Commentary

In the United States this year, approximately 288,300 men will be newly diagnosed with prostate cancer and about 34,700 men will die from this disease. It is the second leading cause of cancer in men, and one out of every eight men will be diagnosed with this cancer at some point in their lives.

As primary care physicians, a large part of our role is to prevent or detect cancers early. Patients look to us for this guidance. However, prostate cancer screening has long been a controversial issue. Earlier this year, the American Urological Association along with the Society of Urologic Oncology published updated guidelines.

Clear recommendations that come from this set of guidelines that are relevant to primary care physicians include:

• using PSA as the screening test of choice.
• repeating PSA in patients with newly elevated results before moving on to other test.
• offering PSA screening every 2-4 years in patients aged 50-69 years.
• offering baseline screening in those between 45-50 years of age.

In high-risk patients, screening can be initiated at 40-45 years of age. All of these recommendations come with the caveat that we give the patient all the pros and cons and leave it up to their “values and preferences.”

The guidelines make recommendations regarding PSA screening and biopsy standards. These guidelines are very specific in their recommendations; however, the question about whether to do PSA screening in the first place is left open to debate. While shared decision-making is important with any testing, it is more difficult with prostate cancer screening. Patients need to understand that there are possible adverse events that can result because of an elevated PSA, such as unneeded biopsies that may come with complications.

The authors of this set of guidelines suggest that physicians talk to patients more often about the benefits of the screening than they do about the negative consequences. This assumes that a negative biopsy result is an unnecessary test, which is not a fair assessment. Negative test results can provide useful clinical information. While a PSA result may lead to a biopsy that could have possibly been avoided, we don’t have any better screening tests available. Missing a prostate cancer that could have been detected by PSA screening is also very harmful. Deciding whether to do PSA screening for any given patient then becomes a difficult question.

More research into biomarkers to detect prostate cancer is needed, as suggested by the guideline authors. As primary care doctors, we’re the first ones to order these tests and make decisions regarding the results. While we may not be the ones to do the biopsies, we do need to know when to refer the patients to specialists or when we can just repeat the test.

Population health is often the benchmark used when looking at screening guidelines. But in the primary care setting, we are responsible for individual patients. Applying guidelines that take whole populations into consideration often doesn’t translate well to single patients. We do need to make them responsible for their own health care decisions but, at the same time, we need to offer them some guidance. If the guidelines are clear, this is easy. When they suggest giving patients all the pros and cons and letting them make their own decision, this is hard. Some of them want us to tell them what to do.

Additionally, patients in the primary care setting develop close relationships with their physicians. They are not an elevated PSA test or a negative biopsy result. They have concerns and fears. When they are high risk, the advice is easy. Keeping in mind that prostate cancer is the second leading cause of cancer in men in the United States, we should have clear screening guidelines, such as we do with mammograms in women. Yes, shared decision-making is important, but we also need to know the answer when our patients ask us whether or not they should have a PSA test done.
 

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J.

In the United States this year, approximately 288,300 men will be newly diagnosed with prostate cancer and about 34,700 men will die from this disease. It is the second leading cause of cancer in men, and one out of every eight men will be diagnosed with this cancer at some point in their lives.

As primary care physicians, a large part of our role is to prevent or detect cancers early. Patients look to us for this guidance. However, prostate cancer screening has long been a controversial issue. Earlier this year, the American Urological Association along with the Society of Urologic Oncology published updated guidelines.

Clear recommendations that come from this set of guidelines that are relevant to primary care physicians include:

• using PSA as the screening test of choice.
• repeating PSA in patients with newly elevated results before moving on to other test.
• offering PSA screening every 2-4 years in patients aged 50-69 years.
• offering baseline screening in those between 45-50 years of age.

In high-risk patients, screening can be initiated at 40-45 years of age. All of these recommendations come with the caveat that we give the patient all the pros and cons and leave it up to their “values and preferences.”

The guidelines make recommendations regarding PSA screening and biopsy standards. These guidelines are very specific in their recommendations; however, the question about whether to do PSA screening in the first place is left open to debate. While shared decision-making is important with any testing, it is more difficult with prostate cancer screening. Patients need to understand that there are possible adverse events that can result because of an elevated PSA, such as unneeded biopsies that may come with complications.

The authors of this set of guidelines suggest that physicians talk to patients more often about the benefits of the screening than they do about the negative consequences. This assumes that a negative biopsy result is an unnecessary test, which is not a fair assessment. Negative test results can provide useful clinical information. While a PSA result may lead to a biopsy that could have possibly been avoided, we don’t have any better screening tests available. Missing a prostate cancer that could have been detected by PSA screening is also very harmful. Deciding whether to do PSA screening for any given patient then becomes a difficult question.

More research into biomarkers to detect prostate cancer is needed, as suggested by the guideline authors. As primary care doctors, we’re the first ones to order these tests and make decisions regarding the results. While we may not be the ones to do the biopsies, we do need to know when to refer the patients to specialists or when we can just repeat the test.

Population health is often the benchmark used when looking at screening guidelines. But in the primary care setting, we are responsible for individual patients. Applying guidelines that take whole populations into consideration often doesn’t translate well to single patients. We do need to make them responsible for their own health care decisions but, at the same time, we need to offer them some guidance. If the guidelines are clear, this is easy. When they suggest giving patients all the pros and cons and letting them make their own decision, this is hard. Some of them want us to tell them what to do.

Additionally, patients in the primary care setting develop close relationships with their physicians. They are not an elevated PSA test or a negative biopsy result. They have concerns and fears. When they are high risk, the advice is easy. Keeping in mind that prostate cancer is the second leading cause of cancer in men in the United States, we should have clear screening guidelines, such as we do with mammograms in women. Yes, shared decision-making is important, but we also need to know the answer when our patients ask us whether or not they should have a PSA test done.
 

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J.

In the United States this year, approximately 288,300 men will be newly diagnosed with prostate cancer and about 34,700 men will die from this disease. It is the second leading cause of cancer in men, and one out of every eight men will be diagnosed with this cancer at some point in their lives.

As primary care physicians, a large part of our role is to prevent or detect cancers early. Patients look to us for this guidance. However, prostate cancer screening has long been a controversial issue. Earlier this year, the American Urological Association along with the Society of Urologic Oncology published updated guidelines.

Clear recommendations that come from this set of guidelines that are relevant to primary care physicians include:

• using PSA as the screening test of choice.
• repeating PSA in patients with newly elevated results before moving on to other test.
• offering PSA screening every 2-4 years in patients aged 50-69 years.
• offering baseline screening in those between 45-50 years of age.

In high-risk patients, screening can be initiated at 40-45 years of age. All of these recommendations come with the caveat that we give the patient all the pros and cons and leave it up to their “values and preferences.”

The guidelines make recommendations regarding PSA screening and biopsy standards. These guidelines are very specific in their recommendations; however, the question about whether to do PSA screening in the first place is left open to debate. While shared decision-making is important with any testing, it is more difficult with prostate cancer screening. Patients need to understand that there are possible adverse events that can result because of an elevated PSA, such as unneeded biopsies that may come with complications.

The authors of this set of guidelines suggest that physicians talk to patients more often about the benefits of the screening than they do about the negative consequences. This assumes that a negative biopsy result is an unnecessary test, which is not a fair assessment. Negative test results can provide useful clinical information. While a PSA result may lead to a biopsy that could have possibly been avoided, we don’t have any better screening tests available. Missing a prostate cancer that could have been detected by PSA screening is also very harmful. Deciding whether to do PSA screening for any given patient then becomes a difficult question.

More research into biomarkers to detect prostate cancer is needed, as suggested by the guideline authors. As primary care doctors, we’re the first ones to order these tests and make decisions regarding the results. While we may not be the ones to do the biopsies, we do need to know when to refer the patients to specialists or when we can just repeat the test.

Population health is often the benchmark used when looking at screening guidelines. But in the primary care setting, we are responsible for individual patients. Applying guidelines that take whole populations into consideration often doesn’t translate well to single patients. We do need to make them responsible for their own health care decisions but, at the same time, we need to offer them some guidance. If the guidelines are clear, this is easy. When they suggest giving patients all the pros and cons and letting them make their own decision, this is hard. Some of them want us to tell them what to do.

Additionally, patients in the primary care setting develop close relationships with their physicians. They are not an elevated PSA test or a negative biopsy result. They have concerns and fears. When they are high risk, the advice is easy. Keeping in mind that prostate cancer is the second leading cause of cancer in men in the United States, we should have clear screening guidelines, such as we do with mammograms in women. Yes, shared decision-making is important, but we also need to know the answer when our patients ask us whether or not they should have a PSA test done.
 

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J.

It is difficult to go through any publication or website these days without finding an article about artificial intelligence (AI). Many discuss its current status, while others speculate on potential future applications. Often, AI is described as an “existential threat to human health” by commentators who aren’t even aware of the definition of that term as Kierkegaard conceived it, the role of the individual to breathe meaning into life. Others characterize such cataclysmic predictions as “overblown and misdirected”.

The long-term potential for abuse of AI requires discussion, and should be addressed by policy makers, but that is beyond the scope of this column.

Meanwhile, there are many near-term opportunities for AI to improve health care and reduce tedious and time consuming tasks. Specifically, some AI-based tools are available to use in your office right now, with no “existential” threat to anybody.

The most popular current AI-based medical applications are automated scribes. They transcribe live consultations between physician and patient automatically and create a searchable report, plus notes for charts and billing.

I’ve written about AI scribes before, but the quality and user-friendliness of these products have improved dramatically in recent years. Language processing capabilities now permit you to speak naturally, without having to memorize specific commands. Some scribes can mimic your writing style based on sample notes that you enter into the system. Others allow you to integrate your own knowledge base, or a bibliography of research studies. With some systems, you can dictate notes directly into most EHR software, ask questions regarding medication dosages, or access a patient’s medical history from hospitals or other offices.

Current popular medical scribe products include DeepCura, DeepScribe, Nuance, Suki, Augmedix, Tali AI, Iodine Software, and ScribeLink. Amazon Web Services recently launched its own product, HealthScribe, as well. (As always, I have no financial interest in any product or service mentioned in this column.)

AI scribes aren’t entirely autonomous, of course; you need to read the output and check for potential inaccuracies. Still, users claim that they substantially reduce documentation and charting time, permitting more patient visits and less after-hours work.

AI can also be used to provide useful content for your patients. If you are not particularly good at writing, or don’t have the time for it, generative algorithms like the much-vaunted ChatGPT can generate posts, FAQs, and other informational content for your website, blog, or social media pages. You can ask for ideas about timely health topics and write general information articles, or create content specific to your location or specialty. You can use it to write emails informing your patients about upcoming office events or educate them on a range of topics, from getting their annual flu shots to scheduling regular screening skin exams.

With some of the same techniques and additional software, you can create entire videos for your website at a fraction of the cost of hiring a video production team. After using ChatGPT to write the content – for example, a 5-minute script on the importance of sunscreen in preventing skin cancer – you can employ a text-to-speech algorithm such as Revoicer to transform the script into audio content, and then a preproduction algorithm like Yepic or Synthesia to generate a video with a synthetic human. 

If you are unhappy with your current online presence, you can use AI to create an entire website. Through a series of questions, AI website builders such as Wix ADI, Jimdo, Hostinger, and 10Web gather all the information needed to set up a website draft that is already personalized with medical-specific content. Most offer the option to connect to Instagram, Facebook, Google My Business, and similar sites, to which they can import your office’s logo, images, and descriptive texts.

Some of them are capable of pulling up responsive site pages that automatically adjust to the device – mobile or computer – that the visitor is using. This is important, as I’ve written before, because more than half of all searches for doctors are now made on smartphones, so the more “mobile friendly” your site is, the higher it will be ranked. You can test how easily a visitor can use your website on a mobile device with Google’s free Mobile-Friendly Test.

If you give talks at medical meetings, you know how cumbersome and time-consuming it can be to create Powerpoint presentations. Once again, AI can save you time and trouble. Presentation designers such as Presentations.AI, Deck Robot, iA Presenter, and Beautiful.AI can assemble very acceptable presentations from your primary inputs. You typically choose a template, input your basic data, and AI will format the slides and offer you visuals, animations, voice-overs, and other fancy features. You will also have flexibility in changing segments or images or sizes you don’t like.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

It is difficult to go through any publication or website these days without finding an article about artificial intelligence (AI). Many discuss its current status, while others speculate on potential future applications. Often, AI is described as an “existential threat to human health” by commentators who aren’t even aware of the definition of that term as Kierkegaard conceived it, the role of the individual to breathe meaning into life. Others characterize such cataclysmic predictions as “overblown and misdirected”.

The long-term potential for abuse of AI requires discussion, and should be addressed by policy makers, but that is beyond the scope of this column.

Meanwhile, there are many near-term opportunities for AI to improve health care and reduce tedious and time consuming tasks. Specifically, some AI-based tools are available to use in your office right now, with no “existential” threat to anybody.

The most popular current AI-based medical applications are automated scribes. They transcribe live consultations between physician and patient automatically and create a searchable report, plus notes for charts and billing.

I’ve written about AI scribes before, but the quality and user-friendliness of these products have improved dramatically in recent years. Language processing capabilities now permit you to speak naturally, without having to memorize specific commands. Some scribes can mimic your writing style based on sample notes that you enter into the system. Others allow you to integrate your own knowledge base, or a bibliography of research studies. With some systems, you can dictate notes directly into most EHR software, ask questions regarding medication dosages, or access a patient’s medical history from hospitals or other offices.

Current popular medical scribe products include DeepCura, DeepScribe, Nuance, Suki, Augmedix, Tali AI, Iodine Software, and ScribeLink. Amazon Web Services recently launched its own product, HealthScribe, as well. (As always, I have no financial interest in any product or service mentioned in this column.)

AI scribes aren’t entirely autonomous, of course; you need to read the output and check for potential inaccuracies. Still, users claim that they substantially reduce documentation and charting time, permitting more patient visits and less after-hours work.

AI can also be used to provide useful content for your patients. If you are not particularly good at writing, or don’t have the time for it, generative algorithms like the much-vaunted ChatGPT can generate posts, FAQs, and other informational content for your website, blog, or social media pages. You can ask for ideas about timely health topics and write general information articles, or create content specific to your location or specialty. You can use it to write emails informing your patients about upcoming office events or educate them on a range of topics, from getting their annual flu shots to scheduling regular screening skin exams.

With some of the same techniques and additional software, you can create entire videos for your website at a fraction of the cost of hiring a video production team. After using ChatGPT to write the content – for example, a 5-minute script on the importance of sunscreen in preventing skin cancer – you can employ a text-to-speech algorithm such as Revoicer to transform the script into audio content, and then a preproduction algorithm like Yepic or Synthesia to generate a video with a synthetic human. 

If you are unhappy with your current online presence, you can use AI to create an entire website. Through a series of questions, AI website builders such as Wix ADI, Jimdo, Hostinger, and 10Web gather all the information needed to set up a website draft that is already personalized with medical-specific content. Most offer the option to connect to Instagram, Facebook, Google My Business, and similar sites, to which they can import your office’s logo, images, and descriptive texts.

Some of them are capable of pulling up responsive site pages that automatically adjust to the device – mobile or computer – that the visitor is using. This is important, as I’ve written before, because more than half of all searches for doctors are now made on smartphones, so the more “mobile friendly” your site is, the higher it will be ranked. You can test how easily a visitor can use your website on a mobile device with Google’s free Mobile-Friendly Test.

If you give talks at medical meetings, you know how cumbersome and time-consuming it can be to create Powerpoint presentations. Once again, AI can save you time and trouble. Presentation designers such as Presentations.AI, Deck Robot, iA Presenter, and Beautiful.AI can assemble very acceptable presentations from your primary inputs. You typically choose a template, input your basic data, and AI will format the slides and offer you visuals, animations, voice-overs, and other fancy features. You will also have flexibility in changing segments or images or sizes you don’t like.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

It is difficult to go through any publication or website these days without finding an article about artificial intelligence (AI). Many discuss its current status, while others speculate on potential future applications. Often, AI is described as an “existential threat to human health” by commentators who aren’t even aware of the definition of that term as Kierkegaard conceived it, the role of the individual to breathe meaning into life. Others characterize such cataclysmic predictions as “overblown and misdirected”.

The long-term potential for abuse of AI requires discussion, and should be addressed by policy makers, but that is beyond the scope of this column.

Meanwhile, there are many near-term opportunities for AI to improve health care and reduce tedious and time consuming tasks. Specifically, some AI-based tools are available to use in your office right now, with no “existential” threat to anybody.

The most popular current AI-based medical applications are automated scribes. They transcribe live consultations between physician and patient automatically and create a searchable report, plus notes for charts and billing.

I’ve written about AI scribes before, but the quality and user-friendliness of these products have improved dramatically in recent years. Language processing capabilities now permit you to speak naturally, without having to memorize specific commands. Some scribes can mimic your writing style based on sample notes that you enter into the system. Others allow you to integrate your own knowledge base, or a bibliography of research studies. With some systems, you can dictate notes directly into most EHR software, ask questions regarding medication dosages, or access a patient’s medical history from hospitals or other offices.

Current popular medical scribe products include DeepCura, DeepScribe, Nuance, Suki, Augmedix, Tali AI, Iodine Software, and ScribeLink. Amazon Web Services recently launched its own product, HealthScribe, as well. (As always, I have no financial interest in any product or service mentioned in this column.)

AI scribes aren’t entirely autonomous, of course; you need to read the output and check for potential inaccuracies. Still, users claim that they substantially reduce documentation and charting time, permitting more patient visits and less after-hours work.

AI can also be used to provide useful content for your patients. If you are not particularly good at writing, or don’t have the time for it, generative algorithms like the much-vaunted ChatGPT can generate posts, FAQs, and other informational content for your website, blog, or social media pages. You can ask for ideas about timely health topics and write general information articles, or create content specific to your location or specialty. You can use it to write emails informing your patients about upcoming office events or educate them on a range of topics, from getting their annual flu shots to scheduling regular screening skin exams.

With some of the same techniques and additional software, you can create entire videos for your website at a fraction of the cost of hiring a video production team. After using ChatGPT to write the content – for example, a 5-minute script on the importance of sunscreen in preventing skin cancer – you can employ a text-to-speech algorithm such as Revoicer to transform the script into audio content, and then a preproduction algorithm like Yepic or Synthesia to generate a video with a synthetic human. 

