Jon O. Ebbert, MD

Recently, I was critically reminded of the effect that certain medications have on the QT interval. My longtime patient with a history of depression and insomnia presented to me with chest pain symptoms. An ECG was ordered. Within an hour, our QT prolongation warning system notified me that her corrected QT interval (QTc) had prolonged to 530 milliseconds. Her previous QTc was 479 milliseconds. Electrolytes were normal. She was taking paroxetine for depression and trazodone for insomnia. Both were tapered and discontinued over the next several days, with return of her QTc to 473 milliseconds. Crisis averted.

A prolonged QT interval reflects abnormal repolarization (electrical recharging) and may lead to torsades de pointes and sudden cardiac death. A long QT interval can be associated with congenital long QT syndrome, electrolyte abnormalities, or medications. The greatest risk factors for an adverse event such as sudden death or aborted cardiac arrest are associated with a QTc of more than 500 milliseconds and a history of nonvasovagal syncope.

In my patient population surviving into their later years, iatrogenic causes of prolonged QTc are far and away the most common etiologies. And with my patient population either becoming more depressed – or me becoming more adept at diagnosing it – antidepressants are high on the list of offenders.

So which ones are the ones that we should be most concerned about? And is there a dose effect?

Dr. Victor M. Castro and his team published a case-control study (BMJ 2013;346:f288) quantifying the impact of citalopram and other selective serotonin reuptake inhibitors on the QT interval. Patients were at least 18 years of age with at least one prescription of an antidepressant or methadone between 1990 and 2011. Methadone is known to prolong the QT interval and was used to verify the sensitivity of the analysis.

The antidepressants analyzed were citalopram, escitalopram, fluoxetine, paroxetine, sertraline, amitriptyline, bupropion, duloxetine, mirtazapine, nortriptyline, and venlafaxine. Patients’ ECGs were selected for analysis if they occurred at least 14 days after a prescription. Of the study patients receiving a medication of interest, 38,397 patients had an ECG in the specified 14- to 90-day window. Analyses of QTc were adjusted for potential confounders such as preexisting cardiovascular disease.

In this population, 20.4% of individuals were characterized as having abnormal or high QTc values. Methadone predictably increased QTc. Dose was observed to be a significant predictor of QTc with citalopram (10-20 mg), escitalopram (5-10 mg and 10-20 mg), and amitriptyline (25-50 mg). Bupropion was found to significantly decrease QTc (P less than .05). Notably, 13.1% of patients who started citalopram with a QTc in the normal range shifted to abnormal after a dose increase.

In this study, one-fifth of patients had an abnormal QTc. But QTc is only considered a proxy measure for torsades de pointes. So, whether we should be routinely ordering ECGs for patients started on citalopram, escitalopram, or amitriptyline, or for whom the dose of these drugs has been changed, remains uncertain.

When my patient’s depression ferociously returned, I restarted paroxetine. This time, I ordered a follow-up ECG, which showed no QT prolongation. Crisis averted.

Recently, I was critically reminded of the effect that certain medications have on the QT interval. My longtime patient with a history of depression and insomnia presented to me with chest pain symptoms. An ECG was ordered. Within an hour, our QT prolongation warning system notified me that her corrected QT interval (QTc) had prolonged to 530 milliseconds. Her previous QTc was 479 milliseconds. Electrolytes were normal. She was taking paroxetine for depression and trazodone for insomnia. Both were tapered and discontinued over the next several days, with return of her QTc to 473 milliseconds. Crisis averted.

A prolonged QT interval reflects abnormal repolarization (electrical recharging) and may lead to torsades de pointes and sudden cardiac death. A long QT interval can be associated with congenital long QT syndrome, electrolyte abnormalities, or medications. The greatest risk factors for an adverse event such as sudden death or aborted cardiac arrest are associated with a QTc of more than 500 milliseconds and a history of nonvasovagal syncope.

In my patient population surviving into their later years, iatrogenic causes of prolonged QTc are far and away the most common etiologies. And with my patient population either becoming more depressed – or me becoming more adept at diagnosing it – antidepressants are high on the list of offenders.

So which ones are the ones that we should be most concerned about? And is there a dose effect?

Dr. Victor M. Castro and his team published a case-control study (BMJ 2013;346:f288) quantifying the impact of citalopram and other selective serotonin reuptake inhibitors on the QT interval. Patients were at least 18 years of age with at least one prescription of an antidepressant or methadone between 1990 and 2011. Methadone is known to prolong the QT interval and was used to verify the sensitivity of the analysis.

The antidepressants analyzed were citalopram, escitalopram, fluoxetine, paroxetine, sertraline, amitriptyline, bupropion, duloxetine, mirtazapine, nortriptyline, and venlafaxine. Patients’ ECGs were selected for analysis if they occurred at least 14 days after a prescription. Of the study patients receiving a medication of interest, 38,397 patients had an ECG in the specified 14- to 90-day window. Analyses of QTc were adjusted for potential confounders such as preexisting cardiovascular disease.

In this population, 20.4% of individuals were characterized as having abnormal or high QTc values. Methadone predictably increased QTc. Dose was observed to be a significant predictor of QTc with citalopram (10-20 mg), escitalopram (5-10 mg and 10-20 mg), and amitriptyline (25-50 mg). Bupropion was found to significantly decrease QTc (P less than .05). Notably, 13.1% of patients who started citalopram with a QTc in the normal range shifted to abnormal after a dose increase.

In this study, one-fifth of patients had an abnormal QTc. But QTc is only considered a proxy measure for torsades de pointes. So, whether we should be routinely ordering ECGs for patients started on citalopram, escitalopram, or amitriptyline, or for whom the dose of these drugs has been changed, remains uncertain.

When my patient’s depression ferociously returned, I restarted paroxetine. This time, I ordered a follow-up ECG, which showed no QT prolongation. Crisis averted.

Recently, I was critically reminded of the effect that certain medications have on the QT interval. My longtime patient with a history of depression and insomnia presented to me with chest pain symptoms. An ECG was ordered. Within an hour, our QT prolongation warning system notified me that her corrected QT interval (QTc) had prolonged to 530 milliseconds. Her previous QTc was 479 milliseconds. Electrolytes were normal. She was taking paroxetine for depression and trazodone for insomnia. Both were tapered and discontinued over the next several days, with return of her QTc to 473 milliseconds. Crisis averted.

A prolonged QT interval reflects abnormal repolarization (electrical recharging) and may lead to torsades de pointes and sudden cardiac death. A long QT interval can be associated with congenital long QT syndrome, electrolyte abnormalities, or medications. The greatest risk factors for an adverse event such as sudden death or aborted cardiac arrest are associated with a QTc of more than 500 milliseconds and a history of nonvasovagal syncope.

In my patient population surviving into their later years, iatrogenic causes of prolonged QTc are far and away the most common etiologies. And with my patient population either becoming more depressed – or me becoming more adept at diagnosing it – antidepressants are high on the list of offenders.

So which ones are the ones that we should be most concerned about? And is there a dose effect?

Dr. Victor M. Castro and his team published a case-control study (BMJ 2013;346:f288) quantifying the impact of citalopram and other selective serotonin reuptake inhibitors on the QT interval. Patients were at least 18 years of age with at least one prescription of an antidepressant or methadone between 1990 and 2011. Methadone is known to prolong the QT interval and was used to verify the sensitivity of the analysis.

