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I’m Dr. Neil Skolnik. The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.
We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.
I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.
When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).
Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.
For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.
Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.
Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.
To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.
Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.
After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.
Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.
In summary:
- Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
- Initially evaluate with an NT-proBNP level and an echocardiogram.
- First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.
This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
I’m Dr. Neil Skolnik. The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.
We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.
I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.
When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).
Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.
For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.
Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.
Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.
To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.
Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.
After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.
Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.
In summary:
- Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
- Initially evaluate with an NT-proBNP level and an echocardiogram.
- First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.
This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
I’m Dr. Neil Skolnik. The incidence of HFpEF is increasing, yet it’s underrecognized. Now that there are evidence-based treatment approaches that improve outcomes, we’ve started to look for this condition and are diagnosing it more often. HFpEF is commonly encountered in primary care.
We should be thinking about HFpEF when we see adults with shortness of breath and/or fatigue and reduced exercise capacity, particularly in the settings of obesity, hypertension, or diabetes. It may not be simple deconditioning; it could be HFpEF.
I’ll organize this discussion into three topics: when to think about HFpEF, how to diagnosis it. and how to treat it.
When to think about HFpEF. When we see a person with risk factors (e.g., older age, obesity, diabetes, hypertension) experiencing dyspnea or fatigue with physical activity, their symptoms are not always from simple deconditioning. HFpEF should be on our differential as well as chronic obstructive pulmonary disease (COPD).
Making the diagnosis. HFpEF is defined as a clinical diagnosis of HR with left ventricular EF (LVEF) greater than 50%. Remember, in HF with reduced EF (HFrEF), the EF is less than 40%, and the EF in midrange HF is 40%-50%. See this recent HF review for more details on reduced and midrange ejection fractions.
For practical purposes, to diagnose HFpEF, check for an elevated N-terminal pro B-type natriuretic peptide (NT-proBNP) (> 125 pg/mL) and evidence of diastolic dysfunction on echocardiogram. Be aware that patients with obesity and HFpEF have lower BNP concentrations than those without obesity, and one professional society has suggested that a 50% reduction in BNP cutoff values should be used when making the diagnosis in patients with obesity.
Of course, we evaluate for other causes of dyspnea and/or edema including lung (most commonly COPD), liver, or kidney disease. When the diagnosis of HFpEF is made, consider whether further evaluation is warranted for specific underlying causes of HFpEF, such as amyloidosis, sarcoid, hemochromatosis, or hypertrophic cardiomyopathy.
Treatment. The evolution of the management of HFpEF has been intriguing. I recommend that people take a look at the guidelines and read the supporting trials. Finding effective therapies has taken longer than it did for HFrEF, but finally, an effective therapy for HFpEF is available.
To quote the guidelines, diuretics should be used “judiciously as needed” to reduce pulmonary congestion and improve symptoms. But here’s the big deal. The mainstays of treatment for HFpEF are the sodium-glucose cotransporter 2 (SGLT2) inhibitors on the basis of the findings of two trials: DELIVER (dapagliflozin) and EMPEROR-Preserved (empagliflozin), both of which have shown very impressive levels of benefit.
Both trials lasted a little over 2 years and found a statistically significant approximately 30% decline in HF hospitalizations and a numerical reduction of about 10% in cardiovascular death, which was statistically significant in meta-analysis. That’s over 2 years! That’s a large level of effect. They also showed improvements in symptoms and health status. Therefore, SGLT2 inhibitors are first-line treatment for all individuals with HFpEF, currently graded as a Class 2a (moderate) recommendation, but likely soon to be upgraded to Class 1 (strong) recommendation.
After the SGLT2 inhibitors, treatment is based on evidence which is not as strong and the recommendations are graded as Class 2b (weak) recommendations. In men with an LVEF less than 55%-60% and for women with any EF, use of a mineralocorticoid antagonist (MRA), an angiotensin receptor-neprilysin inhibitor, or if an ARN inhibitor is not feasible, an angiotensin receptor blocker (ARB) may be considered.
Nonpharmacologic management is also important. Exercise and weight loss (if the patient is overweight) can improve symptoms and quality of life. A new intervention, an implantable ambulatory pulmonary artery sensor, called CardioMEMS, has been evaluated in two trials, showing a decrease in HF hospitalizations. This may be considered for those who experience hospitalizations for HF and continue to experience New York Heart Association functional Class 3 symptoms despite optimal guideline-directed medical therapy or those who have lability in volume status or other medical problems (such as obesity or COPD) that make it difficult to tell whether their symptoms are from HFpEF or a comorbid condition.
In summary:
- Have a low threshold to evaluate for HFpEF in any patients who have shortness of breath, fatigue with exertion, or fluid overload.
- Initially evaluate with an NT-proBNP level and an echocardiogram.
- First-line treatment is an evidence-based SGLT2 inhibitor along with exercise and perhaps weight loss if needed. A loop diuretic can be used as needed to control volume status. Then you can consider, based on symptoms and details discussed above, an MRA, ARN inhibitor, or ARB.
This is important information for a diagnosis that is common in primary care, HFpEF, and for which we now have impressive, effective treatment.
Dr. Skolnik is a professor in the department of family medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the department of family medicine at Abington (Pa.) Jefferson Health. He disclosed conflicts of interest with AstraZeneca, Teva, Eli Lilly, Boehringer Ingelheim; Sanofi, Sanofi Pasteur, GlaxoSmithKline, Merck, and Bayer.
A version of this article first appeared on Medscape.com.