If you are unhappy with your current online presence, you can use AI to create an entire website. Through a series of questions, AI website builders such as Wix ADI, Jimdo, Hostinger, and 10Web gather all the information needed to set up a website draft that is already personalized with medical-specific content. Most offer the option to connect to Instagram, Facebook, Google My Business, and similar sites, to which they can import your office’s logo, images, and descriptive texts.

Some of them are capable of pulling up responsive site pages that automatically adjust to the device – mobile or computer – that the visitor is using. This is important, as I’ve written before, because more than half of all searches for doctors are now made on smartphones, so the more “mobile friendly” your site is, the higher it will be ranked. You can test how easily a visitor can use your website on a mobile device with Google’s free Mobile-Friendly Test.

If you give talks at medical meetings, you know how cumbersome and time-consuming it can be to create Powerpoint presentations. Once again, AI can save you time and trouble. Presentation designers such as Presentations.AI, Deck Robot, iA Presenter, and Beautiful.AI can assemble very acceptable presentations from your primary inputs. You typically choose a template, input your basic data, and AI will format the slides and offer you visuals, animations, voice-overs, and other fancy features. You will also have flexibility in changing segments or images or sizes you don’t like.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Recently, my office received several phone calls from patients asking if I perform “trap tox.” Having not been on social media around that time, I assumed the term had something to do with botulinum toxin and the trapezius muscle, but I had never heard it before. Not too long afterwards, patients were asking me about it in the office, using the same terminology, and I had several calls about it in one day. When I asked one trusted patient where she’d heard this term, which seemed to be trending, she told me that she had seen it on Instagram, as an ad or a “suggested for you” post.

Whether it’s a different name or term for a cosmetic procedure or laser we use that I’ve never heard before – such as “lip flip” or trap tox (also known as “Barbie Botox”) – many of these trendy terms spread like wildfire on social media. Some of the terms may be marketing tools started and spread by doctors who perform aesthetic procedures, something I don’t recommend as it only creates confusion for patients and practitioners, similar to the confusion consumers face regarding the plethora of over-the-counter skin care options and the marketing terms used for them. Other terms and trends are also started by nonphysician or non–professionally trained providers, sometimes leading to an unsafe or misleading term for an aesthetic procedure.

Over the past few years, several articles about the impact of social media in aesthetics have been published. In one recent paper, published in 2022, Boen and Jerdan noted that 72% of people in the United States use social media, up from 5% of American adults in 2005. In the United States, they note, “YouTube is the most popular platform with 73% of adult users, followed by Facebook (69%), Instagram (37%), SnapChat (24%), and Twitter (22%). Of the sites used daily, Facebook has the most activity (74%), followed by Instagram (64%), SnapChat (63%), YouTube (51%), and Twitter (42%).” They argue that the pros of social media in aesthetic medicine include its use as an educational tool by medical professionals to educate and provide accurate information about cosmetic procedures, and that “providing factual and evidence-based medical information to the public can help to counteract the abundant misinformation that is out there.” The cons include misinformation, no credentialing verification of the provider of the information – essentially anyone can be an “influencer” – as well as the addictive nature of social media for the consumer.

Along the same lines, younger patients tend to rely more on social media in choosing treatments and providers, further perpetuating any anxiety created from misinformation and unrealistic expectations from nonmedical influencers regarding procedures, filters used on photographs, photo editing, etc., in achieving an aesthetic result.

Physicians, particularly fellowship-trained aesthetic and surgical dermatologists, plastic and reconstructive surgeons, oculoplastic surgeons, and ENT facial plastic surgeons, who have the most training, knowledge, and expertise about aesthetic procedures, often have the least amount of time to devote to education via social media, compared with nonmedical influencers. Unless sponsored, they are also not being compensated for using it as an educational tool, except for potential indirect compensation from using it as a marketing tool for themselves and their practices. In contrast, nonmedical influencers often have many followers and time to create content, and in some cases, this is their full-time job.

All in all, most authors agree that social media has been associated with an increased acceptance of cosmetic surgery and procedures. Whether it be a trend seen on social media, or viewing one’s appearance in a filtered or photoediting app, or seeing an image of how another person looks (similar to how people in magazines, films and on television, were viewed in the past), social media has piqued people’s interest in aesthetics. It remains a balance for interested physicians to help keep information about cosmetic procedures presented in a healthy, interesting, professional, and accurate manner, and in a non–time-consuming way.

Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to her at [email protected]. She had no relevant disclosures.
 

References

Boen M and Jerdan K. Clin Dermatol. 2022 Jan-Feb;40(1):45-8.

Chen J et al. JAMA Facial Plast Surg. 2019 Sep 1;21(5):361-7.

Chopan M et al. Plast Reconstr Surg. 2019 Apr;143(4):1259-65.

Recently, my office received several phone calls from patients asking if I perform “trap tox.” Having not been on social media around that time, I assumed the term had something to do with botulinum toxin and the trapezius muscle, but I had never heard it before. Not too long afterwards, patients were asking me about it in the office, using the same terminology, and I had several calls about it in one day. When I asked one trusted patient where she’d heard this term, which seemed to be trending, she told me that she had seen it on Instagram, as an ad or a “suggested for you” post.

Whether it’s a different name or term for a cosmetic procedure or laser we use that I’ve never heard before – such as “lip flip” or trap tox (also known as “Barbie Botox”) – many of these trendy terms spread like wildfire on social media. Some of the terms may be marketing tools started and spread by doctors who perform aesthetic procedures, something I don’t recommend as it only creates confusion for patients and practitioners, similar to the confusion consumers face regarding the plethora of over-the-counter skin care options and the marketing terms used for them. Other terms and trends are also started by nonphysician or non–professionally trained providers, sometimes leading to an unsafe or misleading term for an aesthetic procedure.

Over the past few years, several articles about the impact of social media in aesthetics have been published. In one recent paper, published in 2022, Boen and Jerdan noted that 72% of people in the United States use social media, up from 5% of American adults in 2005. In the United States, they note, “YouTube is the most popular platform with 73% of adult users, followed by Facebook (69%), Instagram (37%), SnapChat (24%), and Twitter (22%). Of the sites used daily, Facebook has the most activity (74%), followed by Instagram (64%), SnapChat (63%), YouTube (51%), and Twitter (42%).” They argue that the pros of social media in aesthetic medicine include its use as an educational tool by medical professionals to educate and provide accurate information about cosmetic procedures, and that “providing factual and evidence-based medical information to the public can help to counteract the abundant misinformation that is out there.” The cons include misinformation, no credentialing verification of the provider of the information – essentially anyone can be an “influencer” – as well as the addictive nature of social media for the consumer.

Along the same lines, younger patients tend to rely more on social media in choosing treatments and providers, further perpetuating any anxiety created from misinformation and unrealistic expectations from nonmedical influencers regarding procedures, filters used on photographs, photo editing, etc., in achieving an aesthetic result.

Physicians, particularly fellowship-trained aesthetic and surgical dermatologists, plastic and reconstructive surgeons, oculoplastic surgeons, and ENT facial plastic surgeons, who have the most training, knowledge, and expertise about aesthetic procedures, often have the least amount of time to devote to education via social media, compared with nonmedical influencers. Unless sponsored, they are also not being compensated for using it as an educational tool, except for potential indirect compensation from using it as a marketing tool for themselves and their practices. In contrast, nonmedical influencers often have many followers and time to create content, and in some cases, this is their full-time job.

All in all, most authors agree that social media has been associated with an increased acceptance of cosmetic surgery and procedures. Whether it be a trend seen on social media, or viewing one’s appearance in a filtered or photoediting app, or seeing an image of how another person looks (similar to how people in magazines, films and on television, were viewed in the past), social media has piqued people’s interest in aesthetics. It remains a balance for interested physicians to help keep information about cosmetic procedures presented in a healthy, interesting, professional, and accurate manner, and in a non–time-consuming way.

Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to her at [email protected]. She had no relevant disclosures.
 

References

Boen M and Jerdan K. Clin Dermatol. 2022 Jan-Feb;40(1):45-8.

Chen J et al. JAMA Facial Plast Surg. 2019 Sep 1;21(5):361-7.

Chopan M et al. Plast Reconstr Surg. 2019 Apr;143(4):1259-65.

Recently, my office received several phone calls from patients asking if I perform “trap tox.” Having not been on social media around that time, I assumed the term had something to do with botulinum toxin and the trapezius muscle, but I had never heard it before. Not too long afterwards, patients were asking me about it in the office, using the same terminology, and I had several calls about it in one day. When I asked one trusted patient where she’d heard this term, which seemed to be trending, she told me that she had seen it on Instagram, as an ad or a “suggested for you” post.

Whether it’s a different name or term for a cosmetic procedure or laser we use that I’ve never heard before – such as “lip flip” or trap tox (also known as “Barbie Botox”) – many of these trendy terms spread like wildfire on social media. Some of the terms may be marketing tools started and spread by doctors who perform aesthetic procedures, something I don’t recommend as it only creates confusion for patients and practitioners, similar to the confusion consumers face regarding the plethora of over-the-counter skin care options and the marketing terms used for them. Other terms and trends are also started by nonphysician or non–professionally trained providers, sometimes leading to an unsafe or misleading term for an aesthetic procedure.

Over the past few years, several articles about the impact of social media in aesthetics have been published. In one recent paper, published in 2022, Boen and Jerdan noted that 72% of people in the United States use social media, up from 5% of American adults in 2005. In the United States, they note, “YouTube is the most popular platform with 73% of adult users, followed by Facebook (69%), Instagram (37%), SnapChat (24%), and Twitter (22%). Of the sites used daily, Facebook has the most activity (74%), followed by Instagram (64%), SnapChat (63%), YouTube (51%), and Twitter (42%).” They argue that the pros of social media in aesthetic medicine include its use as an educational tool by medical professionals to educate and provide accurate information about cosmetic procedures, and that “providing factual and evidence-based medical information to the public can help to counteract the abundant misinformation that is out there.” The cons include misinformation, no credentialing verification of the provider of the information – essentially anyone can be an “influencer” – as well as the addictive nature of social media for the consumer.

Along the same lines, younger patients tend to rely more on social media in choosing treatments and providers, further perpetuating any anxiety created from misinformation and unrealistic expectations from nonmedical influencers regarding procedures, filters used on photographs, photo editing, etc., in achieving an aesthetic result.

Physicians, particularly fellowship-trained aesthetic and surgical dermatologists, plastic and reconstructive surgeons, oculoplastic surgeons, and ENT facial plastic surgeons, who have the most training, knowledge, and expertise about aesthetic procedures, often have the least amount of time to devote to education via social media, compared with nonmedical influencers. Unless sponsored, they are also not being compensated for using it as an educational tool, except for potential indirect compensation from using it as a marketing tool for themselves and their practices. In contrast, nonmedical influencers often have many followers and time to create content, and in some cases, this is their full-time job.

All in all, most authors agree that social media has been associated with an increased acceptance of cosmetic surgery and procedures. Whether it be a trend seen on social media, or viewing one’s appearance in a filtered or photoediting app, or seeing an image of how another person looks (similar to how people in magazines, films and on television, were viewed in the past), social media has piqued people’s interest in aesthetics. It remains a balance for interested physicians to help keep information about cosmetic procedures presented in a healthy, interesting, professional, and accurate manner, and in a non–time-consuming way.

Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to her at [email protected]. She had no relevant disclosures.
 

References

Boen M and Jerdan K. Clin Dermatol. 2022 Jan-Feb;40(1):45-8.

Chen J et al. JAMA Facial Plast Surg. 2019 Sep 1;21(5):361-7.

Chopan M et al. Plast Reconstr Surg. 2019 Apr;143(4):1259-65.

This transcript has been edited for clarity.

Today, I’d like to talk about private parts. You know: the genitals, down there.

I hate all of that. I really wish that we can get to a place where we can talk about genitals and sexual health the same way we do about high blood pressure and diabetes. In fact, when a new patient comes in and they get a new diagnosis of diabetes, you spend time explaining to them how their pancreas works. I don’t remember all the details because I’m a urologist. But you explain the details of diabetes, how it works, why therapy is important, and how it’s very important for quality of life.

I would like us to take that same understanding of anatomy and physiology and use it to explain to patients how their sexual health works because when they understand it, they then have the tools to make it better. I say to patients, “You have to know what parts you have in order to figure out how they drive, right?” We want them to drive better.

Let me give you an example. Many men come to see me with complaints of erectile dysfunction. They refuse to take sildenafil and tadalafil (Viagra and Cialis), saying, “Oh my gosh, those are magic pills. I won’t be a man if take them.” We all know that doesn’t make any sense. I explain to them how their penis works: “Your penis is a muscle. The muscle does two things. It contracts and it relaxes, just like your bicep. It’s just that your penis muscle is smooth muscle, which means it responds to fight or flight. It’s on the autonomic nervous system.”

I explain that if the muscle of the penis is relaxed, it fills with blood and expands. It gets big and hard, and it traps the blood. But when the muscles of the penis are contracted, when they are tight, it squeezes out all the blood, like squeezing out a sponge. So the important thing to do if you want to have good erections is to get the muscles to relax. Relaxed muscle increases erections. I get them to understand that sildenafil and tadalafil are phosphodiesterase 5 inhibitors: smooth-muscle relaxants. Instead of saying, “I need to take Viagra or Cialis because I’m broken,” it’s, “Oh hey honey, I need to take my muscle relaxants because my muscles aren’t working the way that they used to.”

In the future, I’ll go into what happens in erectile dysfunction. We’ll go into what can happen with erectile dysfunction and the many reasons why it happens. It’s getting them to understand that if we get the muscles to relax, you will have better erections. This is how the penis works. It’s why the medicine works. The patients will actually try the therapy and they’ll feel so much better about it. They’ll say, “Oh my gosh, this makes so much sense.” They work on their mental muscles to get the muscles of the penis to relax. Understanding anatomy and physiology helps them understand the treatments, which leads to better outcomes.

How about the female side? If a woman comes to see me reporting that she can’t have an orgasm, part of it is education and understanding the anatomy and physiology. The clitoris and the penis are exactly the same thing. The head of the clitoris and the head of the penis are the same. The clitoris has legs that go all the way down to the butt bone. So everyone is sitting on their genitals right now. The butt bones connect to the bottom of the clitoris or the bottom of the penis. They each have legs called crura. When you get patients to understand where their anatomy is and how it functions, they will then understand how to maximize their quality of life.

The clitoris has smooth muscle just like the penis. When that smooth muscle relaxes, it gorges with blood. When you stimulate it, it can lead to orgasm for most people. But, wait a minute. The clitoris is not inside the vagina. It’s outside. It’s behind the labia majora. If you follow the labia minora up, you get to the head of the clitoris. If patients understand that, they then will understand that penetration is not the way the majority of people orgasm.

I love pictures. I show everyone pictures in my office. They help patients to understand why vibration or outside stimulation on the vulva will allow orgasm to happen. And so instead of patients coming in saying, “I’m broken, I can’t orgasm from penetration,” or, “Dr. Rubin, I’m broken because I can’t get erections,” getting them to understand the anatomy and physiology helps them understand the treatment.

As we go forward, I’ll talk more about anatomy and physiology and how to increase the sexual health of our patients. For now though, please stop calling them private parts. Please use your understanding of anatomy and physiology to educate your patients to have better sexual health and higher quality of life. You may be the only clinician to ever do so, and it will make their life so much better.

Dr. Rubin is an assistant clinical professor, department of urology, at Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Today, I’d like to talk about private parts. You know: the genitals, down there.

I hate all of that. I really wish that we can get to a place where we can talk about genitals and sexual health the same way we do about high blood pressure and diabetes. In fact, when a new patient comes in and they get a new diagnosis of diabetes, you spend time explaining to them how their pancreas works. I don’t remember all the details because I’m a urologist. But you explain the details of diabetes, how it works, why therapy is important, and how it’s very important for quality of life.

I would like us to take that same understanding of anatomy and physiology and use it to explain to patients how their sexual health works because when they understand it, they then have the tools to make it better. I say to patients, “You have to know what parts you have in order to figure out how they drive, right?” We want them to drive better.

Let me give you an example. Many men come to see me with complaints of erectile dysfunction. They refuse to take sildenafil and tadalafil (Viagra and Cialis), saying, “Oh my gosh, those are magic pills. I won’t be a man if take them.” We all know that doesn’t make any sense. I explain to them how their penis works: “Your penis is a muscle. The muscle does two things. It contracts and it relaxes, just like your bicep. It’s just that your penis muscle is smooth muscle, which means it responds to fight or flight. It’s on the autonomic nervous system.”

I explain that if the muscle of the penis is relaxed, it fills with blood and expands. It gets big and hard, and it traps the blood. But when the muscles of the penis are contracted, when they are tight, it squeezes out all the blood, like squeezing out a sponge. So the important thing to do if you want to have good erections is to get the muscles to relax. Relaxed muscle increases erections. I get them to understand that sildenafil and tadalafil are phosphodiesterase 5 inhibitors: smooth-muscle relaxants. Instead of saying, “I need to take Viagra or Cialis because I’m broken,” it’s, “Oh hey honey, I need to take my muscle relaxants because my muscles aren’t working the way that they used to.”

In the future, I’ll go into what happens in erectile dysfunction. We’ll go into what can happen with erectile dysfunction and the many reasons why it happens. It’s getting them to understand that if we get the muscles to relax, you will have better erections. This is how the penis works. It’s why the medicine works. The patients will actually try the therapy and they’ll feel so much better about it. They’ll say, “Oh my gosh, this makes so much sense.” They work on their mental muscles to get the muscles of the penis to relax. Understanding anatomy and physiology helps them understand the treatments, which leads to better outcomes.

How about the female side? If a woman comes to see me reporting that she can’t have an orgasm, part of it is education and understanding the anatomy and physiology. The clitoris and the penis are exactly the same thing. The head of the clitoris and the head of the penis are the same. The clitoris has legs that go all the way down to the butt bone. So everyone is sitting on their genitals right now. The butt bones connect to the bottom of the clitoris or the bottom of the penis. They each have legs called crura. When you get patients to understand where their anatomy is and how it functions, they will then understand how to maximize their quality of life.

The clitoris has smooth muscle just like the penis. When that smooth muscle relaxes, it gorges with blood. When you stimulate it, it can lead to orgasm for most people. But, wait a minute. The clitoris is not inside the vagina. It’s outside. It’s behind the labia majora. If you follow the labia minora up, you get to the head of the clitoris. If patients understand that, they then will understand that penetration is not the way the majority of people orgasm.

I love pictures. I show everyone pictures in my office. They help patients to understand why vibration or outside stimulation on the vulva will allow orgasm to happen. And so instead of patients coming in saying, “I’m broken, I can’t orgasm from penetration,” or, “Dr. Rubin, I’m broken because I can’t get erections,” getting them to understand the anatomy and physiology helps them understand the treatment.