The antidepressants analyzed were citalopram, escitalopram, fluoxetine, paroxetine, sertraline, amitriptyline, bupropion, duloxetine, mirtazapine, nortriptyline, and venlafaxine. Patients’ ECGs were selected for analysis if they occurred at least 14 days after a prescription. Of the study patients receiving a medication of interest, 38,397 patients had an ECG in the specified 14- to 90-day window. Analyses of QTc were adjusted for potential confounders such as preexisting cardiovascular disease.

In this population, 20.4% of individuals were characterized as having abnormal or high QTc values. Methadone predictably increased QTc. Dose was observed to be a significant predictor of QTc with citalopram (10-20 mg), escitalopram (5-10 mg and 10-20 mg), and amitriptyline (25-50 mg). Bupropion was found to significantly decrease QTc (P less than .05). Notably, 13.1% of patients who started citalopram with a QTc in the normal range shifted to abnormal after a dose increase.

In this study, one-fifth of patients had an abnormal QTc. But QTc is only considered a proxy measure for torsades de pointes. So, whether we should be routinely ordering ECGs for patients started on citalopram, escitalopram, or amitriptyline, or for whom the dose of these drugs has been changed, remains uncertain.

When my patient’s depression ferociously returned, I restarted paroxetine. This time, I ordered a follow-up ECG, which showed no QT prolongation. Crisis averted.

Male sexual dysfunction is a prevalent disorder and a common presenting clinical complaint. It is especially a challenge when simple "fixes" do not work.

The three major forms of male sexual dysfunction are erectile dysfunction (ED), ejaculatory dysfunction, and decreased libido. In my practice, ED is far and away the issue grappled with most, given the heavy representation of men over the age of 40 years with obesity, hypertension, and polypharmacy.

PDE5 inhibitors are an effective, first-line treatment for men presenting with ED. But discontinuation rates approach 50%, with most men citing lack of consistent efficacy as the cause for stopping. And with the amount of money that patients shell out for these drugs, we should not be surprised. Many of us may try other drugs in the same class, which is commonly an exercise in futility.

What else can we do?

Dr. Farid Dadkhah and colleagues published a randomized, controlled clinical trial evaluating the efficacy of atorvastatin among hyperlipidemic men who were "nonresponders" to sildenafil (Int. J. Impot. Res. 2010;22:51-60). In this study, 131 men were randomized to 40 mg of atorvastatin or matching placebo. Men were 18-70 years of age and had an inadequate response to sildenafil 100 mg, LDL cholesterol less than 160 mg/dL, and ED for more than 6 months. Potential subjects were excluded if they were currently using antilipidemics. Patients were asked to have sexual intercourse at least once per week, and they received medication for 12 weeks. Erectile function was assessed using the International Index of Erectile Function (IIEF-5).

The main outcome was improvement in the IIEF-5 total score. A global efficacy question (GEQ) was used that asked, "Did the treatment you were taking improve your erections?"

Atorvastatin was associated with a statistically significant improvement in the mean IIEF-5 score (P = .01) and GEQ (P = .001). Although 37% of subjects improved, none of the patients regained completely normal erectile function as defined by an IIEF-5 score greater than 21.

The study’s authors note that oxidized LDL inhibits vascular smooth-muscle relaxation. Statins decrease the action of oxidized LDL on endothelial cells, which increases the activity of nitric oxide,* the main vasodilator in penile erection. The investigators also remind us that PDE5 inhibitors are palliative, not curative.

But for our men with ED and dyslipidemia, adding atorvastatin to sildenafil can potentially provide both palliation and cure.

This column, "What Matters," regularly appears in Internal Medicine News, a publication of Frontline Medical Communications. Dr. Ebbert is professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

 * Corrected from earlier version of article.

Male sexual dysfunction is a prevalent disorder and a common presenting clinical complaint. It is especially a challenge when simple "fixes" do not work.

The three major forms of male sexual dysfunction are erectile dysfunction (ED), ejaculatory dysfunction, and decreased libido. In my practice, ED is far and away the issue grappled with most, given the heavy representation of men over the age of 40 years with obesity, hypertension, and polypharmacy.

PDE5 inhibitors are an effective, first-line treatment for men presenting with ED. But discontinuation rates approach 50%, with most men citing lack of consistent efficacy as the cause for stopping. And with the amount of money that patients shell out for these drugs, we should not be surprised. Many of us may try other drugs in the same class, which is commonly an exercise in futility.

What else can we do?

Dr. Farid Dadkhah and colleagues published a randomized, controlled clinical trial evaluating the efficacy of atorvastatin among hyperlipidemic men who were "nonresponders" to sildenafil (Int. J. Impot. Res. 2010;22:51-60). In this study, 131 men were randomized to 40 mg of atorvastatin or matching placebo. Men were 18-70 years of age and had an inadequate response to sildenafil 100 mg, LDL cholesterol less than 160 mg/dL, and ED for more than 6 months. Potential subjects were excluded if they were currently using antilipidemics. Patients were asked to have sexual intercourse at least once per week, and they received medication for 12 weeks. Erectile function was assessed using the International Index of Erectile Function (IIEF-5).

The main outcome was improvement in the IIEF-5 total score. A global efficacy question (GEQ) was used that asked, "Did the treatment you were taking improve your erections?"

Atorvastatin was associated with a statistically significant improvement in the mean IIEF-5 score (P = .01) and GEQ (P = .001). Although 37% of subjects improved, none of the patients regained completely normal erectile function as defined by an IIEF-5 score greater than 21.

The study’s authors note that oxidized LDL inhibits vascular smooth-muscle relaxation. Statins decrease the action of oxidized LDL on endothelial cells, which increases the activity of nitric oxide,* the main vasodilator in penile erection. The investigators also remind us that PDE5 inhibitors are palliative, not curative.

But for our men with ED and dyslipidemia, adding atorvastatin to sildenafil can potentially provide both palliation and cure.

This column, "What Matters," regularly appears in Internal Medicine News, a publication of Frontline Medical Communications. Dr. Ebbert is professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

 * Corrected from earlier version of article.

Male sexual dysfunction is a prevalent disorder and a common presenting clinical complaint. It is especially a challenge when simple "fixes" do not work.

The three major forms of male sexual dysfunction are erectile dysfunction (ED), ejaculatory dysfunction, and decreased libido. In my practice, ED is far and away the issue grappled with most, given the heavy representation of men over the age of 40 years with obesity, hypertension, and polypharmacy.

PDE5 inhibitors are an effective, first-line treatment for men presenting with ED. But discontinuation rates approach 50%, with most men citing lack of consistent efficacy as the cause for stopping. And with the amount of money that patients shell out for these drugs, we should not be surprised. Many of us may try other drugs in the same class, which is commonly an exercise in futility.

What else can we do?

Dr. Farid Dadkhah and colleagues published a randomized, controlled clinical trial evaluating the efficacy of atorvastatin among hyperlipidemic men who were "nonresponders" to sildenafil (Int. J. Impot. Res. 2010;22:51-60). In this study, 131 men were randomized to 40 mg of atorvastatin or matching placebo. Men were 18-70 years of age and had an inadequate response to sildenafil 100 mg, LDL cholesterol less than 160 mg/dL, and ED for more than 6 months. Potential subjects were excluded if they were currently using antilipidemics. Patients were asked to have sexual intercourse at least once per week, and they received medication for 12 weeks. Erectile function was assessed using the International Index of Erectile Function (IIEF-5).

The main outcome was improvement in the IIEF-5 total score. A global efficacy question (GEQ) was used that asked, "Did the treatment you were taking improve your erections?"