As we go forward, I’ll talk more about anatomy and physiology and how to increase the sexual health of our patients. For now though, please stop calling them private parts. Please use your understanding of anatomy and physiology to educate your patients to have better sexual health and higher quality of life. You may be the only clinician to ever do so, and it will make their life so much better.

Dr. Rubin is an assistant clinical professor, department of urology, at Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Today, I’d like to talk about private parts. You know: the genitals, down there.

I hate all of that. I really wish that we can get to a place where we can talk about genitals and sexual health the same way we do about high blood pressure and diabetes. In fact, when a new patient comes in and they get a new diagnosis of diabetes, you spend time explaining to them how their pancreas works. I don’t remember all the details because I’m a urologist. But you explain the details of diabetes, how it works, why therapy is important, and how it’s very important for quality of life.

I would like us to take that same understanding of anatomy and physiology and use it to explain to patients how their sexual health works because when they understand it, they then have the tools to make it better. I say to patients, “You have to know what parts you have in order to figure out how they drive, right?” We want them to drive better.

Let me give you an example. Many men come to see me with complaints of erectile dysfunction. They refuse to take sildenafil and tadalafil (Viagra and Cialis), saying, “Oh my gosh, those are magic pills. I won’t be a man if take them.” We all know that doesn’t make any sense. I explain to them how their penis works: “Your penis is a muscle. The muscle does two things. It contracts and it relaxes, just like your bicep. It’s just that your penis muscle is smooth muscle, which means it responds to fight or flight. It’s on the autonomic nervous system.”

I explain that if the muscle of the penis is relaxed, it fills with blood and expands. It gets big and hard, and it traps the blood. But when the muscles of the penis are contracted, when they are tight, it squeezes out all the blood, like squeezing out a sponge. So the important thing to do if you want to have good erections is to get the muscles to relax. Relaxed muscle increases erections. I get them to understand that sildenafil and tadalafil are phosphodiesterase 5 inhibitors: smooth-muscle relaxants. Instead of saying, “I need to take Viagra or Cialis because I’m broken,” it’s, “Oh hey honey, I need to take my muscle relaxants because my muscles aren’t working the way that they used to.”

In the future, I’ll go into what happens in erectile dysfunction. We’ll go into what can happen with erectile dysfunction and the many reasons why it happens. It’s getting them to understand that if we get the muscles to relax, you will have better erections. This is how the penis works. It’s why the medicine works. The patients will actually try the therapy and they’ll feel so much better about it. They’ll say, “Oh my gosh, this makes so much sense.” They work on their mental muscles to get the muscles of the penis to relax. Understanding anatomy and physiology helps them understand the treatments, which leads to better outcomes.

How about the female side? If a woman comes to see me reporting that she can’t have an orgasm, part of it is education and understanding the anatomy and physiology. The clitoris and the penis are exactly the same thing. The head of the clitoris and the head of the penis are the same. The clitoris has legs that go all the way down to the butt bone. So everyone is sitting on their genitals right now. The butt bones connect to the bottom of the clitoris or the bottom of the penis. They each have legs called crura. When you get patients to understand where their anatomy is and how it functions, they will then understand how to maximize their quality of life.

The clitoris has smooth muscle just like the penis. When that smooth muscle relaxes, it gorges with blood. When you stimulate it, it can lead to orgasm for most people. But, wait a minute. The clitoris is not inside the vagina. It’s outside. It’s behind the labia majora. If you follow the labia minora up, you get to the head of the clitoris. If patients understand that, they then will understand that penetration is not the way the majority of people orgasm.

I love pictures. I show everyone pictures in my office. They help patients to understand why vibration or outside stimulation on the vulva will allow orgasm to happen. And so instead of patients coming in saying, “I’m broken, I can’t orgasm from penetration,” or, “Dr. Rubin, I’m broken because I can’t get erections,” getting them to understand the anatomy and physiology helps them understand the treatment.

As we go forward, I’ll talk more about anatomy and physiology and how to increase the sexual health of our patients. For now though, please stop calling them private parts. Please use your understanding of anatomy and physiology to educate your patients to have better sexual health and higher quality of life. You may be the only clinician to ever do so, and it will make their life so much better.

Dr. Rubin is an assistant clinical professor, department of urology, at Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

A version of this article first appeared on Medscape.com.

David Nichols, PhD, a leading expert in the field of psychedelic research and the founding president of the Heffter Research Institute, often answers the question, “What is a psychedelic?” by saying, “The scientific definition I always use is that they are substances that produce changes in thought, mood, and affect, which only occur during dreaming or religious exaltation.”^1,2 However, this definition does not account for the experiences of naturally occurring psychoses, such as those seen in schizophrenia.

Lasha Khetsuriani

The phenomenology of psychotic experiences between drug-induced and naturally occurring psychoses differs, and the use of psychedelics does not necessarily replicate or simulate the symptoms of schizophrenia. For example, drug induced hallucinations are often described as more intense and vivid, while those associated with schizophrenia are described as more persistent and distressing.³

An altered state of consciousness is a hallmark of a psychedelic trip, but not a characteristic of schizophrenia. Patients with schizophrenia who have used psychedelics typically report that their experiences under the influence of these drugs are distinct from their usual experiences with the condition. Additionally, according to many experts, the underlying neurobiological mechanisms are different, with psychedelics affecting serotonin receptors and schizophrenia thought to be linked more to dopamine dysregulation, among other factors.

However, there are some instances of naturally occurring psychoses that are difficult to distinguish from the experiences reported by those who take psychedelics. This article explores the similarities between psychedelic experiences induced by serotonergic psychedelics, 5-HT2A agonists, such as LSD, psilocybin, and mescaline, and a rare psychiatric disorder known as the “oneiroid state.”
 

Origins and definitions

The term “oneiroia” is derived from the Greek words for “sleep” and “similar,” referring to the dreamlike character of the condition. It is widely acknowledged that psychedelics can temporarily induce dreamlike states,⁴ but this article focuses specifically on the naturally occurring, endogenous dreamlike state.

Oneiroid state was first described by German psychiatrist Wilhelm Mayer-Gross in the early 20th century and was once well-known among European psychiatrists. Some classified it as a part of schizophrenia, others saw it as an unusual manifestation of affective disorder, and still others considered it an atypical psychosis. Nevertheless, this phenomenon has received limited attention in American psychiatric journals.

The key characteristic of this condition is a distinctive state of consciousness marked by vivid and florid hallucinations, and a succession of constantly shifting dreamlike or surrealistic visuals and imagery often similar to mystical or cosmic experiences. Self-awareness and orientation in time and place are often disturbed, and delusions are experienced within this altered state.⁵

To gain a better understanding of the oneiroid state, it may be helpful to turn to European or other schools of psychiatry with a history of studying this phenomenon, as American psychiatry has limited knowledge in this area.

As described in the “Handbook of Psychiatry” by Russian psychiatrist A.V. Snezhnevsky, published in 1983, oneiroid state, also known as oneiroid syndrome, is a dreamlike and imaginative state characterized by a bizarre combination of reality and vivid phantasmagoric imaginations.⁶ In this state, individuals are completely detached from their surroundings and experience a change in self-awareness, often displaying either a lack of movement or senseless excitement.

Patients often experience the oneiroid state as active participants, as if they are in a movie theater, not only watching the story, but also being part of it, reacting to it with either “external immobility” or senseless excitement, completely detached from their surroundings. This is similar to the portrayal of the emotions of the characters in Steven Spielberg’s film “Ready Player One.”

The entry in Dr. Snezhnevsky’s “Handbook” states: “Some patients in Oneiroid State experience travels to other worlds, such as interacting with inhabitants on Mars, collecting gems on the moon, exploring invisible cities, participating in conspiracies and insurrections, fighting with pirates, chasing The Flying Dutchman, wandering through ancient Rome, and even visiting heaven or hell. At times, the patient’s imagination reaches a state of mystical contemplation.”⁶

In contrast to delirium, which never impairs self-awareness, oneiroid state is marked by drastic changes in the sense of self. The memory of the subjective experience during the oneiroia is much more vivid and consistent than in delirium. Patients who have experienced the oneiroid state often have complete recall of their experience, as if they have just woken up from a dream.

It was commonly thought that oneiroid state was part of the group of functional psychoses, rather than organic psychoses, and was not considered to be a result of mind-altering psychedelics. It was not considered a manifestation of epilepsy either. Oneiroid state could last for weeks or even months, making it unlikely to be related to an epileptic seizure. Furthermore, EEG results did not show any seizurelike activity during the state.

An excellent case study on oneiroid state was published in Israel in 2000. The authors described two patients who experienced the oneiroid state for several days or even weeks.⁷ One of the patients reported that during the illness, he experienced himself aboard a spaceship as a cosmonaut, heading for a different universe. On another occasion, the patient perceived himself as a person living 2,000 years ago and being guilty of Christ’s death.

The second patient reported that everything around her appeared “like in the movies,” and she saw others as characters from comic strips. Both patients alternated between catatonic excitement and sluggishness and would sometimes come back to reality for a few minutes to respond to questions. Physical exams, laboratory tests, neurological tests, and a brain scan were all normal in both cases.
 

Conclusions

As mentioned earlier, oneiroid state is not widely discussed in American psychiatric journals and is now considered a rare condition globally, despite being a common occurrence in the past century. A diagnosis similar to oneiroid state, known as bouffée délirante, is still in use in some French-speaking countries, with a noticeable decline in frequency.^2,8 The widespread acceptance of international classification systems such as the ICD-10, which does not recognize the diagnosis, is likely one of the reasons for this decline.

However, the decrease in the prevalence of the oneiroid state is not unique, as other forms of mental illness, such as the catatonic subtype of schizophrenia, are also becoming less prevalent. The cause of this decline is uncertain. Could changes in the way mental disorders affect 5HT2A receptors be a contributing factor?

In conclusion, as the field of psychedelic research experiences a resurgence, this little-known manifestation of mental illness, oneiroid state, may be worth reexamining.

With the expected approval and regulation of psilocybin and MDMA by the FDA, and classical psychedelics widely regarded as nonaddictive and safer than other recreational drugs, the phenomenological similarity between the naturally occurring impaired consciousness of the oneiroid state and the altered states of consciousness brought about by entheogenic substances should be seen as a possibility for enhanced understanding, rather than as a cause for concern.

Dr. Khetsuriani is a supervising psychiatrist at the Bronx Psychiatric Center in Bronx, N.Y., and has a private psychiatric practice located in Manhattan, N.Y.

References

1. Nichols DE. Keynote address, 39th Telluride Mushroom Festival, Aug. 15-18, 2019. https://www.youtube.com/watch?v=RlDCM5JQzRk.

2. Nichols DE. Psychedelics. Pharmacol Rev. 2016 Apr;68(2):264-355. doi: 10.1124/pr.115.011478.

3. Leptourgos P et al. Hallucinations Under Psychedelics and in the Schizophrenia Spectrum: An Interdisciplinary and Multiscale Comparison. Schizophr Bull. 2020 Dec 1;46(6):1396-1408. doi: 10.1093/schbul/sbaa117.

4. Kraehenmann R. Dreams and Psychedelics: Neurophenomenological Comparison and Therapeutic Implications. Curr Neuropharmacol. 2017;15(7):1032-42. doi: 10.2174/1573413713666170619092629.

5. Henri EY et al. “Acute Delusional Psychosis” in Hirsch SR and Shepherd M, eds. Themes and variations in European psychiatry: An anthology. Charlottesville: University Press of Virginia, 1974.

6. Snezhnevsky A, ed. Handbook of Psychiatry. Moscow: Meditsina, 1983.

7. Kaptsan A et al. Oneiroid syndrome: A concept of use for Western psychiatry. Isr J Psychiatry Relat Sci. 2000;37(4):278-85.

8. https://en.wikipedia.org/wiki/Bouff%C3%A9e_d%C3%A9lirante.

David Nichols, PhD, a leading expert in the field of psychedelic research and the founding president of the Heffter Research Institute, often answers the question, “What is a psychedelic?” by saying, “The scientific definition I always use is that they are substances that produce changes in thought, mood, and affect, which only occur during dreaming or religious exaltation.”^1,2 However, this definition does not account for the experiences of naturally occurring psychoses, such as those seen in schizophrenia.

Lasha Khetsuriani

The phenomenology of psychotic experiences between drug-induced and naturally occurring psychoses differs, and the use of psychedelics does not necessarily replicate or simulate the symptoms of schizophrenia. For example, drug induced hallucinations are often described as more intense and vivid, while those associated with schizophrenia are described as more persistent and distressing.³

An altered state of consciousness is a hallmark of a psychedelic trip, but not a characteristic of schizophrenia. Patients with schizophrenia who have used psychedelics typically report that their experiences under the influence of these drugs are distinct from their usual experiences with the condition. Additionally, according to many experts, the underlying neurobiological mechanisms are different, with psychedelics affecting serotonin receptors and schizophrenia thought to be linked more to dopamine dysregulation, among other factors.

However, there are some instances of naturally occurring psychoses that are difficult to distinguish from the experiences reported by those who take psychedelics. This article explores the similarities between psychedelic experiences induced by serotonergic psychedelics, 5-HT2A agonists, such as LSD, psilocybin, and mescaline, and a rare psychiatric disorder known as the “oneiroid state.”
 

Origins and definitions

The term “oneiroia” is derived from the Greek words for “sleep” and “similar,” referring to the dreamlike character of the condition. It is widely acknowledged that psychedelics can temporarily induce dreamlike states,⁴ but this article focuses specifically on the naturally occurring, endogenous dreamlike state.

Oneiroid state was first described by German psychiatrist Wilhelm Mayer-Gross in the early 20th century and was once well-known among European psychiatrists. Some classified it as a part of schizophrenia, others saw it as an unusual manifestation of affective disorder, and still others considered it an atypical psychosis. Nevertheless, this phenomenon has received limited attention in American psychiatric journals.

The key characteristic of this condition is a distinctive state of consciousness marked by vivid and florid hallucinations, and a succession of constantly shifting dreamlike or surrealistic visuals and imagery often similar to mystical or cosmic experiences. Self-awareness and orientation in time and place are often disturbed, and delusions are experienced within this altered state.⁵

To gain a better understanding of the oneiroid state, it may be helpful to turn to European or other schools of psychiatry with a history of studying this phenomenon, as American psychiatry has limited knowledge in this area.

As described in the “Handbook of Psychiatry” by Russian psychiatrist A.V. Snezhnevsky, published in 1983, oneiroid state, also known as oneiroid syndrome, is a dreamlike and imaginative state characterized by a bizarre combination of reality and vivid phantasmagoric imaginations.⁶ In this state, individuals are completely detached from their surroundings and experience a change in self-awareness, often displaying either a lack of movement or senseless excitement.

Patients often experience the oneiroid state as active participants, as if they are in a movie theater, not only watching the story, but also being part of it, reacting to it with either “external immobility” or senseless excitement, completely detached from their surroundings. This is similar to the portrayal of the emotions of the characters in Steven Spielberg’s film “Ready Player One.”

The entry in Dr. Snezhnevsky’s “Handbook” states: “Some patients in Oneiroid State experience travels to other worlds, such as interacting with inhabitants on Mars, collecting gems on the moon, exploring invisible cities, participating in conspiracies and insurrections, fighting with pirates, chasing The Flying Dutchman, wandering through ancient Rome, and even visiting heaven or hell. At times, the patient’s imagination reaches a state of mystical contemplation.”⁶

In contrast to delirium, which never impairs self-awareness, oneiroid state is marked by drastic changes in the sense of self. The memory of the subjective experience during the oneiroia is much more vivid and consistent than in delirium. Patients who have experienced the oneiroid state often have complete recall of their experience, as if they have just woken up from a dream.

It was commonly thought that oneiroid state was part of the group of functional psychoses, rather than organic psychoses, and was not considered to be a result of mind-altering psychedelics. It was not considered a manifestation of epilepsy either. Oneiroid state could last for weeks or even months, making it unlikely to be related to an epileptic seizure. Furthermore, EEG results did not show any seizurelike activity during the state.

An excellent case study on oneiroid state was published in Israel in 2000. The authors described two patients who experienced the oneiroid state for several days or even weeks.⁷ One of the patients reported that during the illness, he experienced himself aboard a spaceship as a cosmonaut, heading for a different universe. On another occasion, the patient perceived himself as a person living 2,000 years ago and being guilty of Christ’s death.

The second patient reported that everything around her appeared “like in the movies,” and she saw others as characters from comic strips. Both patients alternated between catatonic excitement and sluggishness and would sometimes come back to reality for a few minutes to respond to questions. Physical exams, laboratory tests, neurological tests, and a brain scan were all normal in both cases.
 

Conclusions

As mentioned earlier, oneiroid state is not widely discussed in American psychiatric journals and is now considered a rare condition globally, despite being a common occurrence in the past century. A diagnosis similar to oneiroid state, known as bouffée délirante, is still in use in some French-speaking countries, with a noticeable decline in frequency.^2,8 The widespread acceptance of international classification systems such as the ICD-10, which does not recognize the diagnosis, is likely one of the reasons for this decline.

However, the decrease in the prevalence of the oneiroid state is not unique, as other forms of mental illness, such as the catatonic subtype of schizophrenia, are also becoming less prevalent. The cause of this decline is uncertain. Could changes in the way mental disorders affect 5HT2A receptors be a contributing factor?

In conclusion, as the field of psychedelic research experiences a resurgence, this little-known manifestation of mental illness, oneiroid state, may be worth reexamining.

With the expected approval and regulation of psilocybin and MDMA by the FDA, and classical psychedelics widely regarded as nonaddictive and safer than other recreational drugs, the phenomenological similarity between the naturally occurring impaired consciousness of the oneiroid state and the altered states of consciousness brought about by entheogenic substances should be seen as a possibility for enhanced understanding, rather than as a cause for concern.

Dr. Khetsuriani is a supervising psychiatrist at the Bronx Psychiatric Center in Bronx, N.Y., and has a private psychiatric practice located in Manhattan, N.Y.

References

1. Nichols DE. Keynote address, 39th Telluride Mushroom Festival, Aug. 15-18, 2019. https://www.youtube.com/watch?v=RlDCM5JQzRk.

2. Nichols DE. Psychedelics. Pharmacol Rev. 2016 Apr;68(2):264-355. doi: 10.1124/pr.115.011478.

3. Leptourgos P et al. Hallucinations Under Psychedelics and in the Schizophrenia Spectrum: An Interdisciplinary and Multiscale Comparison. Schizophr Bull. 2020 Dec 1;46(6):1396-1408. doi: 10.1093/schbul/sbaa117.

4. Kraehenmann R. Dreams and Psychedelics: Neurophenomenological Comparison and Therapeutic Implications. Curr Neuropharmacol. 2017;15(7):1032-42. doi: 10.2174/1573413713666170619092629.

5. Henri EY et al. “Acute Delusional Psychosis” in Hirsch SR and Shepherd M, eds. Themes and variations in European psychiatry: An anthology. Charlottesville: University Press of Virginia, 1974.

6. Snezhnevsky A, ed. Handbook of Psychiatry. Moscow: Meditsina, 1983.

7. Kaptsan A et al. Oneiroid syndrome: A concept of use for Western psychiatry. Isr J Psychiatry Relat Sci. 2000;37(4):278-85.

8. https://en.wikipedia.org/wiki/Bouff%C3%A9e_d%C3%A9lirante.

David Nichols, PhD, a leading expert in the field of psychedelic research and the founding president of the Heffter Research Institute, often answers the question, “What is a psychedelic?” by saying, “The scientific definition I always use is that they are substances that produce changes in thought, mood, and affect, which only occur during dreaming or religious exaltation.”^1,2 However, this definition does not account for the experiences of naturally occurring psychoses, such as those seen in schizophrenia.

Lasha Khetsuriani

The phenomenology of psychotic experiences between drug-induced and naturally occurring psychoses differs, and the use of psychedelics does not necessarily replicate or simulate the symptoms of schizophrenia. For example, drug induced hallucinations are often described as more intense and vivid, while those associated with schizophrenia are described as more persistent and distressing.³

An altered state of consciousness is a hallmark of a psychedelic trip, but not a characteristic of schizophrenia. Patients with schizophrenia who have used psychedelics typically report that their experiences under the influence of these drugs are distinct from their usual experiences with the condition. Additionally, according to many experts, the underlying neurobiological mechanisms are different, with psychedelics affecting serotonin receptors and schizophrenia thought to be linked more to dopamine dysregulation, among other factors.

However, there are some instances of naturally occurring psychoses that are difficult to distinguish from the experiences reported by those who take psychedelics. This article explores the similarities between psychedelic experiences induced by serotonergic psychedelics, 5-HT2A agonists, such as LSD, psilocybin, and mescaline, and a rare psychiatric disorder known as the “oneiroid state.”
 

Origins and definitions

The term “oneiroia” is derived from the Greek words for “sleep” and “similar,” referring to the dreamlike character of the condition. It is widely acknowledged that psychedelics can temporarily induce dreamlike states,⁴ but this article focuses specifically on the naturally occurring, endogenous dreamlike state.

Oneiroid state was first described by German psychiatrist Wilhelm Mayer-Gross in the early 20th century and was once well-known among European psychiatrists. Some classified it as a part of schizophrenia, others saw it as an unusual manifestation of affective disorder, and still others considered it an atypical psychosis. Nevertheless, this phenomenon has received limited attention in American psychiatric journals.

The key characteristic of this condition is a distinctive state of consciousness marked by vivid and florid hallucinations, and a succession of constantly shifting dreamlike or surrealistic visuals and imagery often similar to mystical or cosmic experiences. Self-awareness and orientation in time and place are often disturbed, and delusions are experienced within this altered state.⁵

To gain a better understanding of the oneiroid state, it may be helpful to turn to European or other schools of psychiatry with a history of studying this phenomenon, as American psychiatry has limited knowledge in this area.

As described in the “Handbook of Psychiatry” by Russian psychiatrist A.V. Snezhnevsky, published in 1983, oneiroid state, also known as oneiroid syndrome, is a dreamlike and imaginative state characterized by a bizarre combination of reality and vivid phantasmagoric imaginations.⁶ In this state, individuals are completely detached from their surroundings and experience a change in self-awareness, often displaying either a lack of movement or senseless excitement.

Patients often experience the oneiroid state as active participants, as if they are in a movie theater, not only watching the story, but also being part of it, reacting to it with either “external immobility” or senseless excitement, completely detached from their surroundings. This is similar to the portrayal of the emotions of the characters in Steven Spielberg’s film “Ready Player One.”

The entry in Dr. Snezhnevsky’s “Handbook” states: “Some patients in Oneiroid State experience travels to other worlds, such as interacting with inhabitants on Mars, collecting gems on the moon, exploring invisible cities, participating in conspiracies and insurrections, fighting with pirates, chasing The Flying Dutchman, wandering through ancient Rome, and even visiting heaven or hell. At times, the patient’s imagination reaches a state of mystical contemplation.”⁶

In contrast to delirium, which never impairs self-awareness, oneiroid state is marked by drastic changes in the sense of self. The memory of the subjective experience during the oneiroia is much more vivid and consistent than in delirium. Patients who have experienced the oneiroid state often have complete recall of their experience, as if they have just woken up from a dream.

It was commonly thought that oneiroid state was part of the group of functional psychoses, rather than organic psychoses, and was not considered to be a result of mind-altering psychedelics. It was not considered a manifestation of epilepsy either. Oneiroid state could last for weeks or even months, making it unlikely to be related to an epileptic seizure. Furthermore, EEG results did not show any seizurelike activity during the state.

An excellent case study on oneiroid state was published in Israel in 2000. The authors described two patients who experienced the oneiroid state for several days or even weeks.⁷ One of the patients reported that during the illness, he experienced himself aboard a spaceship as a cosmonaut, heading for a different universe. On another occasion, the patient perceived himself as a person living 2,000 years ago and being guilty of Christ’s death.

The second patient reported that everything around her appeared “like in the movies,” and she saw others as characters from comic strips. Both patients alternated between catatonic excitement and sluggishness and would sometimes come back to reality for a few minutes to respond to questions. Physical exams, laboratory tests, neurological tests, and a brain scan were all normal in both cases.
 

Conclusions

As mentioned earlier, oneiroid state is not widely discussed in American psychiatric journals and is now considered a rare condition globally, despite being a common occurrence in the past century. A diagnosis similar to oneiroid state, known as bouffée délirante, is still in use in some French-speaking countries, with a noticeable decline in frequency.^2,8 The widespread acceptance of international classification systems such as the ICD-10, which does not recognize the diagnosis, is likely one of the reasons for this decline.

However, the decrease in the prevalence of the oneiroid state is not unique, as other forms of mental illness, such as the catatonic subtype of schizophrenia, are also becoming less prevalent. The cause of this decline is uncertain. Could changes in the way mental disorders affect 5HT2A receptors be a contributing factor?

In conclusion, as the field of psychedelic research experiences a resurgence, this little-known manifestation of mental illness, oneiroid state, may be worth reexamining.

With the expected approval and regulation of psilocybin and MDMA by the FDA, and classical psychedelics widely regarded as nonaddictive and safer than other recreational drugs, the phenomenological similarity between the naturally occurring impaired consciousness of the oneiroid state and the altered states of consciousness brought about by entheogenic substances should be seen as a possibility for enhanced understanding, rather than as a cause for concern.

Dr. Khetsuriani is a supervising psychiatrist at the Bronx Psychiatric Center in Bronx, N.Y., and has a private psychiatric practice located in Manhattan, N.Y.

References

1. Nichols DE. Keynote address, 39th Telluride Mushroom Festival, Aug. 15-18, 2019. https://www.youtube.com/watch?v=RlDCM5JQzRk.

2. Nichols DE. Psychedelics. Pharmacol Rev. 2016 Apr;68(2):264-355. doi: 10.1124/pr.115.011478.

3. Leptourgos P et al. Hallucinations Under Psychedelics and in the Schizophrenia Spectrum: An Interdisciplinary and Multiscale Comparison. Schizophr Bull. 2020 Dec 1;46(6):1396-1408. doi: 10.1093/schbul/sbaa117.

4. Kraehenmann R. Dreams and Psychedelics: Neurophenomenological Comparison and Therapeutic Implications. Curr Neuropharmacol. 2017;15(7):1032-42. doi: 10.2174/1573413713666170619092629.

5. Henri EY et al. “Acute Delusional Psychosis” in Hirsch SR and Shepherd M, eds. Themes and variations in European psychiatry: An anthology. Charlottesville: University Press of Virginia, 1974.

6. Snezhnevsky A, ed. Handbook of Psychiatry. Moscow: Meditsina, 1983.

7. Kaptsan A et al. Oneiroid syndrome: A concept of use for Western psychiatry. Isr J Psychiatry Relat Sci. 2000;37(4):278-85.

8. https://en.wikipedia.org/wiki/Bouff%C3%A9e_d%C3%A9lirante.

This transcript has been edited for clarity.

How do you tell if a condition is caused by an infection?

It seems like an obvious question, right? In the post–van Leeuwenhoek era we can look at whatever part of the body is diseased under a microscope and see microbes – you know, the usual suspects.

Except when we can’t. And there are plenty of cases where we can’t: where the microbe is too small to be seen without more advanced imaging techniques, like with viruses; or when the pathogen is sparsely populated or hard to culture, like Mycobacterium.

Finding out that a condition is the result of an infection is not only an exercise for 19th century physicians. After all, it was 2008 when Barry Marshall and Robin Warren won their Nobel Prize for proving that stomach ulcers, long thought to be due to “stress,” were actually caused by a tiny microbe called Helicobacter pylori.

And this week, we are looking at a study which, once again, begins to suggest that a condition thought to be more or less random – cerebral amyloid angiopathy – may actually be the result of an infectious disease.

We’re talking about this paper, appearing in JAMA, which is just a great example of old-fashioned shoe-leather epidemiology. But let’s get up to speed on cerebral amyloid angiopathy (CAA) first.

CAA is characterized by the deposition of amyloid protein in the brain. While there are some genetic causes, they are quite rare, and most cases are thought to be idiopathic. Recent analyses suggest that somewhere between 5% and 7% of cognitively normal older adults have CAA, but the rate is much higher among those with intracerebral hemorrhage – brain bleeds. In fact, CAA is the second-most common cause of bleeding in the brain, second only to severe hypertension.

Most of the textbooks continue to describe CAA as a sporadic condition, but there have been some intriguing studies that suggest it may be transmissible. An article in Nature highlights cases that seemed to develop after the administration of cadaveric pituitary hormone.

Other studies have shown potential transmission via dura mater grafts and neurosurgical instruments. But despite those clues, no infectious organism has been identified. Some have suggested that the long latent period and difficulty of finding a responsible microbe points to a prion-like disease not yet known. But these studies are more or less case series. The new JAMA paper gives us, if not a smoking gun, a pretty decent set of fingerprints.

Here’s the idea: If CAA is caused by some infectious agent, it may be transmitted in the blood. We know that a decent percentage of people who have spontaneous brain bleeds have CAA. If those people donated blood in the past, maybe the people who received that blood would be at risk for brain bleeds too.

courtesy Dr. F. Perry Wilson

courtesy Dr. F. Perry Wilson

courtesy Dr. F. Perry Wilson

courtesy JAMA Internal Medicine

Dr. F. Perry Wilson is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.
 

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

How do you tell if a condition is caused by an infection?

It seems like an obvious question, right? In the post–van Leeuwenhoek era we can look at whatever part of the body is diseased under a microscope and see microbes – you know, the usual suspects.

Except when we can’t. And there are plenty of cases where we can’t: where the microbe is too small to be seen without more advanced imaging techniques, like with viruses; or when the pathogen is sparsely populated or hard to culture, like Mycobacterium.

Finding out that a condition is the result of an infection is not only an exercise for 19th century physicians. After all, it was 2008 when Barry Marshall and Robin Warren won their Nobel Prize for proving that stomach ulcers, long thought to be due to “stress,” were actually caused by a tiny microbe called Helicobacter pylori.

And this week, we are looking at a study which, once again, begins to suggest that a condition thought to be more or less random – cerebral amyloid angiopathy – may actually be the result of an infectious disease.

We’re talking about this paper, appearing in JAMA, which is just a great example of old-fashioned shoe-leather epidemiology. But let’s get up to speed on cerebral amyloid angiopathy (CAA) first.

CAA is characterized by the deposition of amyloid protein in the brain. While there are some genetic causes, they are quite rare, and most cases are thought to be idiopathic. Recent analyses suggest that somewhere between 5% and 7% of cognitively normal older adults have CAA, but the rate is much higher among those with intracerebral hemorrhage – brain bleeds. In fact, CAA is the second-most common cause of bleeding in the brain, second only to severe hypertension.

Most of the textbooks continue to describe CAA as a sporadic condition, but there have been some intriguing studies that suggest it may be transmissible. An article in Nature highlights cases that seemed to develop after the administration of cadaveric pituitary hormone.

Other studies have shown potential transmission via dura mater grafts and neurosurgical instruments. But despite those clues, no infectious organism has been identified. Some have suggested that the long latent period and difficulty of finding a responsible microbe points to a prion-like disease not yet known. But these studies are more or less case series. The new JAMA paper gives us, if not a smoking gun, a pretty decent set of fingerprints.

Here’s the idea: If CAA is caused by some infectious agent, it may be transmitted in the blood. We know that a decent percentage of people who have spontaneous brain bleeds have CAA. If those people donated blood in the past, maybe the people who received that blood would be at risk for brain bleeds too.

courtesy Dr. F. Perry Wilson

courtesy Dr. F. Perry Wilson

courtesy Dr. F. Perry Wilson

courtesy JAMA Internal Medicine

Dr. F. Perry Wilson is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.
 

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

How do you tell if a condition is caused by an infection?

It seems like an obvious question, right? In the post–van Leeuwenhoek era we can look at whatever part of the body is diseased under a microscope and see microbes – you know, the usual suspects.

Except when we can’t. And there are plenty of cases where we can’t: where the microbe is too small to be seen without more advanced imaging techniques, like with viruses; or when the pathogen is sparsely populated or hard to culture, like Mycobacterium.

Finding out that a condition is the result of an infection is not only an exercise for 19th century physicians. After all, it was 2008 when Barry Marshall and Robin Warren won their Nobel Prize for proving that stomach ulcers, long thought to be due to “stress,” were actually caused by a tiny microbe called Helicobacter pylori.

And this week, we are looking at a study which, once again, begins to suggest that a condition thought to be more or less random – cerebral amyloid angiopathy – may actually be the result of an infectious disease.

We’re talking about this paper, appearing in JAMA, which is just a great example of old-fashioned shoe-leather epidemiology. But let’s get up to speed on cerebral amyloid angiopathy (CAA) first.

CAA is characterized by the deposition of amyloid protein in the brain. While there are some genetic causes, they are quite rare, and most cases are thought to be idiopathic. Recent analyses suggest that somewhere between 5% and 7% of cognitively normal older adults have CAA, but the rate is much higher among those with intracerebral hemorrhage – brain bleeds. In fact, CAA is the second-most common cause of bleeding in the brain, second only to severe hypertension.

Most of the textbooks continue to describe CAA as a sporadic condition, but there have been some intriguing studies that suggest it may be transmissible. An article in Nature highlights cases that seemed to develop after the administration of cadaveric pituitary hormone.

Other studies have shown potential transmission via dura mater grafts and neurosurgical instruments. But despite those clues, no infectious organism has been identified. Some have suggested that the long latent period and difficulty of finding a responsible microbe points to a prion-like disease not yet known. But these studies are more or less case series. The new JAMA paper gives us, if not a smoking gun, a pretty decent set of fingerprints.

Here’s the idea: If CAA is caused by some infectious agent, it may be transmitted in the blood. We know that a decent percentage of people who have spontaneous brain bleeds have CAA. If those people donated blood in the past, maybe the people who received that blood would be at risk for brain bleeds too.

courtesy Dr. F. Perry Wilson

courtesy Dr. F. Perry Wilson

courtesy Dr. F. Perry Wilson

courtesy JAMA Internal Medicine

Dr. F. Perry Wilson is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.
 

A version of this article first appeared on Medscape.com.

What happens to grief when those around you don’t understand it? Where does it go? How do you process it?

Disenfranchised grief, when someone or society more generally doesn’t see a loss as worthy of mourning, can deprive people of experiencing or processing their sadness. This grief, which may be triggered by the death of an ex-spouse, a pet, a failed adoption, can be painful and long-lasting.

Here, we reflect as physicians on our own experiences and memories of this phenomenon.
 

Suzanne Cole, MD: ‘I didn’t feel the right to grieve’

During the COVID-19 pandemic, my little sister unexpectedly died. Though she was not one of the nearly 7 million people who died of the virus, in 2021 she became another type of statistic: one of the 109,699 people in the United State who died from a drug overdose. Hers was from fentanyl laced with methamphetamines.

Her death unraveled me. I felt deep guilt that I could not pull her from the sweeping current that had wrenched her from mainstream society into the underbelly of sex work and toward the solace of mind-altering drugs.

But I did not feel the right to grieve for her as I have grieved for other loved ones who were not blamed for their exit from this world. My sister was living a sordid life on the fringes of society. My grief felt invalid, undeserved. Yet, in the eyes of other “upstanding citizens,” her life was not as worth grieving – or so I thought. I tucked my sorrow into a small corner of my soul so no one would see, and I carried on.

To this day, the shame I feel robbed me of the ability to freely talk about her or share the searing pain I feel. Tears still prick my eyes when I think of her, but I have become adept at swallowing them, shaking off the waves of grief as though nothing happened. Even now, I cannot shake the pervasive feeling that my silent tears don’t deserve to be wept.
 

Don S. Dizon, MD: Working through tragedy

As a medical student, I worked with an outpatient physician as part of a third-year rotation. When we met, the first thing that struck me was how disheveled he looked. His clothes were wrinkled, and his pants were baggy. He took cigarette breaks, which I found disturbing.

But I quickly came to admire him. Despite my first impression, he was the type of doctor I aspired to be. He didn’t need to look at a patient’s chart to recall who they were. He just knew them. He greeted patients warmly, asked about their family. He even remembered the special occasions his patients had mentioned since their past visit. He epitomized empathy and connectedness.

Spending one day in clinic brought to light the challenges of forming such bonds with patients. A man came into the cancer clinic reporting chest pain and was triaged to an exam room. Soon after, the patient was found unresponsive on the floor. Nurses were yelling for help, and the doctor ran in and started CPR while minutes ticked by waiting for an ambulance that could take him to the ED.

By the time help arrived, the patient was blue.

He had died in the clinic in the middle of the day, as the waiting room filled. After the body was taken away, the doctor went into the bathroom. About 20 minutes later, he came out, eyes bloodshot, and continued with the rest of his day, ensuring each patient was seen and cared for.