Atorvastatin was associated with a statistically significant improvement in the mean IIEF-5 score (P = .01) and GEQ (P = .001). Although 37% of subjects improved, none of the patients regained completely normal erectile function as defined by an IIEF-5 score greater than 21.

The study’s authors note that oxidized LDL inhibits vascular smooth-muscle relaxation. Statins decrease the action of oxidized LDL on endothelial cells, which increases the activity of nitric oxide,* the main vasodilator in penile erection. The investigators also remind us that PDE5 inhibitors are palliative, not curative.

But for our men with ED and dyslipidemia, adding atorvastatin to sildenafil can potentially provide both palliation and cure.

This column, "What Matters," regularly appears in Internal Medicine News, a publication of Frontline Medical Communications. Dr. Ebbert is professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

 * Corrected from earlier version of article.

Most likely I am not alone with the feeling that we spend a lot of resources diagnosing sleep apnea, meticulously titrating CPAP devices, and patiently listening to some of our patients as they list the reasons for not using it.

Many times, the patients have been back to the sleep specialists, who try in earnest to make it work because we all know the litany of potential adverse downstream effects if apnea is left untreated.

We all also know that frightening our patients ("untreated sleep apnea can increase the risk for sudden cardiac death and heart failure. ...") into CPAP compliance is ineffective. So, for the lucky patients whose insurance coverage facilitates the fitting of oral appliances, such as the mandibular advancement device (MAD), we can try these.

Although the reduction in overall apneic episodes is less with MAD than with CPAP devices, the adherence to the MAD may be higher.

So how do CPAP and oral appliances fare head-to-head?

Australian investigators conducted a randomized controlled clinical trial evaluating the health outcomes of patients using the MAD or CPAP for obstructive sleep apnea (Am. J. Respir. Crit. Care Med. Feb. 14, 2013 [doi:10.1164/rccm.201212-2223OC]).

In this study, 126 patients with moderate to severe OSA were randomly assigned to use of MAD or CPAP for 1 month. Patients were excluded if they had central sleep apnea, need for immediate treatment, a coexisting sleep disorder, regular use of sedatives or narcotics, or pre-existing lung or psychiatric disease.

The primary outcome was a difference in 24-hour mean arterial blood pressure. Secondary outcomes included cardiovascular events and arterial stiffness. Neurobehavioral function and quality of life also were measured.

CPAP was significantly more effective than MAD for reducing the apnea-hypopnea index (AHI), but compliance was significantly greater with MAD (6.5 hours per night vs. 5.2 hours per night). No differences in the 24-hour mean arterial pressure were observed, though neither treatment improved blood pressure. Sleepiness, driving stimulator performance, and disease-specific quality of life improved with both treatments by similar amounts. MAD was superior to CPAP on several quality-of-life domains.

This study is extremely informative for our practices in which we cannot consistently provide either motivational enhancement or interventions to improve adherence with CPAP. For CPAP-nonadherent patients for whom an appliance seems like an appropriate next step, this should be pursued. In the case of sleep apnea, we should not let perfect be the enemy of good.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

Most likely I am not alone with the feeling that we spend a lot of resources diagnosing sleep apnea, meticulously titrating CPAP devices, and patiently listening to some of our patients as they list the reasons for not using it.

Many times, the patients have been back to the sleep specialists, who try in earnest to make it work because we all know the litany of potential adverse downstream effects if apnea is left untreated.

We all also know that frightening our patients ("untreated sleep apnea can increase the risk for sudden cardiac death and heart failure. ...") into CPAP compliance is ineffective. So, for the lucky patients whose insurance coverage facilitates the fitting of oral appliances, such as the mandibular advancement device (MAD), we can try these.

Although the reduction in overall apneic episodes is less with MAD than with CPAP devices, the adherence to the MAD may be higher.

So how do CPAP and oral appliances fare head-to-head?

Australian investigators conducted a randomized controlled clinical trial evaluating the health outcomes of patients using the MAD or CPAP for obstructive sleep apnea (Am. J. Respir. Crit. Care Med. Feb. 14, 2013 [doi:10.1164/rccm.201212-2223OC]).

In this study, 126 patients with moderate to severe OSA were randomly assigned to use of MAD or CPAP for 1 month. Patients were excluded if they had central sleep apnea, need for immediate treatment, a coexisting sleep disorder, regular use of sedatives or narcotics, or pre-existing lung or psychiatric disease.

The primary outcome was a difference in 24-hour mean arterial blood pressure. Secondary outcomes included cardiovascular events and arterial stiffness. Neurobehavioral function and quality of life also were measured.

CPAP was significantly more effective than MAD for reducing the apnea-hypopnea index (AHI), but compliance was significantly greater with MAD (6.5 hours per night vs. 5.2 hours per night). No differences in the 24-hour mean arterial pressure were observed, though neither treatment improved blood pressure. Sleepiness, driving stimulator performance, and disease-specific quality of life improved with both treatments by similar amounts. MAD was superior to CPAP on several quality-of-life domains.

This study is extremely informative for our practices in which we cannot consistently provide either motivational enhancement or interventions to improve adherence with CPAP. For CPAP-nonadherent patients for whom an appliance seems like an appropriate next step, this should be pursued. In the case of sleep apnea, we should not let perfect be the enemy of good.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

Most likely I am not alone with the feeling that we spend a lot of resources diagnosing sleep apnea, meticulously titrating CPAP devices, and patiently listening to some of our patients as they list the reasons for not using it.

Many times, the patients have been back to the sleep specialists, who try in earnest to make it work because we all know the litany of potential adverse downstream effects if apnea is left untreated.

We all also know that frightening our patients ("untreated sleep apnea can increase the risk for sudden cardiac death and heart failure. ...") into CPAP compliance is ineffective. So, for the lucky patients whose insurance coverage facilitates the fitting of oral appliances, such as the mandibular advancement device (MAD), we can try these.

Although the reduction in overall apneic episodes is less with MAD than with CPAP devices, the adherence to the MAD may be higher.

So how do CPAP and oral appliances fare head-to-head?

Australian investigators conducted a randomized controlled clinical trial evaluating the health outcomes of patients using the MAD or CPAP for obstructive sleep apnea (Am. J. Respir. Crit. Care Med. Feb. 14, 2013 [doi:10.1164/rccm.201212-2223OC]).

In this study, 126 patients with moderate to severe OSA were randomly assigned to use of MAD or CPAP for 1 month. Patients were excluded if they had central sleep apnea, need for immediate treatment, a coexisting sleep disorder, regular use of sedatives or narcotics, or pre-existing lung or psychiatric disease.

The primary outcome was a difference in 24-hour mean arterial blood pressure. Secondary outcomes included cardiovascular events and arterial stiffness. Neurobehavioral function and quality of life also were measured.

CPAP was significantly more effective than MAD for reducing the apnea-hypopnea index (AHI), but compliance was significantly greater with MAD (6.5 hours per night vs. 5.2 hours per night). No differences in the 24-hour mean arterial pressure were observed, though neither treatment improved blood pressure. Sleepiness, driving stimulator performance, and disease-specific quality of life improved with both treatments by similar amounts. MAD was superior to CPAP on several quality-of-life domains.

This study is extremely informative for our practices in which we cannot consistently provide either motivational enhancement or interventions to improve adherence with CPAP. For CPAP-nonadherent patients for whom an appliance seems like an appropriate next step, this should be pursued. In the case of sleep apnea, we should not let perfect be the enemy of good.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

Recently, my patient presented to our emergency department with a massive acute pulmonary embolism. No clear risk factors were identified.

After about 2 weeks working with our anticoagulation nurses and being unable or unwilling to pay for a home INR monitor, she grew weary. She presented with her husband and asked whether there was anything other than warfarin that they could use that would be safe and effective.

We know alternatives are out there – but are we using them widely, and are they ready for prime time?

The search for new oral anticoagulants (NOACs), which presently includes the major classes of direct thrombin inhibitors (DTIs) and factor Xa (FXa) inhibitors, continues in earnest. The DTI currently on the market is dabigatran. FXa inhibitors include rivaroxaban, apixaban, edoxaban, and betrixaban. NOACs offer the potential advantage of predictable effects and decreased monitoring.

Dr. Soheir S. Adam and her colleagues recently published a systematic review, comparing new oral anticoagulants (NOACs) with warfarin for atrial fibrillation and venous thromboembolism (Ann. Intern. Med. 2012;157:796-807).

The authors identified six randomized clinical trials involving more than 60,000 patients. Three evaluated NOACs for chronic atrial fibrillation (AF), and three evaluated them for venous thromboembolism (VTE). All studies compared these drugs to adjusted-dose warfarin. Data were combined for DTIs and FXa inhibitors.

For AF, NOACs were associated with decreased all-cause mortality (relative risk [RR], 0.88; 95% confidence interval: 0.82-0.96) and hemorrhagic stroke (RR, 0.48; 95% CI: 0.36-0.62), compared with warfarin.

For VTE, no differences between NOACs and warfarin were observed for all-cause mortality, VTE-related mortality, or recurrent deep vein thrombosis and pulmonary embolism. Rates of fatal bleeding were consistently lower with NOACs (RR, 0.60; 95% CI: 0.46-0.77] with no difference by drug class. The risk for gastrointestinal bleeding was increased with NOACs.

Although not statistically significant, the point estimate for the risk of myocardial infarction was higher with dabigatran (RR, 1.35; CI: 0.99-1.85) than with FXa inhibitors. More patients discontinued dabigatran (RR 1.62; CI: 1.23-2.15) than did FXa inhibitors.

The authors point out that the FDA has reported that dabigatran and warfarin were first and second, respectively, among anticoagulant drugs with reported adverse event reports. Dabigatran was associated with hemorrhages, renal failure, strokes, deaths, and cases of renal failure.

Overall, the findings suggest that bleeding risk may be increased with dabigatran among older patients or those with impaired renal function. Risk for MI also might be increased.

Rivaroxaban is approved by the FDA for the treatment of acute pulmonary embolism. Rivaroxaban should not be used in patients with a creatinine clearance of 30 mL/min or less, significant hepatic impairment, or during pregnancy. But if my patient is willing to pay the higher cost of this medication and assume the possible increased risk for GI bleeding, it may be reasonable to try.

Recently, my patient presented to our emergency department with a massive acute pulmonary embolism. No clear risk factors were identified.

After about 2 weeks working with our anticoagulation nurses and being unable or unwilling to pay for a home INR monitor, she grew weary. She presented with her husband and asked whether there was anything other than warfarin that they could use that would be safe and effective.

We know alternatives are out there – but are we using them widely, and are they ready for prime time?

The search for new oral anticoagulants (NOACs), which presently includes the major classes of direct thrombin inhibitors (DTIs) and factor Xa (FXa) inhibitors, continues in earnest. The DTI currently on the market is dabigatran. FXa inhibitors include rivaroxaban, apixaban, edoxaban, and betrixaban. NOACs offer the potential advantage of predictable effects and decreased monitoring.

Dr. Soheir S. Adam and her colleagues recently published a systematic review, comparing new oral anticoagulants (NOACs) with warfarin for atrial fibrillation and venous thromboembolism (Ann. Intern. Med. 2012;157:796-807).

The authors identified six randomized clinical trials involving more than 60,000 patients. Three evaluated NOACs for chronic atrial fibrillation (AF), and three evaluated them for venous thromboembolism (VTE). All studies compared these drugs to adjusted-dose warfarin. Data were combined for DTIs and FXa inhibitors.

For AF, NOACs were associated with decreased all-cause mortality (relative risk [RR], 0.88; 95% confidence interval: 0.82-0.96) and hemorrhagic stroke (RR, 0.48; 95% CI: 0.36-0.62), compared with warfarin.

For VTE, no differences between NOACs and warfarin were observed for all-cause mortality, VTE-related mortality, or recurrent deep vein thrombosis and pulmonary embolism. Rates of fatal bleeding were consistently lower with NOACs (RR, 0.60; 95% CI: 0.46-0.77] with no difference by drug class. The risk for gastrointestinal bleeding was increased with NOACs.

Although not statistically significant, the point estimate for the risk of myocardial infarction was higher with dabigatran (RR, 1.35; CI: 0.99-1.85) than with FXa inhibitors. More patients discontinued dabigatran (RR 1.62; CI: 1.23-2.15) than did FXa inhibitors.

The authors point out that the FDA has reported that dabigatran and warfarin were first and second, respectively, among anticoagulant drugs with reported adverse event reports. Dabigatran was associated with hemorrhages, renal failure, strokes, deaths, and cases of renal failure.

Overall, the findings suggest that bleeding risk may be increased with dabigatran among older patients or those with impaired renal function. Risk for MI also might be increased.

Rivaroxaban is approved by the FDA for the treatment of acute pulmonary embolism. Rivaroxaban should not be used in patients with a creatinine clearance of 30 mL/min or less, significant hepatic impairment, or during pregnancy. But if my patient is willing to pay the higher cost of this medication and assume the possible increased risk for GI bleeding, it may be reasonable to try.

Recently, my patient presented to our emergency department with a massive acute pulmonary embolism. No clear risk factors were identified.

After about 2 weeks working with our anticoagulation nurses and being unable or unwilling to pay for a home INR monitor, she grew weary. She presented with her husband and asked whether there was anything other than warfarin that they could use that would be safe and effective.

We know alternatives are out there – but are we using them widely, and are they ready for prime time?

The search for new oral anticoagulants (NOACs), which presently includes the major classes of direct thrombin inhibitors (DTIs) and factor Xa (FXa) inhibitors, continues in earnest. The DTI currently on the market is dabigatran. FXa inhibitors include rivaroxaban, apixaban, edoxaban, and betrixaban. NOACs offer the potential advantage of predictable effects and decreased monitoring.

Dr. Soheir S. Adam and her colleagues recently published a systematic review, comparing new oral anticoagulants (NOACs) with warfarin for atrial fibrillation and venous thromboembolism (Ann. Intern. Med. 2012;157:796-807).

The authors identified six randomized clinical trials involving more than 60,000 patients. Three evaluated NOACs for chronic atrial fibrillation (AF), and three evaluated them for venous thromboembolism (VTE). All studies compared these drugs to adjusted-dose warfarin. Data were combined for DTIs and FXa inhibitors.

For AF, NOACs were associated with decreased all-cause mortality (relative risk [RR], 0.88; 95% confidence interval: 0.82-0.96) and hemorrhagic stroke (RR, 0.48; 95% CI: 0.36-0.62), compared with warfarin.

For VTE, no differences between NOACs and warfarin were observed for all-cause mortality, VTE-related mortality, or recurrent deep vein thrombosis and pulmonary embolism. Rates of fatal bleeding were consistently lower with NOACs (RR, 0.60; 95% CI: 0.46-0.77] with no difference by drug class. The risk for gastrointestinal bleeding was increased with NOACs.