As a medical student, it hit me how hard it must be to see something so tragic like the end of a life and then continue with your day as if nothing had happened. This is an experience of grief I later came to know well after nearly 30 years treating patients with advanced cancers: compartmentalizing it and carrying on.
 

A space for grieving: The Schwartz Center Rounds

Disenfranchised grief, the grief that is hard to share and often seems wrong to feel in the first place, can be triggered in many situations. Losing a person others don’t believe deserve to be grieved, such as an abusive partner or someone who committed a crime; losing someone you cared for in a professional role; a loss experienced in a breakup or same-sex partnership, if that relationship was not accepted by one’s family; loss from infertility, miscarriage, stillbirth, or failed adoption; loss that may be taboo or stigmatized, such as deaths via suicide or abortion; and loss of a job, home, or possession that you treasure.

Many of us have had similar situations or will, and the feeling that no one understands the need to mourn can be paralyzing and alienating. In the early days, intense, crushing feelings can cause intrusive, distracting thoughts, and over time, that grief can linger and find a permanent place in our minds.

More and more, though, we are being given opportunities to reflect on these sad moments.

The Schwartz Rounds are an example of such an opportunity. In these rounds, we gather to talk about the experience of caring for people, not the science of medicine.

During one particularly powerful rounds, I spoke to my colleagues about my initial meeting with a patient who was very sick. I detailed the experience of telling her children and her at that initial consult how I thought she was dying and that I did not recommend therapy. I remember how they cried. And I remembered how powerless I felt.

As I recalled that memory during Schwartz Rounds, I could not stop from crying. The unfairness of being a physician meeting someone for the first time and having to tell them such bad news overwhelmed me.

Even more poignant, I had the chance to reconnect with this woman’s children, who were present that day, not as audience members but as participants. Their presence may have brought my emotions to the surface more strongly. In that moment, I could show them the feelings I had bottled up for the sake of professionalism. Ultimately, I felt relieved, freer somehow, as if this burden my soul was carrying had been lifted.

Although we are both grateful for forums like this, these opportunities to share and express the grief we may have hidden away are not as common as they should be.

As physicians, we may express grief by shedding tears at the bedside of a patient nearing the end of life or through the anxiety we feel when our patient suffers a severe reaction to treatment. But we tend to put it away, to go on with our day, because there are others to be seen and cared for and more work to be done. Somehow, we move forward, shedding tears in one room and celebrating victories in another.

We need to create more spaces to express and feel grief, so we don’t get lost in it. Because understanding how grief impacts us, as people and as providers, is one of the most important realizations we can make as we go about our time-honored profession as healers.

Dr. Dizon is the director of women’s cancers at Lifespan Cancer Institute, director of medical oncology at Rhode Island Hospital, and a professor of medicine at Brown University, all in Providence. He reported conflicts of interest with Regeneron, AstraZeneca, Clovis, Bristol-Myers Squibb, and Kazia.

A version of this article first appeared on Medscape.com.

What happens to grief when those around you don’t understand it? Where does it go? How do you process it?

Disenfranchised grief, when someone or society more generally doesn’t see a loss as worthy of mourning, can deprive people of experiencing or processing their sadness. This grief, which may be triggered by the death of an ex-spouse, a pet, a failed adoption, can be painful and long-lasting.

Here, we reflect as physicians on our own experiences and memories of this phenomenon.
 

Suzanne Cole, MD: ‘I didn’t feel the right to grieve’

During the COVID-19 pandemic, my little sister unexpectedly died. Though she was not one of the nearly 7 million people who died of the virus, in 2021 she became another type of statistic: one of the 109,699 people in the United State who died from a drug overdose. Hers was from fentanyl laced with methamphetamines.

Her death unraveled me. I felt deep guilt that I could not pull her from the sweeping current that had wrenched her from mainstream society into the underbelly of sex work and toward the solace of mind-altering drugs.

But I did not feel the right to grieve for her as I have grieved for other loved ones who were not blamed for their exit from this world. My sister was living a sordid life on the fringes of society. My grief felt invalid, undeserved. Yet, in the eyes of other “upstanding citizens,” her life was not as worth grieving – or so I thought. I tucked my sorrow into a small corner of my soul so no one would see, and I carried on.

To this day, the shame I feel robbed me of the ability to freely talk about her or share the searing pain I feel. Tears still prick my eyes when I think of her, but I have become adept at swallowing them, shaking off the waves of grief as though nothing happened. Even now, I cannot shake the pervasive feeling that my silent tears don’t deserve to be wept.
 

Don S. Dizon, MD: Working through tragedy

As a medical student, I worked with an outpatient physician as part of a third-year rotation. When we met, the first thing that struck me was how disheveled he looked. His clothes were wrinkled, and his pants were baggy. He took cigarette breaks, which I found disturbing.

But I quickly came to admire him. Despite my first impression, he was the type of doctor I aspired to be. He didn’t need to look at a patient’s chart to recall who they were. He just knew them. He greeted patients warmly, asked about their family. He even remembered the special occasions his patients had mentioned since their past visit. He epitomized empathy and connectedness.

Spending one day in clinic brought to light the challenges of forming such bonds with patients. A man came into the cancer clinic reporting chest pain and was triaged to an exam room. Soon after, the patient was found unresponsive on the floor. Nurses were yelling for help, and the doctor ran in and started CPR while minutes ticked by waiting for an ambulance that could take him to the ED.

By the time help arrived, the patient was blue.

He had died in the clinic in the middle of the day, as the waiting room filled. After the body was taken away, the doctor went into the bathroom. About 20 minutes later, he came out, eyes bloodshot, and continued with the rest of his day, ensuring each patient was seen and cared for.

As a medical student, it hit me how hard it must be to see something so tragic like the end of a life and then continue with your day as if nothing had happened. This is an experience of grief I later came to know well after nearly 30 years treating patients with advanced cancers: compartmentalizing it and carrying on.
 

A space for grieving: The Schwartz Center Rounds

Disenfranchised grief, the grief that is hard to share and often seems wrong to feel in the first place, can be triggered in many situations. Losing a person others don’t believe deserve to be grieved, such as an abusive partner or someone who committed a crime; losing someone you cared for in a professional role; a loss experienced in a breakup or same-sex partnership, if that relationship was not accepted by one’s family; loss from infertility, miscarriage, stillbirth, or failed adoption; loss that may be taboo or stigmatized, such as deaths via suicide or abortion; and loss of a job, home, or possession that you treasure.

Many of us have had similar situations or will, and the feeling that no one understands the need to mourn can be paralyzing and alienating. In the early days, intense, crushing feelings can cause intrusive, distracting thoughts, and over time, that grief can linger and find a permanent place in our minds.

More and more, though, we are being given opportunities to reflect on these sad moments.

The Schwartz Rounds are an example of such an opportunity. In these rounds, we gather to talk about the experience of caring for people, not the science of medicine.

During one particularly powerful rounds, I spoke to my colleagues about my initial meeting with a patient who was very sick. I detailed the experience of telling her children and her at that initial consult how I thought she was dying and that I did not recommend therapy. I remember how they cried. And I remembered how powerless I felt.

As I recalled that memory during Schwartz Rounds, I could not stop from crying. The unfairness of being a physician meeting someone for the first time and having to tell them such bad news overwhelmed me.

Even more poignant, I had the chance to reconnect with this woman’s children, who were present that day, not as audience members but as participants. Their presence may have brought my emotions to the surface more strongly. In that moment, I could show them the feelings I had bottled up for the sake of professionalism. Ultimately, I felt relieved, freer somehow, as if this burden my soul was carrying had been lifted.

Although we are both grateful for forums like this, these opportunities to share and express the grief we may have hidden away are not as common as they should be.

As physicians, we may express grief by shedding tears at the bedside of a patient nearing the end of life or through the anxiety we feel when our patient suffers a severe reaction to treatment. But we tend to put it away, to go on with our day, because there are others to be seen and cared for and more work to be done. Somehow, we move forward, shedding tears in one room and celebrating victories in another.

We need to create more spaces to express and feel grief, so we don’t get lost in it. Because understanding how grief impacts us, as people and as providers, is one of the most important realizations we can make as we go about our time-honored profession as healers.

Dr. Dizon is the director of women’s cancers at Lifespan Cancer Institute, director of medical oncology at Rhode Island Hospital, and a professor of medicine at Brown University, all in Providence. He reported conflicts of interest with Regeneron, AstraZeneca, Clovis, Bristol-Myers Squibb, and Kazia.

A version of this article first appeared on Medscape.com.

What happens to grief when those around you don’t understand it? Where does it go? How do you process it?

Disenfranchised grief, when someone or society more generally doesn’t see a loss as worthy of mourning, can deprive people of experiencing or processing their sadness. This grief, which may be triggered by the death of an ex-spouse, a pet, a failed adoption, can be painful and long-lasting.

Here, we reflect as physicians on our own experiences and memories of this phenomenon.
 

Suzanne Cole, MD: ‘I didn’t feel the right to grieve’

During the COVID-19 pandemic, my little sister unexpectedly died. Though she was not one of the nearly 7 million people who died of the virus, in 2021 she became another type of statistic: one of the 109,699 people in the United State who died from a drug overdose. Hers was from fentanyl laced with methamphetamines.

Her death unraveled me. I felt deep guilt that I could not pull her from the sweeping current that had wrenched her from mainstream society into the underbelly of sex work and toward the solace of mind-altering drugs.

But I did not feel the right to grieve for her as I have grieved for other loved ones who were not blamed for their exit from this world. My sister was living a sordid life on the fringes of society. My grief felt invalid, undeserved. Yet, in the eyes of other “upstanding citizens,” her life was not as worth grieving – or so I thought. I tucked my sorrow into a small corner of my soul so no one would see, and I carried on.

To this day, the shame I feel robbed me of the ability to freely talk about her or share the searing pain I feel. Tears still prick my eyes when I think of her, but I have become adept at swallowing them, shaking off the waves of grief as though nothing happened. Even now, I cannot shake the pervasive feeling that my silent tears don’t deserve to be wept.
 

Don S. Dizon, MD: Working through tragedy

As a medical student, I worked with an outpatient physician as part of a third-year rotation. When we met, the first thing that struck me was how disheveled he looked. His clothes were wrinkled, and his pants were baggy. He took cigarette breaks, which I found disturbing.

But I quickly came to admire him. Despite my first impression, he was the type of doctor I aspired to be. He didn’t need to look at a patient’s chart to recall who they were. He just knew them. He greeted patients warmly, asked about their family. He even remembered the special occasions his patients had mentioned since their past visit. He epitomized empathy and connectedness.

Spending one day in clinic brought to light the challenges of forming such bonds with patients. A man came into the cancer clinic reporting chest pain and was triaged to an exam room. Soon after, the patient was found unresponsive on the floor. Nurses were yelling for help, and the doctor ran in and started CPR while minutes ticked by waiting for an ambulance that could take him to the ED.

By the time help arrived, the patient was blue.

He had died in the clinic in the middle of the day, as the waiting room filled. After the body was taken away, the doctor went into the bathroom. About 20 minutes later, he came out, eyes bloodshot, and continued with the rest of his day, ensuring each patient was seen and cared for.

As a medical student, it hit me how hard it must be to see something so tragic like the end of a life and then continue with your day as if nothing had happened. This is an experience of grief I later came to know well after nearly 30 years treating patients with advanced cancers: compartmentalizing it and carrying on.
 

A space for grieving: The Schwartz Center Rounds

Disenfranchised grief, the grief that is hard to share and often seems wrong to feel in the first place, can be triggered in many situations. Losing a person others don’t believe deserve to be grieved, such as an abusive partner or someone who committed a crime; losing someone you cared for in a professional role; a loss experienced in a breakup or same-sex partnership, if that relationship was not accepted by one’s family; loss from infertility, miscarriage, stillbirth, or failed adoption; loss that may be taboo or stigmatized, such as deaths via suicide or abortion; and loss of a job, home, or possession that you treasure.

Many of us have had similar situations or will, and the feeling that no one understands the need to mourn can be paralyzing and alienating. In the early days, intense, crushing feelings can cause intrusive, distracting thoughts, and over time, that grief can linger and find a permanent place in our minds.

More and more, though, we are being given opportunities to reflect on these sad moments.

The Schwartz Rounds are an example of such an opportunity. In these rounds, we gather to talk about the experience of caring for people, not the science of medicine.

During one particularly powerful rounds, I spoke to my colleagues about my initial meeting with a patient who was very sick. I detailed the experience of telling her children and her at that initial consult how I thought she was dying and that I did not recommend therapy. I remember how they cried. And I remembered how powerless I felt.

As I recalled that memory during Schwartz Rounds, I could not stop from crying. The unfairness of being a physician meeting someone for the first time and having to tell them such bad news overwhelmed me.

Even more poignant, I had the chance to reconnect with this woman’s children, who were present that day, not as audience members but as participants. Their presence may have brought my emotions to the surface more strongly. In that moment, I could show them the feelings I had bottled up for the sake of professionalism. Ultimately, I felt relieved, freer somehow, as if this burden my soul was carrying had been lifted.

Although we are both grateful for forums like this, these opportunities to share and express the grief we may have hidden away are not as common as they should be.

As physicians, we may express grief by shedding tears at the bedside of a patient nearing the end of life or through the anxiety we feel when our patient suffers a severe reaction to treatment. But we tend to put it away, to go on with our day, because there are others to be seen and cared for and more work to be done. Somehow, we move forward, shedding tears in one room and celebrating victories in another.

We need to create more spaces to express and feel grief, so we don’t get lost in it. Because understanding how grief impacts us, as people and as providers, is one of the most important realizations we can make as we go about our time-honored profession as healers.

Dr. Dizon is the director of women’s cancers at Lifespan Cancer Institute, director of medical oncology at Rhode Island Hospital, and a professor of medicine at Brown University, all in Providence. He reported conflicts of interest with Regeneron, AstraZeneca, Clovis, Bristol-Myers Squibb, and Kazia.

A version of this article first appeared on Medscape.com.

A very good thing happened this summer for patients with anxiety and the psychiatrists, psychologists, and other mental health professionals who provide treatment for them. The U.S. Preventive Services Task Force recommended anxiety screening for all adults younger than 65.

On the surface, this is a great recommendation for recognition and caring for those who deal with and suffer from an anxiety disorder or multiple anxiety disorders. Although the USPSTF recommendations are independent of the U.S. government and are not an official position of the Department of Health & Human Services, they are a wonderful start at recognizing the importance of mental health care.

Robert T. London

After all, anxiety disorders are the most commonly experienced and diagnosed mental disorders, according to the DSM-5.

They range mainly from generalized anxiety disorder (GAD), to panic attacks and panic disorder, separation anxiety, specific type phobias (bridges, tunnels, insects, snakes, and the list goes on), to other phobias, including agoraphobia, social phobia, and of course, anxiety caused by medical conditions. GAD alone occurs in, at least, more than 3% of the population.

Those of us who have been treating anxiety disorders for decades recognize them as an issue affecting both mental and physical well-being, not only because of the emotional causes but the physical distress and illnesses that anxiety may precipitate or worsen.

For example, blood pressure– and heart-related issues, GI disorders, and musculoskeletal issues are just a few examples of how our bodies and organ systems are affected by anxiety. Just the momentary physical symptoms of tachycardia or the “runs” before an exam are fine examples of how anxiety may affect patients physically, and an ongoing, consistent anxiety is potentially more harmful.

In fact, a first panic attack or episode of generalized anxiety may be so serious that an emergency department or physician visit is necessary to rule out a heart attack, asthma, or breathing issues – even a hormone or thyroid emergency, or a cardiac arrhythmia. Panic attacks alone create a high number of ED visits.

Treatments mainly include medication management and a variety of psychotherapy techniques. Currently, the most preferred, first-choice medications are the SSRI antidepressants, which are Food and Drug Administration approved for anxiety as well. These include Zoloft (sertraline), Prozac/Sarafem (fluoxetine), Celexa (citalopram), and Lexapro (escitalopram).

For many years, benzodiazepines (that is, tranquillizers) such as Valium (diazepam), Ativan (lorazepam), and Klonopin/Rivotril (clonazepam) to name a few, were the mainstay of anxiety treatment, but they have proven addictive and may affect cognition and memory. As the current opioid epidemic has shown, when combined with opioids, benzodiazepines are a potentially lethal combination and when used, they need to be for shorter-term care and monitored very judiciously.

It should be noted that after ongoing long-term use of an SSRI for anxiety or depression, it should not be stopped abruptly, as a variety of physical symptoms (for example, flu-like symptoms) may occur.
 

Benefits of nonmedicinal therapies

There are a variety of talk therapies, from dynamic psychotherapies to cognitive-behavioral therapies (CBT), plus relaxation techniques and guided imagery that have all had a good amount of success in treating generalized anxiety, panic disorder, as well as various types of phobias.

When medications are stopped, the anxiety symptoms may well return. But when using nonmedicinal therapies, clinicians have discovered that when patients develop a new perspective on the anxiety problem or have a new technique to treat anxiety, it may well be long lasting.

For me, using CBT, relaxation techniques, hypnosis, and guided imagery has been very successful in treating anxiety disorders with long-lasting results. Once a person learns to relax, whether it’s from deep breathing exercises, hypnosis (which is not sleep), mindfulness, or meditation, a strategy of guided imagery can be taught, which allows a person to practice as well as control their anxiety as a lifetime process. For example, I like imagining a large movie screen to desensitize and project anxieties.

In many instances, a combination of a medication and a talk therapy approach works best, but there are an equal number of instances in which just medication or just talk therapy is needed. Once again, knowledge, clinical judgment, and the art of care are required to make these assessments.

In other words, recognizing and treating anxiety requires highly specialized training, which is why I thought the USPSTF recommendations raise a few critical questions.
 

Questions and concerns

One issue, of course, is the exclusion of those patients over age 65 because of a lack of “data.” Why such an exclusion? Does this mean that data are lacking for this age group?

The concept of using solely evidenced-based data in psychiatry is itself an interesting concept because our profession, like many other medical specialties, requires practitioners to use a combination of art and science. And much can be said either way about the clarity of accuracy in the diversity of issues that arise when treating emotional disorders.

When looking at the over-65 population, has anyone thought of clinical knowledge, judgment, experience, observation, and, of course, common sense?

Just consider the worry (a cardinal feature of anxiety) that besets people over 65 when it comes to issues such as retirement, financial security, “empty nesting,” physical health issues, decreased socialization that resulted from the COVID-19 pandemic, and the perpetual loss of relatives and friends.