Although not statistically significant, the point estimate for the risk of myocardial infarction was higher with dabigatran (RR, 1.35; CI: 0.99-1.85) than with FXa inhibitors. More patients discontinued dabigatran (RR 1.62; CI: 1.23-2.15) than did FXa inhibitors.

The authors point out that the FDA has reported that dabigatran and warfarin were first and second, respectively, among anticoagulant drugs with reported adverse event reports. Dabigatran was associated with hemorrhages, renal failure, strokes, deaths, and cases of renal failure.

Overall, the findings suggest that bleeding risk may be increased with dabigatran among older patients or those with impaired renal function. Risk for MI also might be increased.

Rivaroxaban is approved by the FDA for the treatment of acute pulmonary embolism. Rivaroxaban should not be used in patients with a creatinine clearance of 30 mL/min or less, significant hepatic impairment, or during pregnancy. But if my patient is willing to pay the higher cost of this medication and assume the possible increased risk for GI bleeding, it may be reasonable to try.

Throughout history, medicine has a habit of seeking out and holding up to scrutiny various panaceas. Vitamin D had its moment in the sun a few years ago. Now probiotics are perhaps enjoying theirs.

If your practice is like mine, daylight is frequently consumed by chronicity, intractability, and preauthorization forms. One may find it enjoyable to occasionally see a member of the "walking well" with a simple problem – opening the exam room door to spend a few minutes proffering advice to enhance health and prevent disease.

Entertaining the idea of recommending probiotics to prevent the common cold is attractive and energizing, especially because probiotics do not require a prescription or a preauthorization.

So, what’s the evidence?

En-Jin Kang and colleagues at Hallym University College of Medicine in Seoul, South Korea, conducted a systematic review of randomized trials evaluating probiotic administration for reducing the incidence of colds and cold symptoms. Studies were excluded if they focused on sinusitis, tonsillitis, laryngitis, otitis media, and lower respiratory tract diseases such as bronchitis or pneumonia (Korean J. Fam. Med. 2013;34:2-10).

Seven randomized, controlled trials were selected and included in the final analysis. The quality of the studies was high overall, and the researchers detected no tendency for only positive studies to be published.

The relative risk of developing a cold or cold symptoms was 0.82 (95% CI: 0.70-0.97) when probiotics were administered for less than 3 months. But the relative risk rose to 1.0 (95% CI: 0.92-1.09) if administration was longer than 3 months.

When probiotics were administered with vitamins and minerals, the relative risk was 0.87 (95% CI: 0.78-0.97), though it climbed to 0.97 when the researchers discarded two studies that may not have used placebo.

One of the difficulties with this type of meta-analysis may be the heterogeneity of the types of bacteria in the probiotics administered in the different studies. Lactobacillus and Bifidobacterium were the most commonly used genera.

But remember that cold symptoms result from our response to an offending virus, so the type of bacteria in the probiotic may not be relevant. Why not? Some experts have theorized that probiotics may be effective because they reduce our body’s overall inflammatory response.

Except in the relatively rare circumstances of immunocompromised hosts, probiotics are safe. The biggest downside for patients may be cost. But with U.S. patients spending $34 billion per year on alternative therapies, they likely won’t mind the cost – as long as there is at least some evidence they could avoid a cold.

Throughout history, medicine has a habit of seeking out and holding up to scrutiny various panaceas. Vitamin D had its moment in the sun a few years ago. Now probiotics are perhaps enjoying theirs.

If your practice is like mine, daylight is frequently consumed by chronicity, intractability, and preauthorization forms. One may find it enjoyable to occasionally see a member of the "walking well" with a simple problem – opening the exam room door to spend a few minutes proffering advice to enhance health and prevent disease.

Entertaining the idea of recommending probiotics to prevent the common cold is attractive and energizing, especially because probiotics do not require a prescription or a preauthorization.

So, what’s the evidence?

En-Jin Kang and colleagues at Hallym University College of Medicine in Seoul, South Korea, conducted a systematic review of randomized trials evaluating probiotic administration for reducing the incidence of colds and cold symptoms. Studies were excluded if they focused on sinusitis, tonsillitis, laryngitis, otitis media, and lower respiratory tract diseases such as bronchitis or pneumonia (Korean J. Fam. Med. 2013;34:2-10).

Seven randomized, controlled trials were selected and included in the final analysis. The quality of the studies was high overall, and the researchers detected no tendency for only positive studies to be published.

The relative risk of developing a cold or cold symptoms was 0.82 (95% CI: 0.70-0.97) when probiotics were administered for less than 3 months. But the relative risk rose to 1.0 (95% CI: 0.92-1.09) if administration was longer than 3 months.

When probiotics were administered with vitamins and minerals, the relative risk was 0.87 (95% CI: 0.78-0.97), though it climbed to 0.97 when the researchers discarded two studies that may not have used placebo.

One of the difficulties with this type of meta-analysis may be the heterogeneity of the types of bacteria in the probiotics administered in the different studies. Lactobacillus and Bifidobacterium were the most commonly used genera.

But remember that cold symptoms result from our response to an offending virus, so the type of bacteria in the probiotic may not be relevant. Why not? Some experts have theorized that probiotics may be effective because they reduce our body’s overall inflammatory response.

Except in the relatively rare circumstances of immunocompromised hosts, probiotics are safe. The biggest downside for patients may be cost. But with U.S. patients spending $34 billion per year on alternative therapies, they likely won’t mind the cost – as long as there is at least some evidence they could avoid a cold.

Throughout history, medicine has a habit of seeking out and holding up to scrutiny various panaceas. Vitamin D had its moment in the sun a few years ago. Now probiotics are perhaps enjoying theirs.

If your practice is like mine, daylight is frequently consumed by chronicity, intractability, and preauthorization forms. One may find it enjoyable to occasionally see a member of the "walking well" with a simple problem – opening the exam room door to spend a few minutes proffering advice to enhance health and prevent disease.

Entertaining the idea of recommending probiotics to prevent the common cold is attractive and energizing, especially because probiotics do not require a prescription or a preauthorization.

So, what’s the evidence?

En-Jin Kang and colleagues at Hallym University College of Medicine in Seoul, South Korea, conducted a systematic review of randomized trials evaluating probiotic administration for reducing the incidence of colds and cold symptoms. Studies were excluded if they focused on sinusitis, tonsillitis, laryngitis, otitis media, and lower respiratory tract diseases such as bronchitis or pneumonia (Korean J. Fam. Med. 2013;34:2-10).

Seven randomized, controlled trials were selected and included in the final analysis. The quality of the studies was high overall, and the researchers detected no tendency for only positive studies to be published.

The relative risk of developing a cold or cold symptoms was 0.82 (95% CI: 0.70-0.97) when probiotics were administered for less than 3 months. But the relative risk rose to 1.0 (95% CI: 0.92-1.09) if administration was longer than 3 months.

When probiotics were administered with vitamins and minerals, the relative risk was 0.87 (95% CI: 0.78-0.97), though it climbed to 0.97 when the researchers discarded two studies that may not have used placebo.

One of the difficulties with this type of meta-analysis may be the heterogeneity of the types of bacteria in the probiotics administered in the different studies. Lactobacillus and Bifidobacterium were the most commonly used genera.

But remember that cold symptoms result from our response to an offending virus, so the type of bacteria in the probiotic may not be relevant. Why not? Some experts have theorized that probiotics may be effective because they reduce our body’s overall inflammatory response.

Except in the relatively rare circumstances of immunocompromised hosts, probiotics are safe. The biggest downside for patients may be cost. But with U.S. patients spending $34 billion per year on alternative therapies, they likely won’t mind the cost – as long as there is at least some evidence they could avoid a cold.