In addition, as we age, anxiety can come simply from the loss of identity as active lifestyles decrease and the reality of nearing life’s end becomes more of a reality. It would seem that this population would benefit enormously from anxiety screening and possible treatment.

Another major concern is that the screening and potential treatment of patients is aimed at primary care physicians. Putting the sole responsibility of providing mental health care on these overworked PCPs defies common sense unless we’re okay with 1- to 2-minute assessments of mental health issues and no doubt, a pharmacology-only approach.

If this follows the same route as well-intentioned PCPs treating depression, where 5-minute medication management is far too common, the only proper diagnostic course – the in-depth interview necessary to make a proper diagnosis – is often missing.

For example, in depression alone, it takes psychiatric experience and time to differentiate a major depressive disorder from a bipolar depression and to provide the appropriate medication and treatment plan with careful follow-up. In my experience, this usually does not happen in the exceedingly overworked, time-driven day of a PCP.

Anxiety disorders and depression can prove debilitating, and if a PCP wants the responsibility of treatment, a mandated mental health program should be followed – just as here in New York, prescribers are mandated to take a pain control, opioid, and infection control CME course to keep our licenses up to date.

Short of mandating a mental health program for PCPs, it should be part of training and CME courses that whenever PCPs diagnose a mental illness, a proper referral to a psychiatrist or psychologist should be made – whether for a consultation or for shared care. Psychiatry is a super specialty, much like orthopedics and ophthalmology, and primary care physicians should never hesitate to make referrals to the specialist.

The big picture for me, and I hope for us all, is that the USPSTF has started things rolling by making it clear that PCPs and other health care clinicians need to screen for anxiety as a disabling disorder that is quite treatable.

This approach will help to advance the destigmatization of mental health disorders. But as result, with more patients diagnosed, there will be a need for more psychiatrists – and psychologists with PhDs or PsyDs – to fill the gaps in mental health care.

Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

A very good thing happened this summer for patients with anxiety and the psychiatrists, psychologists, and other mental health professionals who provide treatment for them. The U.S. Preventive Services Task Force recommended anxiety screening for all adults younger than 65.

On the surface, this is a great recommendation for recognition and caring for those who deal with and suffer from an anxiety disorder or multiple anxiety disorders. Although the USPSTF recommendations are independent of the U.S. government and are not an official position of the Department of Health & Human Services, they are a wonderful start at recognizing the importance of mental health care.

Robert T. London

After all, anxiety disorders are the most commonly experienced and diagnosed mental disorders, according to the DSM-5.

They range mainly from generalized anxiety disorder (GAD), to panic attacks and panic disorder, separation anxiety, specific type phobias (bridges, tunnels, insects, snakes, and the list goes on), to other phobias, including agoraphobia, social phobia, and of course, anxiety caused by medical conditions. GAD alone occurs in, at least, more than 3% of the population.

Those of us who have been treating anxiety disorders for decades recognize them as an issue affecting both mental and physical well-being, not only because of the emotional causes but the physical distress and illnesses that anxiety may precipitate or worsen.

For example, blood pressure– and heart-related issues, GI disorders, and musculoskeletal issues are just a few examples of how our bodies and organ systems are affected by anxiety. Just the momentary physical symptoms of tachycardia or the “runs” before an exam are fine examples of how anxiety may affect patients physically, and an ongoing, consistent anxiety is potentially more harmful.

In fact, a first panic attack or episode of generalized anxiety may be so serious that an emergency department or physician visit is necessary to rule out a heart attack, asthma, or breathing issues – even a hormone or thyroid emergency, or a cardiac arrhythmia. Panic attacks alone create a high number of ED visits.

Treatments mainly include medication management and a variety of psychotherapy techniques. Currently, the most preferred, first-choice medications are the SSRI antidepressants, which are Food and Drug Administration approved for anxiety as well. These include Zoloft (sertraline), Prozac/Sarafem (fluoxetine), Celexa (citalopram), and Lexapro (escitalopram).

For many years, benzodiazepines (that is, tranquillizers) such as Valium (diazepam), Ativan (lorazepam), and Klonopin/Rivotril (clonazepam) to name a few, were the mainstay of anxiety treatment, but they have proven addictive and may affect cognition and memory. As the current opioid epidemic has shown, when combined with opioids, benzodiazepines are a potentially lethal combination and when used, they need to be for shorter-term care and monitored very judiciously.

It should be noted that after ongoing long-term use of an SSRI for anxiety or depression, it should not be stopped abruptly, as a variety of physical symptoms (for example, flu-like symptoms) may occur.
 

Benefits of nonmedicinal therapies

There are a variety of talk therapies, from dynamic psychotherapies to cognitive-behavioral therapies (CBT), plus relaxation techniques and guided imagery that have all had a good amount of success in treating generalized anxiety, panic disorder, as well as various types of phobias.

When medications are stopped, the anxiety symptoms may well return. But when using nonmedicinal therapies, clinicians have discovered that when patients develop a new perspective on the anxiety problem or have a new technique to treat anxiety, it may well be long lasting.

For me, using CBT, relaxation techniques, hypnosis, and guided imagery has been very successful in treating anxiety disorders with long-lasting results. Once a person learns to relax, whether it’s from deep breathing exercises, hypnosis (which is not sleep), mindfulness, or meditation, a strategy of guided imagery can be taught, which allows a person to practice as well as control their anxiety as a lifetime process. For example, I like imagining a large movie screen to desensitize and project anxieties.

In many instances, a combination of a medication and a talk therapy approach works best, but there are an equal number of instances in which just medication or just talk therapy is needed. Once again, knowledge, clinical judgment, and the art of care are required to make these assessments.

In other words, recognizing and treating anxiety requires highly specialized training, which is why I thought the USPSTF recommendations raise a few critical questions.
 

Questions and concerns

One issue, of course, is the exclusion of those patients over age 65 because of a lack of “data.” Why such an exclusion? Does this mean that data are lacking for this age group?

The concept of using solely evidenced-based data in psychiatry is itself an interesting concept because our profession, like many other medical specialties, requires practitioners to use a combination of art and science. And much can be said either way about the clarity of accuracy in the diversity of issues that arise when treating emotional disorders.

When looking at the over-65 population, has anyone thought of clinical knowledge, judgment, experience, observation, and, of course, common sense?

Just consider the worry (a cardinal feature of anxiety) that besets people over 65 when it comes to issues such as retirement, financial security, “empty nesting,” physical health issues, decreased socialization that resulted from the COVID-19 pandemic, and the perpetual loss of relatives and friends.

In addition, as we age, anxiety can come simply from the loss of identity as active lifestyles decrease and the reality of nearing life’s end becomes more of a reality. It would seem that this population would benefit enormously from anxiety screening and possible treatment.

Another major concern is that the screening and potential treatment of patients is aimed at primary care physicians. Putting the sole responsibility of providing mental health care on these overworked PCPs defies common sense unless we’re okay with 1- to 2-minute assessments of mental health issues and no doubt, a pharmacology-only approach.

If this follows the same route as well-intentioned PCPs treating depression, where 5-minute medication management is far too common, the only proper diagnostic course – the in-depth interview necessary to make a proper diagnosis – is often missing.

For example, in depression alone, it takes psychiatric experience and time to differentiate a major depressive disorder from a bipolar depression and to provide the appropriate medication and treatment plan with careful follow-up. In my experience, this usually does not happen in the exceedingly overworked, time-driven day of a PCP.

Anxiety disorders and depression can prove debilitating, and if a PCP wants the responsibility of treatment, a mandated mental health program should be followed – just as here in New York, prescribers are mandated to take a pain control, opioid, and infection control CME course to keep our licenses up to date.

Short of mandating a mental health program for PCPs, it should be part of training and CME courses that whenever PCPs diagnose a mental illness, a proper referral to a psychiatrist or psychologist should be made – whether for a consultation or for shared care. Psychiatry is a super specialty, much like orthopedics and ophthalmology, and primary care physicians should never hesitate to make referrals to the specialist.

The big picture for me, and I hope for us all, is that the USPSTF has started things rolling by making it clear that PCPs and other health care clinicians need to screen for anxiety as a disabling disorder that is quite treatable.

This approach will help to advance the destigmatization of mental health disorders. But as result, with more patients diagnosed, there will be a need for more psychiatrists – and psychologists with PhDs or PsyDs – to fill the gaps in mental health care.

Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

A very good thing happened this summer for patients with anxiety and the psychiatrists, psychologists, and other mental health professionals who provide treatment for them. The U.S. Preventive Services Task Force recommended anxiety screening for all adults younger than 65.

On the surface, this is a great recommendation for recognition and caring for those who deal with and suffer from an anxiety disorder or multiple anxiety disorders. Although the USPSTF recommendations are independent of the U.S. government and are not an official position of the Department of Health & Human Services, they are a wonderful start at recognizing the importance of mental health care.

Robert T. London

After all, anxiety disorders are the most commonly experienced and diagnosed mental disorders, according to the DSM-5.

They range mainly from generalized anxiety disorder (GAD), to panic attacks and panic disorder, separation anxiety, specific type phobias (bridges, tunnels, insects, snakes, and the list goes on), to other phobias, including agoraphobia, social phobia, and of course, anxiety caused by medical conditions. GAD alone occurs in, at least, more than 3% of the population.

Those of us who have been treating anxiety disorders for decades recognize them as an issue affecting both mental and physical well-being, not only because of the emotional causes but the physical distress and illnesses that anxiety may precipitate or worsen.

For example, blood pressure– and heart-related issues, GI disorders, and musculoskeletal issues are just a few examples of how our bodies and organ systems are affected by anxiety. Just the momentary physical symptoms of tachycardia or the “runs” before an exam are fine examples of how anxiety may affect patients physically, and an ongoing, consistent anxiety is potentially more harmful.

In fact, a first panic attack or episode of generalized anxiety may be so serious that an emergency department or physician visit is necessary to rule out a heart attack, asthma, or breathing issues – even a hormone or thyroid emergency, or a cardiac arrhythmia. Panic attacks alone create a high number of ED visits.

Treatments mainly include medication management and a variety of psychotherapy techniques. Currently, the most preferred, first-choice medications are the SSRI antidepressants, which are Food and Drug Administration approved for anxiety as well. These include Zoloft (sertraline), Prozac/Sarafem (fluoxetine), Celexa (citalopram), and Lexapro (escitalopram).

For many years, benzodiazepines (that is, tranquillizers) such as Valium (diazepam), Ativan (lorazepam), and Klonopin/Rivotril (clonazepam) to name a few, were the mainstay of anxiety treatment, but they have proven addictive and may affect cognition and memory. As the current opioid epidemic has shown, when combined with opioids, benzodiazepines are a potentially lethal combination and when used, they need to be for shorter-term care and monitored very judiciously.

It should be noted that after ongoing long-term use of an SSRI for anxiety or depression, it should not be stopped abruptly, as a variety of physical symptoms (for example, flu-like symptoms) may occur.
 

Benefits of nonmedicinal therapies

There are a variety of talk therapies, from dynamic psychotherapies to cognitive-behavioral therapies (CBT), plus relaxation techniques and guided imagery that have all had a good amount of success in treating generalized anxiety, panic disorder, as well as various types of phobias.

When medications are stopped, the anxiety symptoms may well return. But when using nonmedicinal therapies, clinicians have discovered that when patients develop a new perspective on the anxiety problem or have a new technique to treat anxiety, it may well be long lasting.

For me, using CBT, relaxation techniques, hypnosis, and guided imagery has been very successful in treating anxiety disorders with long-lasting results. Once a person learns to relax, whether it’s from deep breathing exercises, hypnosis (which is not sleep), mindfulness, or meditation, a strategy of guided imagery can be taught, which allows a person to practice as well as control their anxiety as a lifetime process. For example, I like imagining a large movie screen to desensitize and project anxieties.

In many instances, a combination of a medication and a talk therapy approach works best, but there are an equal number of instances in which just medication or just talk therapy is needed. Once again, knowledge, clinical judgment, and the art of care are required to make these assessments.

In other words, recognizing and treating anxiety requires highly specialized training, which is why I thought the USPSTF recommendations raise a few critical questions.
 

Questions and concerns

One issue, of course, is the exclusion of those patients over age 65 because of a lack of “data.” Why such an exclusion? Does this mean that data are lacking for this age group?

The concept of using solely evidenced-based data in psychiatry is itself an interesting concept because our profession, like many other medical specialties, requires practitioners to use a combination of art and science. And much can be said either way about the clarity of accuracy in the diversity of issues that arise when treating emotional disorders.

When looking at the over-65 population, has anyone thought of clinical knowledge, judgment, experience, observation, and, of course, common sense?

Just consider the worry (a cardinal feature of anxiety) that besets people over 65 when it comes to issues such as retirement, financial security, “empty nesting,” physical health issues, decreased socialization that resulted from the COVID-19 pandemic, and the perpetual loss of relatives and friends.

In addition, as we age, anxiety can come simply from the loss of identity as active lifestyles decrease and the reality of nearing life’s end becomes more of a reality. It would seem that this population would benefit enormously from anxiety screening and possible treatment.

Another major concern is that the screening and potential treatment of patients is aimed at primary care physicians. Putting the sole responsibility of providing mental health care on these overworked PCPs defies common sense unless we’re okay with 1- to 2-minute assessments of mental health issues and no doubt, a pharmacology-only approach.

If this follows the same route as well-intentioned PCPs treating depression, where 5-minute medication management is far too common, the only proper diagnostic course – the in-depth interview necessary to make a proper diagnosis – is often missing.

For example, in depression alone, it takes psychiatric experience and time to differentiate a major depressive disorder from a bipolar depression and to provide the appropriate medication and treatment plan with careful follow-up. In my experience, this usually does not happen in the exceedingly overworked, time-driven day of a PCP.

Anxiety disorders and depression can prove debilitating, and if a PCP wants the responsibility of treatment, a mandated mental health program should be followed – just as here in New York, prescribers are mandated to take a pain control, opioid, and infection control CME course to keep our licenses up to date.

Short of mandating a mental health program for PCPs, it should be part of training and CME courses that whenever PCPs diagnose a mental illness, a proper referral to a psychiatrist or psychologist should be made – whether for a consultation or for shared care. Psychiatry is a super specialty, much like orthopedics and ophthalmology, and primary care physicians should never hesitate to make referrals to the specialist.

The big picture for me, and I hope for us all, is that the USPSTF has started things rolling by making it clear that PCPs and other health care clinicians need to screen for anxiety as a disabling disorder that is quite treatable.

This approach will help to advance the destigmatization of mental health disorders. But as result, with more patients diagnosed, there will be a need for more psychiatrists – and psychologists with PhDs or PsyDs – to fill the gaps in mental health care.

Dr. London is a practicing psychiatrist and has been a newspaper columnist for 35 years, specializing in and writing about short-term therapy, including cognitive-behavioral therapy and guided imagery. He is author of “Find Freedom Fast” (New York: Kettlehole Publishing, 2019). He has no conflicts of interest.

Erythema chronicum migrans (ECM) is the classical dermatologic manifestation of Lyme disease, a condition caused by Borrelia burgdorferi, a bacterial spirochete. Lyme disease is the most commonly transmitted tick-borne illness in the United States. This infection is typically transmitted through a bite by the Ixodes tick commonly found in the Midwest, Northeast, and mid-Atlantic regions; however, the geographical distribution continues to expand over time in the United States. Ticks must be attached for 24-48 hours to transmit the pathogen. There are three general stages of the disease: early localized, early disseminated, and late disseminated.

The most common presentation is the early localized disease, which manifests between 3 and 30 days after an infected tick bite. Approximately 70%-80% of cases feature a targetlike lesion that expands centrifugally at the site of the bite. Most commonly, lesions appear on the abdomen, groin, axilla, and popliteal fossa. The diagnosis of ECM requires lesions at least 5 cm in size. Lesions may be asymptomatic, although burning may occur in half of patients. Atypical presentations include bullous, vesicular, hemorrhagic, or necrotic lesions. Up to half of patients may develop multiple ECM lesions. Palms and soles are spared. Differential diagnoses include arthropod reactions, pyoderma gangrenosum, cellulitis, herpes simplex virus and varicella zoster virus, contact dermatitis, or granuloma annulare. The rash is often accompanied by systemic symptoms including fatigue, myalgia, headache, and fever.

The next two stages include early and late disseminated infection. Early disseminated infection often occurs 3-12 weeks after infection and is characterized by muscle pain, dizziness, headache, and cardiac symptoms. CNS involvement occurs in about 20% of patients. Joint involvement may include the knee, ankle, and wrist. If symptoms are only in one joint, septic arthritis is part of the differential diagnosis, so clinical correlation and labs must be considered. Late disseminated infection occurs months or years after initial infection and includes neurologic and rheumatologic symptoms including meningitis, Bell’s palsy, arthritis, and dysesthesia. Knee arthritis is a key feature of this stage. Patients commonly have radicular pain and fibromyalgia-type pain. More severe disease processes include encephalomyelitis, arrhythmias, and heart block.

ECM is often a clinical diagnosis because serologic testing may not be positive during the first 2 weeks of infection. The screening serologic test is the ELISA, and a Western blot confirms the results. Skin histopathology for Lyme disease is often nonspecific and reveals a perivascular infiltrate of histiocytes, plasma cells, and lymphocytes. Silver stain or antibody testing may be used to identify the spirochete. In acrodermatitis chronica atrophicans, late Lyme disease presenting on the distal extremities, lymphocytic and plasma cell infiltrates are present. In borrelial lymphocytoma, a dense dermal lymphocytic infiltrate is present.

The standard for treatment of early localized disease is oral doxycycline in adults. Alternatives may be used if a patient is allergic or for children under 9. Disseminated disease may be treated with IV ceftriaxone and topical steroids are used if ocular symptoms are involved. Early treatment is often curative.

This patient’s antibodies were negative initially, but became positive after 6 weeks. He was treated empirically at the time of his office visit with doxycycline for 1 month.

This case and the photo were submitted by Lucas Shapiro, BS, of Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Fla., and Susannah Berke, MD, Three Rivers Dermatology, Coraopolis, Pa. The column was edited by Donna Bilu Martin, MD.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to [email protected].

References
 

Carriveau A et al. Nurs Clin North Am. 2019 Jun;54(2):261-75.

Skar GL and Simonsen KA. Lyme Disease. [Updated 2023 May 31]. In: “StatPearls” [Internet]. Treasure Island, Fla.: StatPearls Publishing; 2023 Jan.

Tiger JB et al. J Am Acad Dermatol. 2014 Oct;71(4):e133-4.