The Affordable Care Act authorized the creation of the Medicare Shared Savings Program, which in turn allows Medicare to contract with accountable care organizations. ACOs, in turn, will be motivated to reduce discretionary office visits.

As the Centers for Medicare and Medicaid Services explains, the MSSP "promotes accountability for a patient population, coordinates items and services under part A and B, and encourages investment in infrastructure and redesigned care processes for high quality and efficient service delivery."

Some of us believe that the Medicare fee-for-service payment model will remain on the table in the future but that it will become de-incentivized relative to an ACO model. Many challenges remain, however. At its core, an ACO model of care is designed to promote high-quality clinical care and cost controls by providing incentives for care coordination, improved patient experiences and safety, and preventive health.

To control costs, the low-hanging fruit may be office visits. Office visits require staff, and we all know that some patient complaints could be handled differently. To this end, it is important to understand why people visit health care providers in primary care.

Our research group at the Mayo Clinic analyzed data from the Rochester Epidemiology Project (REP) to determine the most common nonacute clinical diagnoses in a well-defined population (Mayo Clin. Proc. 2013;88:56-67). The REP records linkage system includes the medical records of patients residing in Olmsted County, Minn., who receive the vast majority of their medical care through the Mayo Clinic, Olmsted Medical Center, and the Rochester Family Medicine Clinic.

For this study, we searched the REP electronically to extract the ICD-9 codes in the medical records of members assigned by any health care institution from Jan. 1, 2005, through Dec. 31, 2009. Diagnoses were assigned based upon clinical visit assessments and subsequent assigned and billed diagnoses.

Among 142,377 patients, skin disorders (42.7%), osteoarthritis and joint disorders (33.6%), back problems (23.9%), disorders of lipid metabolism (22.4%), and upper respiratory tract disease (22.1%, excluding asthma) were the most prevalent diagnoses.

If we have an understanding of the resources needed to address the most common issues, we can creatively explore how to accomplish the same amount of work while streamlining care and reducing costs.

Is teledermatology ready for prime time in the United States? Perhaps not, but embedding orthopedic specialty colleagues in the primary care practice, as we have done at our institution, may reduce downstream utilization and has an evidence base to support it. Addressing all lipid disorders telephonically with nurse protocols certainly seems like fertile ground for exploration. Enhanced phone triage for respiratory tract conditions also may decrease visits.

If we are planning on bravely surviving into the future of medicine, knowing why patients visit us is the first step in developing care models to alleviate the need to do so.

The Affordable Care Act authorized the creation of the Medicare Shared Savings Program, which in turn allows Medicare to contract with accountable care organizations. ACOs, in turn, will be motivated to reduce discretionary office visits.

As the Centers for Medicare and Medicaid Services explains, the MSSP "promotes accountability for a patient population, coordinates items and services under part A and B, and encourages investment in infrastructure and redesigned care processes for high quality and efficient service delivery."

Some of us believe that the Medicare fee-for-service payment model will remain on the table in the future but that it will become de-incentivized relative to an ACO model. Many challenges remain, however. At its core, an ACO model of care is designed to promote high-quality clinical care and cost controls by providing incentives for care coordination, improved patient experiences and safety, and preventive health.

To control costs, the low-hanging fruit may be office visits. Office visits require staff, and we all know that some patient complaints could be handled differently. To this end, it is important to understand why people visit health care providers in primary care.

Our research group at the Mayo Clinic analyzed data from the Rochester Epidemiology Project (REP) to determine the most common nonacute clinical diagnoses in a well-defined population (Mayo Clin. Proc. 2013;88:56-67). The REP records linkage system includes the medical records of patients residing in Olmsted County, Minn., who receive the vast majority of their medical care through the Mayo Clinic, Olmsted Medical Center, and the Rochester Family Medicine Clinic.

For this study, we searched the REP electronically to extract the ICD-9 codes in the medical records of members assigned by any health care institution from Jan. 1, 2005, through Dec. 31, 2009. Diagnoses were assigned based upon clinical visit assessments and subsequent assigned and billed diagnoses.

Among 142,377 patients, skin disorders (42.7%), osteoarthritis and joint disorders (33.6%), back problems (23.9%), disorders of lipid metabolism (22.4%), and upper respiratory tract disease (22.1%, excluding asthma) were the most prevalent diagnoses.

If we have an understanding of the resources needed to address the most common issues, we can creatively explore how to accomplish the same amount of work while streamlining care and reducing costs.

Is teledermatology ready for prime time in the United States? Perhaps not, but embedding orthopedic specialty colleagues in the primary care practice, as we have done at our institution, may reduce downstream utilization and has an evidence base to support it. Addressing all lipid disorders telephonically with nurse protocols certainly seems like fertile ground for exploration. Enhanced phone triage for respiratory tract conditions also may decrease visits.

If we are planning on bravely surviving into the future of medicine, knowing why patients visit us is the first step in developing care models to alleviate the need to do so.

The Affordable Care Act authorized the creation of the Medicare Shared Savings Program, which in turn allows Medicare to contract with accountable care organizations. ACOs, in turn, will be motivated to reduce discretionary office visits.

As the Centers for Medicare and Medicaid Services explains, the MSSP "promotes accountability for a patient population, coordinates items and services under part A and B, and encourages investment in infrastructure and redesigned care processes for high quality and efficient service delivery."

Some of us believe that the Medicare fee-for-service payment model will remain on the table in the future but that it will become de-incentivized relative to an ACO model. Many challenges remain, however. At its core, an ACO model of care is designed to promote high-quality clinical care and cost controls by providing incentives for care coordination, improved patient experiences and safety, and preventive health.

To control costs, the low-hanging fruit may be office visits. Office visits require staff, and we all know that some patient complaints could be handled differently. To this end, it is important to understand why people visit health care providers in primary care.

Our research group at the Mayo Clinic analyzed data from the Rochester Epidemiology Project (REP) to determine the most common nonacute clinical diagnoses in a well-defined population (Mayo Clin. Proc. 2013;88:56-67). The REP records linkage system includes the medical records of patients residing in Olmsted County, Minn., who receive the vast majority of their medical care through the Mayo Clinic, Olmsted Medical Center, and the Rochester Family Medicine Clinic.

For this study, we searched the REP electronically to extract the ICD-9 codes in the medical records of members assigned by any health care institution from Jan. 1, 2005, through Dec. 31, 2009. Diagnoses were assigned based upon clinical visit assessments and subsequent assigned and billed diagnoses.

Among 142,377 patients, skin disorders (42.7%), osteoarthritis and joint disorders (33.6%), back problems (23.9%), disorders of lipid metabolism (22.4%), and upper respiratory tract disease (22.1%, excluding asthma) were the most prevalent diagnoses.

If we have an understanding of the resources needed to address the most common issues, we can creatively explore how to accomplish the same amount of work while streamlining care and reducing costs.

Is teledermatology ready for prime time in the United States? Perhaps not, but embedding orthopedic specialty colleagues in the primary care practice, as we have done at our institution, may reduce downstream utilization and has an evidence base to support it. Addressing all lipid disorders telephonically with nurse protocols certainly seems like fertile ground for exploration. Enhanced phone triage for respiratory tract conditions also may decrease visits.

If we are planning on bravely surviving into the future of medicine, knowing why patients visit us is the first step in developing care models to alleviate the need to do so.

During my training, the use of beta-blockers was considered to cause potential harm among patients with heart failure. However, I worked with seasoned cardiologists at Mayo who were convinced of the contrary even before large amounts of data began to emerge supporting their use.

Analyses of the Studies of Left Ventricular Dysfunction (SOLVD) ultimately taught us that the combination of beta-blockers (BBs) and enalapril was associated with a reduction in risk of death. Large meta-analyses also identified reduction in morbidity and mortality, and suggested that they should be routinely offered to all patients with heart failure (HF).

As others have said before me, not all BBs are treated equally. BBs with intrinsic sympathomimetic activity (e.g., acebutolol and pindolol) should generally be avoided in patients with HF. But do clinically important differences exist between BBs with beta-nonselective activity (carvedilol) and beta₁-selective activity (e.g., atenolol and metoprolol) in patients with HF and acute myocardial infarction (AMI)?

James DiNicolantonio, Pharm.D., and his colleagues conducted a systematic review and meta-analysis comparing outcomes between clinical trial subjects with systolic HF or AMI receiving carvedilol and those receiving beta₁-selective BBs (specifically atenolol, metoprolol, bisoprolol, and nebivolol) (Am. J. Cardiol. 2013 Jan. 7 [doi: 10.1016/j.amjcard.2012.11.031]).

Studies were included if they were randomized, controlled clinical trials including adults older than 18 years. Outcomes included all-cause mortality, cardiovascular events including fatal and nonfatal strokes and MI, HF, and CV-related hospital readmissions. Eleven studies were included in the final meta-analyses.

A significant decrease in all-cause mortality in patients with HF was observed with carvedilol, compared with beta₁-selective BBs (relative risk, 0.85; 95% confidence interval, 0.78-0.93; number needed to treat = 22). In patients with AMI, carvedilol significantly decreased all-cause mortality by 45% (RR, 0.55; 95% CI, 0.32-0.94), compared with beta₁-selective BBs.

No statistically significant benefit of carvedilol was observed for HF readmissions or nonfatal MI in patients with AMIs.

The investigators remind us that in addition to being a beta-nonselective BB and an alpha₁-blocker, carvedilol may have unique vasodilating, antioxidant, and antiarrhythmic effects. The combination of these effects may account for the observed differences.

Dr. DiNicolantonio also highlights our current use and misuse of atenolol. Atenolol continues to be one of the most widely prescribed BBs. This is occurring in spite of the fact that atenolol has not been shown to improve CV prognosis after MI, improve outcomes in HF, or reduce the risk for heart disease despite blood pressure lowering.

Many clinics, including my own, have reminder systems for clinicians to consider the use of ACE-I therapy for patients with HF. To improve patient outcomes, these systems should remind us to consider carvedilol, or at least consider it in lieu of beta₁-selective BBs.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

During my training, the use of beta-blockers was considered to cause potential harm among patients with heart failure. However, I worked with seasoned cardiologists at Mayo who were convinced of the contrary even before large amounts of data began to emerge supporting their use.

Analyses of the Studies of Left Ventricular Dysfunction (SOLVD) ultimately taught us that the combination of beta-blockers (BBs) and enalapril was associated with a reduction in risk of death. Large meta-analyses also identified reduction in morbidity and mortality, and suggested that they should be routinely offered to all patients with heart failure (HF).

As others have said before me, not all BBs are treated equally. BBs with intrinsic sympathomimetic activity (e.g., acebutolol and pindolol) should generally be avoided in patients with HF. But do clinically important differences exist between BBs with beta-nonselective activity (carvedilol) and beta₁-selective activity (e.g., atenolol and metoprolol) in patients with HF and acute myocardial infarction (AMI)?

James DiNicolantonio, Pharm.D., and his colleagues conducted a systematic review and meta-analysis comparing outcomes between clinical trial subjects with systolic HF or AMI receiving carvedilol and those receiving beta₁-selective BBs (specifically atenolol, metoprolol, bisoprolol, and nebivolol) (Am. J. Cardiol. 2013 Jan. 7 [doi: 10.1016/j.amjcard.2012.11.031]).

Studies were included if they were randomized, controlled clinical trials including adults older than 18 years. Outcomes included all-cause mortality, cardiovascular events including fatal and nonfatal strokes and MI, HF, and CV-related hospital readmissions. Eleven studies were included in the final meta-analyses.

A significant decrease in all-cause mortality in patients with HF was observed with carvedilol, compared with beta₁-selective BBs (relative risk, 0.85; 95% confidence interval, 0.78-0.93; number needed to treat = 22). In patients with AMI, carvedilol significantly decreased all-cause mortality by 45% (RR, 0.55; 95% CI, 0.32-0.94), compared with beta₁-selective BBs.

No statistically significant benefit of carvedilol was observed for HF readmissions or nonfatal MI in patients with AMIs.

The investigators remind us that in addition to being a beta-nonselective BB and an alpha₁-blocker, carvedilol may have unique vasodilating, antioxidant, and antiarrhythmic effects. The combination of these effects may account for the observed differences.

Dr. DiNicolantonio also highlights our current use and misuse of atenolol. Atenolol continues to be one of the most widely prescribed BBs. This is occurring in spite of the fact that atenolol has not been shown to improve CV prognosis after MI, improve outcomes in HF, or reduce the risk for heart disease despite blood pressure lowering.

Many clinics, including my own, have reminder systems for clinicians to consider the use of ACE-I therapy for patients with HF. To improve patient outcomes, these systems should remind us to consider carvedilol, or at least consider it in lieu of beta₁-selective BBs.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

During my training, the use of beta-blockers was considered to cause potential harm among patients with heart failure. However, I worked with seasoned cardiologists at Mayo who were convinced of the contrary even before large amounts of data began to emerge supporting their use.

Analyses of the Studies of Left Ventricular Dysfunction (SOLVD) ultimately taught us that the combination of beta-blockers (BBs) and enalapril was associated with a reduction in risk of death. Large meta-analyses also identified reduction in morbidity and mortality, and suggested that they should be routinely offered to all patients with heart failure (HF).

As others have said before me, not all BBs are treated equally. BBs with intrinsic sympathomimetic activity (e.g., acebutolol and pindolol) should generally be avoided in patients with HF. But do clinically important differences exist between BBs with beta-nonselective activity (carvedilol) and beta₁-selective activity (e.g., atenolol and metoprolol) in patients with HF and acute myocardial infarction (AMI)?

James DiNicolantonio, Pharm.D., and his colleagues conducted a systematic review and meta-analysis comparing outcomes between clinical trial subjects with systolic HF or AMI receiving carvedilol and those receiving beta₁-selective BBs (specifically atenolol, metoprolol, bisoprolol, and nebivolol) (Am. J. Cardiol. 2013 Jan. 7 [doi: 10.1016/j.amjcard.2012.11.031]).

Studies were included if they were randomized, controlled clinical trials including adults older than 18 years. Outcomes included all-cause mortality, cardiovascular events including fatal and nonfatal strokes and MI, HF, and CV-related hospital readmissions. Eleven studies were included in the final meta-analyses.

A significant decrease in all-cause mortality in patients with HF was observed with carvedilol, compared with beta₁-selective BBs (relative risk, 0.85; 95% confidence interval, 0.78-0.93; number needed to treat = 22). In patients with AMI, carvedilol significantly decreased all-cause mortality by 45% (RR, 0.55; 95% CI, 0.32-0.94), compared with beta₁-selective BBs.

No statistically significant benefit of carvedilol was observed for HF readmissions or nonfatal MI in patients with AMIs.

The investigators remind us that in addition to being a beta-nonselective BB and an alpha₁-blocker, carvedilol may have unique vasodilating, antioxidant, and antiarrhythmic effects. The combination of these effects may account for the observed differences.