Erythema chronicum migrans (ECM) is the classical dermatologic manifestation of Lyme disease, a condition caused by Borrelia burgdorferi, a bacterial spirochete. Lyme disease is the most commonly transmitted tick-borne illness in the United States. This infection is typically transmitted through a bite by the Ixodes tick commonly found in the Midwest, Northeast, and mid-Atlantic regions; however, the geographical distribution continues to expand over time in the United States. Ticks must be attached for 24-48 hours to transmit the pathogen. There are three general stages of the disease: early localized, early disseminated, and late disseminated.

The most common presentation is the early localized disease, which manifests between 3 and 30 days after an infected tick bite. Approximately 70%-80% of cases feature a targetlike lesion that expands centrifugally at the site of the bite. Most commonly, lesions appear on the abdomen, groin, axilla, and popliteal fossa. The diagnosis of ECM requires lesions at least 5 cm in size. Lesions may be asymptomatic, although burning may occur in half of patients. Atypical presentations include bullous, vesicular, hemorrhagic, or necrotic lesions. Up to half of patients may develop multiple ECM lesions. Palms and soles are spared. Differential diagnoses include arthropod reactions, pyoderma gangrenosum, cellulitis, herpes simplex virus and varicella zoster virus, contact dermatitis, or granuloma annulare. The rash is often accompanied by systemic symptoms including fatigue, myalgia, headache, and fever.

The next two stages include early and late disseminated infection. Early disseminated infection often occurs 3-12 weeks after infection and is characterized by muscle pain, dizziness, headache, and cardiac symptoms. CNS involvement occurs in about 20% of patients. Joint involvement may include the knee, ankle, and wrist. If symptoms are only in one joint, septic arthritis is part of the differential diagnosis, so clinical correlation and labs must be considered. Late disseminated infection occurs months or years after initial infection and includes neurologic and rheumatologic symptoms including meningitis, Bell’s palsy, arthritis, and dysesthesia. Knee arthritis is a key feature of this stage. Patients commonly have radicular pain and fibromyalgia-type pain. More severe disease processes include encephalomyelitis, arrhythmias, and heart block.

ECM is often a clinical diagnosis because serologic testing may not be positive during the first 2 weeks of infection. The screening serologic test is the ELISA, and a Western blot confirms the results. Skin histopathology for Lyme disease is often nonspecific and reveals a perivascular infiltrate of histiocytes, plasma cells, and lymphocytes. Silver stain or antibody testing may be used to identify the spirochete. In acrodermatitis chronica atrophicans, late Lyme disease presenting on the distal extremities, lymphocytic and plasma cell infiltrates are present. In borrelial lymphocytoma, a dense dermal lymphocytic infiltrate is present.

The standard for treatment of early localized disease is oral doxycycline in adults. Alternatives may be used if a patient is allergic or for children under 9. Disseminated disease may be treated with IV ceftriaxone and topical steroids are used if ocular symptoms are involved. Early treatment is often curative.

This patient’s antibodies were negative initially, but became positive after 6 weeks. He was treated empirically at the time of his office visit with doxycycline for 1 month.

This case and the photo were submitted by Lucas Shapiro, BS, of Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Fla., and Susannah Berke, MD, Three Rivers Dermatology, Coraopolis, Pa. The column was edited by Donna Bilu Martin, MD.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to [email protected].

References
 

Carriveau A et al. Nurs Clin North Am. 2019 Jun;54(2):261-75.

Skar GL and Simonsen KA. Lyme Disease. [Updated 2023 May 31]. In: “StatPearls” [Internet]. Treasure Island, Fla.: StatPearls Publishing; 2023 Jan.

Tiger JB et al. J Am Acad Dermatol. 2014 Oct;71(4):e133-4.

Erythema chronicum migrans (ECM) is the classical dermatologic manifestation of Lyme disease, a condition caused by Borrelia burgdorferi, a bacterial spirochete. Lyme disease is the most commonly transmitted tick-borne illness in the United States. This infection is typically transmitted through a bite by the Ixodes tick commonly found in the Midwest, Northeast, and mid-Atlantic regions; however, the geographical distribution continues to expand over time in the United States. Ticks must be attached for 24-48 hours to transmit the pathogen. There are three general stages of the disease: early localized, early disseminated, and late disseminated.

The most common presentation is the early localized disease, which manifests between 3 and 30 days after an infected tick bite. Approximately 70%-80% of cases feature a targetlike lesion that expands centrifugally at the site of the bite. Most commonly, lesions appear on the abdomen, groin, axilla, and popliteal fossa. The diagnosis of ECM requires lesions at least 5 cm in size. Lesions may be asymptomatic, although burning may occur in half of patients. Atypical presentations include bullous, vesicular, hemorrhagic, or necrotic lesions. Up to half of patients may develop multiple ECM lesions. Palms and soles are spared. Differential diagnoses include arthropod reactions, pyoderma gangrenosum, cellulitis, herpes simplex virus and varicella zoster virus, contact dermatitis, or granuloma annulare. The rash is often accompanied by systemic symptoms including fatigue, myalgia, headache, and fever.

The next two stages include early and late disseminated infection. Early disseminated infection often occurs 3-12 weeks after infection and is characterized by muscle pain, dizziness, headache, and cardiac symptoms. CNS involvement occurs in about 20% of patients. Joint involvement may include the knee, ankle, and wrist. If symptoms are only in one joint, septic arthritis is part of the differential diagnosis, so clinical correlation and labs must be considered. Late disseminated infection occurs months or years after initial infection and includes neurologic and rheumatologic symptoms including meningitis, Bell’s palsy, arthritis, and dysesthesia. Knee arthritis is a key feature of this stage. Patients commonly have radicular pain and fibromyalgia-type pain. More severe disease processes include encephalomyelitis, arrhythmias, and heart block.

ECM is often a clinical diagnosis because serologic testing may not be positive during the first 2 weeks of infection. The screening serologic test is the ELISA, and a Western blot confirms the results. Skin histopathology for Lyme disease is often nonspecific and reveals a perivascular infiltrate of histiocytes, plasma cells, and lymphocytes. Silver stain or antibody testing may be used to identify the spirochete. In acrodermatitis chronica atrophicans, late Lyme disease presenting on the distal extremities, lymphocytic and plasma cell infiltrates are present. In borrelial lymphocytoma, a dense dermal lymphocytic infiltrate is present.

The standard for treatment of early localized disease is oral doxycycline in adults. Alternatives may be used if a patient is allergic or for children under 9. Disseminated disease may be treated with IV ceftriaxone and topical steroids are used if ocular symptoms are involved. Early treatment is often curative.

This patient’s antibodies were negative initially, but became positive after 6 weeks. He was treated empirically at the time of his office visit with doxycycline for 1 month.

This case and the photo were submitted by Lucas Shapiro, BS, of Nova Southeastern University College of Osteopathic Medicine, Fort Lauderdale, Fla., and Susannah Berke, MD, Three Rivers Dermatology, Coraopolis, Pa. The column was edited by Donna Bilu Martin, MD.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to [email protected].

References
 

Carriveau A et al. Nurs Clin North Am. 2019 Jun;54(2):261-75.

Skar GL and Simonsen KA. Lyme Disease. [Updated 2023 May 31]. In: “StatPearls” [Internet]. Treasure Island, Fla.: StatPearls Publishing; 2023 Jan.

Tiger JB et al. J Am Acad Dermatol. 2014 Oct;71(4):e133-4.

Recorded Aug. 28, 2023. This transcript has been edited for clarity.
 

John M. Mandrola, MD: I’m here at the European Society of Cardiology meeting, and I’m very excited to have two colleagues whom I met at the Western Atrial Fibrillation Symposium (Western AFib) and who presented the CASTLE-HTx study. This is Christian Sohns and Philipp Sommer, and the CASTLE-HTx study is very exciting.

Before I get into that, I really want to introduce the concept of atrial fibrillation in heart failure. I like to say that there are two big populations of patients with atrial fibrillation, and the vast majority can be treated slowly with reassurance and education. There is a group of patients who have heart failure who, when they develop atrial fibrillation, can degenerate rapidly. The CASTLE-HTx study looked at catheter ablation versus medical therapy in patients with advanced heart failure.

Christian, why don’t you tell us the top-line results and what you found.
 

CASTLE-HTx key findings

Christian Sohns, MD, PhD: Thanks, first of all, for mentioning this special cohort of patients in end-stage heart failure, which is very important. The endpoint of the study was a composite of death from any cause or left ventricular assist device (LVAD) implantation and heart transplantation. These are very hard, strong clinical endpoints, not the rate of rehospitalization or something like that.

Catheter ablation was superior to medical therapy alone in terms of this composite endpoint. That was driven by cardiovascular death and all-cause mortality, which highlights the fact that you should always consider atrial fibrillation ablation in the end-stage heart failure cohort. The findings were driven by the fact that we saw left ventricular reverse remodeling and the reduction of atrial fibrillation in these patients.

Dr. Mandrola: Tell me about how it came about. It was conducted at your center. Who were these patients?

Philipp Sommer, MD: As one of the biggest centers for heart transplantations all over Europe, with roughly 100 transplants per year, we had many patients being referred to our center with the questions of whether those patients are eligible for a heart transplantation. Not all of the patients in our study were listed for a transplant, but all of them were admitted in that end-stage heart failure status to evaluate their eligibility for transplant.

If we look at the baseline data of those patients, they had an ejection fraction of 29%. They had a 6-minute walk test as a functional capacity parameter of around 300 m. Approximately two thirds of them were New York Heart Association class III and IV, which is significantly worse than what we saw in the previous studies dealing with heart failure patients.

I think overall, if you also look at NT-proBNP levels, this is a really sick patient population where some people might doubt if they should admit and refer those patients for an ablation procedure. Therefore, it’s really interesting and fascinating to see the results.

Dr. Mandrola: I did read in the manuscript, and I heard from you, that these were recruited as outpatients. So they were stable outpatients who were referred to the center for consideration of an LVAD or transplant?

Dr. Sohns: The definition of stability is very difficult in these patients because they have hospital stays, they have a history of drug therapy, and they have a history of interventions also behind them – not atrial fibrillation ablation, but others. I think these patients are referred because the referring physicians are done with the case. They can no longer offer any option to the patients other than surgical treatment, assist device, pump implantation, or transplantation.

If you look at the guidelines, they do not comment on atrial fibrillation ablation in this cohort of patients. Also, they have different recommendations between the American societies and the European societies regarding what is end-stage heart failure and how to treat these patients. Therefore, it was a big benefit of CASTLE-HTx that we randomized a cohort of patients with advanced end-stage heart failure.
 

How can AFib ablation have such big, early effects?

Dr. Mandrola: These are very clinically significant findings, with large effect sizes and very early separation of the Kaplan-Meier curves. How do you explain how dramatic an effect that is, and how early of an effect?

Dr. Sommer: That’s one of the key questions at the end of the day. I think our job basically was to provide the data and to ensure that the data are clean and that it’s all perfectly done. The interpretation of these data is really kind of difficult, although we do not have the 100% perfect and obvious explanation why the curves separated so early. Our view on that is that we are talking about a pretty fragile patient population, so little differences like having a tachyarrhythmia of 110 day in, day out or being in sinus rhythm of 60 can make a huge difference. That’s obviously pretty early.

The one that remains in tachyarrhythmia will deteriorate and will require an LVAD after a couple of months, and the one that you may keep in sinus rhythm, even with reduced atrial fibrillation burden – not zero, but reduced atrial fibrillation burden – and improved LV function, all of a sudden this patient will still remain on a low level of being stable, but he or she will remain stable and will not require any surgical interventions for the next 1.5-2 years. If we can manage to do this, just postponing the natural cause of the disease, I think that is a great benefit for the patient.

Dr. Mandrola: One of the things that comes up in our center is that I look at some of these patients and think, there’s no way I can put this patient under general anesthetic and do all of this. Your ablation procedure wasn’t that extensive, was it?

Dr. Sohns: On the one hand, no. On the other hand, yes. You need to take into consideration that it has been performed by experienced physicians with experience in heart failure treatment and atrial fibrillation in heart transplantation centers, though it›s not sure that we can transfer these results one-to-one to all other centers in the world.

It is very clear that we have almost no major complications in these patients. We were able to do these ablation procedures without general anesthesia. We have 60% of patients who had pulmonary vein isolation only and 40% of patients who have PVI and additional therapy. We have a procedure duration of almost 90 minutes during radiofrequency ablation.

We have different categories. When you talk about the different patient cohorts, we also see different stages of myocardial tissue damage, which will be part of another publication for sure. It is, in part, surprising how normal some of the atria were despite having a volume of 180 mL, but they had no fibrosis. That was very interesting.

Dr. Mandrola: How did the persistent vs paroxysmal atrial fibrillation sort out? Were these mostly patients with persistent atrial fibrillation?

Dr. Sommer: Two-thirds were persistent. It would be expected in this patient population that you would not find so many paroxysmal cases. I think it›s very important what Christian was just mentioning that when we discussed the trial design, we were anticipating problems with the sedation, for example. With the follow-up of those procedures, would they decompensate because of the fluid that you have to deliver during such a procedure.

We were quite surprised at the end of the day that the procedures were quite straightforward. Fortunately, we had no major complications. I think there were four complications in the 100 ablated patients. I think we were really positive about how the procedures turned out.

I should mention that one of the exclusion criteria was a left atrial diameter of about 60 mm. The huge ones may be very diseased, and maybe the hopeless ones were excluded from the study. Below 60 mm, we did the ablation.
 

Rhythm control

Dr. Mandrola: One of my colleagues, who is even more skeptical than me, wanted me to ask you, why wouldn’t you take a patient with persistent atrial fibrillation who had heart failure and just cardiovert and use amiodarone and try and maintain sinus rhythm that way?

Dr. Sohns: It is important to mention that 50% of the patients have already had amiodarone before they were randomized and enrolled for the trial. It might bring you a couple of minutes or a couple of hours [of relief], but the patients would get recurrence.

It was very interesting also, and this is in line with the data from Jason Andrade, who demonstrated that we were able to reduce the percentage of patients with persistent atrial fibrillation to paroxysmal. We did a down-staging of the underlying disease. This is not possible with cardioversion or drugs, for example.

Dr. Sommer: What I really like about that question and that comment is the idea that rhythm control in this subset of patients obviously has a role and an importance. It may be a cardioversion initially, giving amiodarone if they didn’t have that before, and you can keep the patient in sinus rhythm with this therapy, I think we’re reaching the same goal.

I think the critical point to get into the mind of physicians who treat heart failure is that sinus rhythm is beneficial, however you get there. Ablation, of course, as in other studies, is the most powerful tool to get there. Cardioversion can be a really good thing to do; you just have to think about it and consider it.

Dr. Mandrola: I do want to say to everybody that there is a tension sometimes between the heart failure community and the electrophysiology community. I think the ideal situation is that we work together, because I think that we can help with the maintenance of sinus rhythm. The control group mortality at 1 year was 20%, and I’ve heard people say that that’s not advanced heart failure. Advanced heart failure patients have much higher mortality than that. My colleague who is a heart failure specialist was criticizing a selection bias in picking the best patients. How would you answer that?

Dr. Sohns: There are data available from Eurotransplant, for example, that the waiting list mortality is 18%, so I think we are almost in line with this 20% mortality in this conservative group. You cannot generalize it. All these patients have different histories. We have 60% dilated cardiomyopathy and 40% ischemic cardiomyopathy. I think it is a very representative group in contrast to your friend who suggests that it is not.

Dr. Sommer: What I like about the discussion is that some approach us to say that the mortality in the control group is much too high – like, what are you doing with those patients that you create so many endpoints? Then others say that it’s not high enough because that is not end-stage heart failure. Come on! We have a patient cohort that is very well described and very well characterized.

If the label is end-stage heart failure, advanced heart failure, or whatever, they are sicker than the patients that we had in earlier trials. The patients that we treated were mostly excluded from all other trials. We opened the door. We found a clear result. I think everyone can see whatever you like to see.

Dr. Mandrola: What would your take-home message be after having done this trial design, the trial was conducted in your single center, and you come up with these amazing results? What would your message be to the whole community?

Dr. Sohns: Taking into consideration how severely sick these patients are, I can just repeat it: They are one step away from death, more or less, or from surgical intervention that can prolong their life. You should also consider that there are options like atrial fibrillation ablation that can buy time, postpone the natural course, or even in some patients replace the destination therapy. Therefore, in my opinion the next guidelines should recommend that every patient should carefully be checked for sinus rhythm before bringing these patients into the environment of transplantation.

Dr. Sommer: My interpretation is that we have to try to bring into physicians’ minds that besides a well-established and well-documented effect of drug therapy with the fabulous four, we may now have the fabulous five, including an ablation option for patients with atrial fibrillation.

Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. Dr. Sohns is deputy director of the Heart and Diabetes Center NRW, Ruhr University Bochum, Bad Oeynhausen, Germany. Dr. Sommer is professor of cardiology at the Heart and Diabetes Center NRW. Dr. Mandrola reported no conflicts of interest. Dr. Sohns reported receiving research funding from Else Kröner–Fresenius–Stiftung. Dr. Sommer reported consulting with Abbott, Biosense Webster, Boston Scientific, and Medtronic USA.


A version of this article first appeared on Medscape.com.

Recorded Aug. 28, 2023. This transcript has been edited for clarity.
 

John M. Mandrola, MD: I’m here at the European Society of Cardiology meeting, and I’m very excited to have two colleagues whom I met at the Western Atrial Fibrillation Symposium (Western AFib) and who presented the CASTLE-HTx study. This is Christian Sohns and Philipp Sommer, and the CASTLE-HTx study is very exciting.

Before I get into that, I really want to introduce the concept of atrial fibrillation in heart failure. I like to say that there are two big populations of patients with atrial fibrillation, and the vast majority can be treated slowly with reassurance and education. There is a group of patients who have heart failure who, when they develop atrial fibrillation, can degenerate rapidly. The CASTLE-HTx study looked at catheter ablation versus medical therapy in patients with advanced heart failure.

Christian, why don’t you tell us the top-line results and what you found.
 

CASTLE-HTx key findings

Christian Sohns, MD, PhD: Thanks, first of all, for mentioning this special cohort of patients in end-stage heart failure, which is very important. The endpoint of the study was a composite of death from any cause or left ventricular assist device (LVAD) implantation and heart transplantation. These are very hard, strong clinical endpoints, not the rate of rehospitalization or something like that.

Catheter ablation was superior to medical therapy alone in terms of this composite endpoint. That was driven by cardiovascular death and all-cause mortality, which highlights the fact that you should always consider atrial fibrillation ablation in the end-stage heart failure cohort. The findings were driven by the fact that we saw left ventricular reverse remodeling and the reduction of atrial fibrillation in these patients.

Dr. Mandrola: Tell me about how it came about. It was conducted at your center. Who were these patients?

Philipp Sommer, MD: As one of the biggest centers for heart transplantations all over Europe, with roughly 100 transplants per year, we had many patients being referred to our center with the questions of whether those patients are eligible for a heart transplantation. Not all of the patients in our study were listed for a transplant, but all of them were admitted in that end-stage heart failure status to evaluate their eligibility for transplant.

If we look at the baseline data of those patients, they had an ejection fraction of 29%. They had a 6-minute walk test as a functional capacity parameter of around 300 m. Approximately two thirds of them were New York Heart Association class III and IV, which is significantly worse than what we saw in the previous studies dealing with heart failure patients.

I think overall, if you also look at NT-proBNP levels, this is a really sick patient population where some people might doubt if they should admit and refer those patients for an ablation procedure. Therefore, it’s really interesting and fascinating to see the results.

Dr. Mandrola: I did read in the manuscript, and I heard from you, that these were recruited as outpatients. So they were stable outpatients who were referred to the center for consideration of an LVAD or transplant?

Dr. Sohns: The definition of stability is very difficult in these patients because they have hospital stays, they have a history of drug therapy, and they have a history of interventions also behind them – not atrial fibrillation ablation, but others. I think these patients are referred because the referring physicians are done with the case. They can no longer offer any option to the patients other than surgical treatment, assist device, pump implantation, or transplantation.

If you look at the guidelines, they do not comment on atrial fibrillation ablation in this cohort of patients. Also, they have different recommendations between the American societies and the European societies regarding what is end-stage heart failure and how to treat these patients. Therefore, it was a big benefit of CASTLE-HTx that we randomized a cohort of patients with advanced end-stage heart failure.
 

How can AFib ablation have such big, early effects?

Dr. Mandrola: These are very clinically significant findings, with large effect sizes and very early separation of the Kaplan-Meier curves. How do you explain how dramatic an effect that is, and how early of an effect?

Dr. Sommer: That’s one of the key questions at the end of the day. I think our job basically was to provide the data and to ensure that the data are clean and that it’s all perfectly done. The interpretation of these data is really kind of difficult, although we do not have the 100% perfect and obvious explanation why the curves separated so early. Our view on that is that we are talking about a pretty fragile patient population, so little differences like having a tachyarrhythmia of 110 day in, day out or being in sinus rhythm of 60 can make a huge difference. That’s obviously pretty early.

The one that remains in tachyarrhythmia will deteriorate and will require an LVAD after a couple of months, and the one that you may keep in sinus rhythm, even with reduced atrial fibrillation burden – not zero, but reduced atrial fibrillation burden – and improved LV function, all of a sudden this patient will still remain on a low level of being stable, but he or she will remain stable and will not require any surgical interventions for the next 1.5-2 years. If we can manage to do this, just postponing the natural cause of the disease, I think that is a great benefit for the patient.

Dr. Mandrola: One of the things that comes up in our center is that I look at some of these patients and think, there’s no way I can put this patient under general anesthetic and do all of this. Your ablation procedure wasn’t that extensive, was it?

Dr. Sohns: On the one hand, no. On the other hand, yes. You need to take into consideration that it has been performed by experienced physicians with experience in heart failure treatment and atrial fibrillation in heart transplantation centers, though it›s not sure that we can transfer these results one-to-one to all other centers in the world.

It is very clear that we have almost no major complications in these patients. We were able to do these ablation procedures without general anesthesia. We have 60% of patients who had pulmonary vein isolation only and 40% of patients who have PVI and additional therapy. We have a procedure duration of almost 90 minutes during radiofrequency ablation.

We have different categories. When you talk about the different patient cohorts, we also see different stages of myocardial tissue damage, which will be part of another publication for sure. It is, in part, surprising how normal some of the atria were despite having a volume of 180 mL, but they had no fibrosis. That was very interesting.

Dr. Mandrola: How did the persistent vs paroxysmal atrial fibrillation sort out? Were these mostly patients with persistent atrial fibrillation?

Dr. Sommer: Two-thirds were persistent. It would be expected in this patient population that you would not find so many paroxysmal cases. I think it›s very important what Christian was just mentioning that when we discussed the trial design, we were anticipating problems with the sedation, for example. With the follow-up of those procedures, would they decompensate because of the fluid that you have to deliver during such a procedure.

We were quite surprised at the end of the day that the procedures were quite straightforward. Fortunately, we had no major complications. I think there were four complications in the 100 ablated patients. I think we were really positive about how the procedures turned out.

I should mention that one of the exclusion criteria was a left atrial diameter of about 60 mm. The huge ones may be very diseased, and maybe the hopeless ones were excluded from the study. Below 60 mm, we did the ablation.
 

Rhythm control

Dr. Mandrola: One of my colleagues, who is even more skeptical than me, wanted me to ask you, why wouldn’t you take a patient with persistent atrial fibrillation who had heart failure and just cardiovert and use amiodarone and try and maintain sinus rhythm that way?

Dr. Sohns: It is important to mention that 50% of the patients have already had amiodarone before they were randomized and enrolled for the trial. It might bring you a couple of minutes or a couple of hours [of relief], but the patients would get recurrence.

It was very interesting also, and this is in line with the data from Jason Andrade, who demonstrated that we were able to reduce the percentage of patients with persistent atrial fibrillation to paroxysmal. We did a down-staging of the underlying disease. This is not possible with cardioversion or drugs, for example.

Dr. Sommer: What I really like about that question and that comment is the idea that rhythm control in this subset of patients obviously has a role and an importance. It may be a cardioversion initially, giving amiodarone if they didn’t have that before, and you can keep the patient in sinus rhythm with this therapy, I think we’re reaching the same goal.

I think the critical point to get into the mind of physicians who treat heart failure is that sinus rhythm is beneficial, however you get there. Ablation, of course, as in other studies, is the most powerful tool to get there. Cardioversion can be a really good thing to do; you just have to think about it and consider it.

Dr. Mandrola: I do want to say to everybody that there is a tension sometimes between the heart failure community and the electrophysiology community. I think the ideal situation is that we work together, because I think that we can help with the maintenance of sinus rhythm. The control group mortality at 1 year was 20%, and I’ve heard people say that that’s not advanced heart failure. Advanced heart failure patients have much higher mortality than that. My colleague who is a heart failure specialist was criticizing a selection bias in picking the best patients. How would you answer that?

Dr. Sohns: There are data available from Eurotransplant, for example, that the waiting list mortality is 18%, so I think we are almost in line with this 20% mortality in this conservative group. You cannot generalize it. All these patients have different histories. We have 60% dilated cardiomyopathy and 40% ischemic cardiomyopathy. I think it is a very representative group in contrast to your friend who suggests that it is not.

Dr. Sommer: What I like about the discussion is that some approach us to say that the mortality in the control group is much too high – like, what are you doing with those patients that you create so many endpoints? Then others say that it’s not high enough because that is not end-stage heart failure. Come on! We have a patient cohort that is very well described and very well characterized.

If the label is end-stage heart failure, advanced heart failure, or whatever, they are sicker than the patients that we had in earlier trials. The patients that we treated were mostly excluded from all other trials. We opened the door. We found a clear result. I think everyone can see whatever you like to see.

Dr. Mandrola: What would your take-home message be after having done this trial design, the trial was conducted in your single center, and you come up with these amazing results? What would your message be to the whole community?

Dr. Sohns: Taking into consideration how severely sick these patients are, I can just repeat it: They are one step away from death, more or less, or from surgical intervention that can prolong their life. You should also consider that there are options like atrial fibrillation ablation that can buy time, postpone the natural course, or even in some patients replace the destination therapy. Therefore, in my opinion the next guidelines should recommend that every patient should carefully be checked for sinus rhythm before bringing these patients into the environment of transplantation.

Dr. Sommer: My interpretation is that we have to try to bring into physicians’ minds that besides a well-established and well-documented effect of drug therapy with the fabulous four, we may now have the fabulous five, including an ablation option for patients with atrial fibrillation.

Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. Dr. Sohns is deputy director of the Heart and Diabetes Center NRW, Ruhr University Bochum, Bad Oeynhausen, Germany. Dr. Sommer is professor of cardiology at the Heart and Diabetes Center NRW. Dr. Mandrola reported no conflicts of interest. Dr. Sohns reported receiving research funding from Else Kröner–Fresenius–Stiftung. Dr. Sommer reported consulting with Abbott, Biosense Webster, Boston Scientific, and Medtronic USA.


A version of this article first appeared on Medscape.com.

Recorded Aug. 28, 2023. This transcript has been edited for clarity.
 

John M. Mandrola, MD: I’m here at the European Society of Cardiology meeting, and I’m very excited to have two colleagues whom I met at the Western Atrial Fibrillation Symposium (Western AFib) and who presented the CASTLE-HTx study. This is Christian Sohns and Philipp Sommer, and the CASTLE-HTx study is very exciting.

Before I get into that, I really want to introduce the concept of atrial fibrillation in heart failure. I like to say that there are two big populations of patients with atrial fibrillation, and the vast majority can be treated slowly with reassurance and education. There is a group of patients who have heart failure who, when they develop atrial fibrillation, can degenerate rapidly. The CASTLE-HTx study looked at catheter ablation versus medical therapy in patients with advanced heart failure.

Christian, why don’t you tell us the top-line results and what you found.
 

CASTLE-HTx key findings

Christian Sohns, MD, PhD: Thanks, first of all, for mentioning this special cohort of patients in end-stage heart failure, which is very important. The endpoint of the study was a composite of death from any cause or left ventricular assist device (LVAD) implantation and heart transplantation. These are very hard, strong clinical endpoints, not the rate of rehospitalization or something like that.

Catheter ablation was superior to medical therapy alone in terms of this composite endpoint. That was driven by cardiovascular death and all-cause mortality, which highlights the fact that you should always consider atrial fibrillation ablation in the end-stage heart failure cohort. The findings were driven by the fact that we saw left ventricular reverse remodeling and the reduction of atrial fibrillation in these patients.

Dr. Mandrola: Tell me about how it came about. It was conducted at your center. Who were these patients?

Philipp Sommer, MD: As one of the biggest centers for heart transplantations all over Europe, with roughly 100 transplants per year, we had many patients being referred to our center with the questions of whether those patients are eligible for a heart transplantation. Not all of the patients in our study were listed for a transplant, but all of them were admitted in that end-stage heart failure status to evaluate their eligibility for transplant.

If we look at the baseline data of those patients, they had an ejection fraction of 29%. They had a 6-minute walk test as a functional capacity parameter of around 300 m. Approximately two thirds of them were New York Heart Association class III and IV, which is significantly worse than what we saw in the previous studies dealing with heart failure patients.

I think overall, if you also look at NT-proBNP levels, this is a really sick patient population where some people might doubt if they should admit and refer those patients for an ablation procedure. Therefore, it’s really interesting and fascinating to see the results.

Dr. Mandrola: I did read in the manuscript, and I heard from you, that these were recruited as outpatients. So they were stable outpatients who were referred to the center for consideration of an LVAD or transplant?

Dr. Sohns: The definition of stability is very difficult in these patients because they have hospital stays, they have a history of drug therapy, and they have a history of interventions also behind them – not atrial fibrillation ablation, but others. I think these patients are referred because the referring physicians are done with the case. They can no longer offer any option to the patients other than surgical treatment, assist device, pump implantation, or transplantation.

If you look at the guidelines, they do not comment on atrial fibrillation ablation in this cohort of patients. Also, they have different recommendations between the American societies and the European societies regarding what is end-stage heart failure and how to treat these patients. Therefore, it was a big benefit of CASTLE-HTx that we randomized a cohort of patients with advanced end-stage heart failure.
 

How can AFib ablation have such big, early effects?

Dr. Mandrola: These are very clinically significant findings, with large effect sizes and very early separation of the Kaplan-Meier curves. How do you explain how dramatic an effect that is, and how early of an effect?

Dr. Sommer: That’s one of the key questions at the end of the day. I think our job basically was to provide the data and to ensure that the data are clean and that it’s all perfectly done. The interpretation of these data is really kind of difficult, although we do not have the 100% perfect and obvious explanation why the curves separated so early. Our view on that is that we are talking about a pretty fragile patient population, so little differences like having a tachyarrhythmia of 110 day in, day out or being in sinus rhythm of 60 can make a huge difference. That’s obviously pretty early.

The one that remains in tachyarrhythmia will deteriorate and will require an LVAD after a couple of months, and the one that you may keep in sinus rhythm, even with reduced atrial fibrillation burden – not zero, but reduced atrial fibrillation burden – and improved LV function, all of a sudden this patient will still remain on a low level of being stable, but he or she will remain stable and will not require any surgical interventions for the next 1.5-2 years. If we can manage to do this, just postponing the natural cause of the disease, I think that is a great benefit for the patient.

Dr. Mandrola: One of the things that comes up in our center is that I look at some of these patients and think, there’s no way I can put this patient under general anesthetic and do all of this. Your ablation procedure wasn’t that extensive, was it?

Dr. Sohns: On the one hand, no. On the other hand, yes. You need to take into consideration that it has been performed by experienced physicians with experience in heart failure treatment and atrial fibrillation in heart transplantation centers, though it›s not sure that we can transfer these results one-to-one to all other centers in the world.

It is very clear that we have almost no major complications in these patients. We were able to do these ablation procedures without general anesthesia. We have 60% of patients who had pulmonary vein isolation only and 40% of patients who have PVI and additional therapy. We have a procedure duration of almost 90 minutes during radiofrequency ablation.

We have different categories. When you talk about the different patient cohorts, we also see different stages of myocardial tissue damage, which will be part of another publication for sure. It is, in part, surprising how normal some of the atria were despite having a volume of 180 mL, but they had no fibrosis. That was very interesting.

Dr. Mandrola: How did the persistent vs paroxysmal atrial fibrillation sort out? Were these mostly patients with persistent atrial fibrillation?

Dr. Sommer: Two-thirds were persistent. It would be expected in this patient population that you would not find so many paroxysmal cases. I think it›s very important what Christian was just mentioning that when we discussed the trial design, we were anticipating problems with the sedation, for example. With the follow-up of those procedures, would they decompensate because of the fluid that you have to deliver during such a procedure.

We were quite surprised at the end of the day that the procedures were quite straightforward. Fortunately, we had no major complications. I think there were four complications in the 100 ablated patients. I think we were really positive about how the procedures turned out.

I should mention that one of the exclusion criteria was a left atrial diameter of about 60 mm. The huge ones may be very diseased, and maybe the hopeless ones were excluded from the study. Below 60 mm, we did the ablation.
 

Rhythm control

Dr. Mandrola: One of my colleagues, who is even more skeptical than me, wanted me to ask you, why wouldn’t you take a patient with persistent atrial fibrillation who had heart failure and just cardiovert and use amiodarone and try and maintain sinus rhythm that way?

Dr. Sohns: It is important to mention that 50% of the patients have already had amiodarone before they were randomized and enrolled for the trial. It might bring you a couple of minutes or a couple of hours [of relief], but the patients would get recurrence.

It was very interesting also, and this is in line with the data from Jason Andrade, who demonstrated that we were able to reduce the percentage of patients with persistent atrial fibrillation to paroxysmal. We did a down-staging of the underlying disease. This is not possible with cardioversion or drugs, for example.

Dr. Sommer: What I really like about that question and that comment is the idea that rhythm control in this subset of patients obviously has a role and an importance. It may be a cardioversion initially, giving amiodarone if they didn’t have that before, and you can keep the patient in sinus rhythm with this therapy, I think we’re reaching the same goal.

I think the critical point to get into the mind of physicians who treat heart failure is that sinus rhythm is beneficial, however you get there. Ablation, of course, as in other studies, is the most powerful tool to get there. Cardioversion can be a really good thing to do; you just have to think about it and consider it.

Dr. Mandrola: I do want to say to everybody that there is a tension sometimes between the heart failure community and the electrophysiology community. I think the ideal situation is that we work together, because I think that we can help with the maintenance of sinus rhythm. The control group mortality at 1 year was 20%, and I’ve heard people say that that’s not advanced heart failure. Advanced heart failure patients have much higher mortality than that. My colleague who is a heart failure specialist was criticizing a selection bias in picking the best patients. How would you answer that?

Dr. Sohns: There are data available from Eurotransplant, for example, that the waiting list mortality is 18%, so I think we are almost in line with this 20% mortality in this conservative group. You cannot generalize it. All these patients have different histories. We have 60% dilated cardiomyopathy and 40% ischemic cardiomyopathy. I think it is a very representative group in contrast to your friend who suggests that it is not.

Dr. Sommer: What I like about the discussion is that some approach us to say that the mortality in the control group is much too high – like, what are you doing with those patients that you create so many endpoints? Then others say that it’s not high enough because that is not end-stage heart failure. Come on! We have a patient cohort that is very well described and very well characterized.

If the label is end-stage heart failure, advanced heart failure, or whatever, they are sicker than the patients that we had in earlier trials. The patients that we treated were mostly excluded from all other trials. We opened the door. We found a clear result. I think everyone can see whatever you like to see.

Dr. Mandrola: What would your take-home message be after having done this trial design, the trial was conducted in your single center, and you come up with these amazing results? What would your message be to the whole community?

Dr. Sohns: Taking into consideration how severely sick these patients are, I can just repeat it: They are one step away from death, more or less, or from surgical intervention that can prolong their life. You should also consider that there are options like atrial fibrillation ablation that can buy time, postpone the natural course, or even in some patients replace the destination therapy. Therefore, in my opinion the next guidelines should recommend that every patient should carefully be checked for sinus rhythm before bringing these patients into the environment of transplantation.

Dr. Sommer: My interpretation is that we have to try to bring into physicians’ minds that besides a well-established and well-documented effect of drug therapy with the fabulous four, we may now have the fabulous five, including an ablation option for patients with atrial fibrillation.

Dr. Mandrola is a clinical electrophysiologist at Baptist Medical Associates, Louisville, Ky. Dr. Sohns is deputy director of the Heart and Diabetes Center NRW, Ruhr University Bochum, Bad Oeynhausen, Germany. Dr. Sommer is professor of cardiology at the Heart and Diabetes Center NRW. Dr. Mandrola reported no conflicts of interest. Dr. Sohns reported receiving research funding from Else Kröner–Fresenius–Stiftung. Dr. Sommer reported consulting with Abbott, Biosense Webster, Boston Scientific, and Medtronic USA.


A version of this article first appeared on Medscape.com.