Dr. DiNicolantonio also highlights our current use and misuse of atenolol. Atenolol continues to be one of the most widely prescribed BBs. This is occurring in spite of the fact that atenolol has not been shown to improve CV prognosis after MI, improve outcomes in HF, or reduce the risk for heart disease despite blood pressure lowering.

Many clinics, including my own, have reminder systems for clinicians to consider the use of ACE-I therapy for patients with HF. To improve patient outcomes, these systems should remind us to consider carvedilol, or at least consider it in lieu of beta₁-selective BBs.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

At the risk of foolishly rushing into topics about which angels commonly fear discourse, we need to continue our journey this year through the clinical management of clinically localized prostate cancer. We – and I am including myself in this – should make a new year’s resolution to be self-reflective, explore our biases and preconceived notions, and observe and chart new and emerging data. Several trials are ongoing which may more brightly illuminate our path.

Dr. Jenny L. Donovan of the University of Bristol (England) recently published an article in the Journal of the National Cancer Institute Mongraphs brilliantly summarizing the current state of the debate (2012;45:191-6). She describes the maturation of our "group think" as we evolved from a strategy of watchful waiting only for those men with limited life expectancy to a deeper realization and appreciation for the downsides of radical intervention for nonaggressive disease.

Clinicians hold an enormous amount of sway in the decisions that patients make about clinical care, and personal and professional biases commonly take the helm. When it comes to complex clinical issues, most of us have neither a firm grasp on the data nor the time to explain it.

Decision aids are an effective clinical tool that can improve the quality of the decisions about screening and treatment. For prostate cancer screening, decision aids enhance patient knowledge, reduce decisional conflict, and reduce interest in prostate-specific antigen screening. Relatively less is known about how treatment should be presented to enhance decision making.

Dr. Donovan describes Prostate Testing for Cancer and Treatment (ProtecT), which has enrolled more than 3,000 men with clinically localized prostate cancer, and compares radical prostatectomy, radiotherapy, and active monitoring.

In the process of recruiting for the study, investigators learned that "watchful waiting" was frequently interpreted as "no treatment." As a result, the term was changed to "active monitoring." Decisions, in clinical medicine, as in business, are contingent upon the salesperson, and word choice is crucial. Data from this trial are expected in 2016.

In the meantime, we can facilitate our decision with the use of an amazingly helpful online decision aid produced by the federal Agency for Healthcare Research and Quality. This tool is designed for patients with clinically localized prostate cancer. This may serve as a useful homework assignment for our Internet-savvy patients.

Providing our patients with this degree of information will empower them and advance our clinical discussions about prostate cancer treatment.

This column, "What Matters," regularly appears in Internal Medicine News, a publication of Frontline Medical Communications. Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

At the risk of foolishly rushing into topics about which angels commonly fear discourse, we need to continue our journey this year through the clinical management of clinically localized prostate cancer. We – and I am including myself in this – should make a new year’s resolution to be self-reflective, explore our biases and preconceived notions, and observe and chart new and emerging data. Several trials are ongoing which may more brightly illuminate our path.

Dr. Jenny L. Donovan of the University of Bristol (England) recently published an article in the Journal of the National Cancer Institute Mongraphs brilliantly summarizing the current state of the debate (2012;45:191-6). She describes the maturation of our "group think" as we evolved from a strategy of watchful waiting only for those men with limited life expectancy to a deeper realization and appreciation for the downsides of radical intervention for nonaggressive disease.

Clinicians hold an enormous amount of sway in the decisions that patients make about clinical care, and personal and professional biases commonly take the helm. When it comes to complex clinical issues, most of us have neither a firm grasp on the data nor the time to explain it.

Decision aids are an effective clinical tool that can improve the quality of the decisions about screening and treatment. For prostate cancer screening, decision aids enhance patient knowledge, reduce decisional conflict, and reduce interest in prostate-specific antigen screening. Relatively less is known about how treatment should be presented to enhance decision making.

Dr. Donovan describes Prostate Testing for Cancer and Treatment (ProtecT), which has enrolled more than 3,000 men with clinically localized prostate cancer, and compares radical prostatectomy, radiotherapy, and active monitoring.

In the process of recruiting for the study, investigators learned that "watchful waiting" was frequently interpreted as "no treatment." As a result, the term was changed to "active monitoring." Decisions, in clinical medicine, as in business, are contingent upon the salesperson, and word choice is crucial. Data from this trial are expected in 2016.

In the meantime, we can facilitate our decision with the use of an amazingly helpful online decision aid produced by the federal Agency for Healthcare Research and Quality. This tool is designed for patients with clinically localized prostate cancer. This may serve as a useful homework assignment for our Internet-savvy patients.

Providing our patients with this degree of information will empower them and advance our clinical discussions about prostate cancer treatment.

This column, "What Matters," regularly appears in Internal Medicine News, a publication of Frontline Medical Communications. Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

At the risk of foolishly rushing into topics about which angels commonly fear discourse, we need to continue our journey this year through the clinical management of clinically localized prostate cancer. We – and I am including myself in this – should make a new year’s resolution to be self-reflective, explore our biases and preconceived notions, and observe and chart new and emerging data. Several trials are ongoing which may more brightly illuminate our path.

Dr. Jenny L. Donovan of the University of Bristol (England) recently published an article in the Journal of the National Cancer Institute Mongraphs brilliantly summarizing the current state of the debate (2012;45:191-6). She describes the maturation of our "group think" as we evolved from a strategy of watchful waiting only for those men with limited life expectancy to a deeper realization and appreciation for the downsides of radical intervention for nonaggressive disease.

Clinicians hold an enormous amount of sway in the decisions that patients make about clinical care, and personal and professional biases commonly take the helm. When it comes to complex clinical issues, most of us have neither a firm grasp on the data nor the time to explain it.

Decision aids are an effective clinical tool that can improve the quality of the decisions about screening and treatment. For prostate cancer screening, decision aids enhance patient knowledge, reduce decisional conflict, and reduce interest in prostate-specific antigen screening. Relatively less is known about how treatment should be presented to enhance decision making.

Dr. Donovan describes Prostate Testing for Cancer and Treatment (ProtecT), which has enrolled more than 3,000 men with clinically localized prostate cancer, and compares radical prostatectomy, radiotherapy, and active monitoring.

In the process of recruiting for the study, investigators learned that "watchful waiting" was frequently interpreted as "no treatment." As a result, the term was changed to "active monitoring." Decisions, in clinical medicine, as in business, are contingent upon the salesperson, and word choice is crucial. Data from this trial are expected in 2016.

In the meantime, we can facilitate our decision with the use of an amazingly helpful online decision aid produced by the federal Agency for Healthcare Research and Quality. This tool is designed for patients with clinically localized prostate cancer. This may serve as a useful homework assignment for our Internet-savvy patients.

Providing our patients with this degree of information will empower them and advance our clinical discussions about prostate cancer treatment.

This column, "What Matters," regularly appears in Internal Medicine News, a publication of Frontline Medical Communications. Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are those of the author. Reply via e-mail at [email protected].

Having just passed the winter solstice, we are reminded that many of our patients may not see much of the sun this time of year. The sun that they do see is tangential – and patients in the northern climes in particular are typically covered from head to toe, tending not to linger outdoors "catching rays.

Available data suggest that people living north of the 37th parallel (north of a line from San Francisco to Richmond, Va.) see so little of the sun that it makes the manufacture of vitamin D nearly impossible.

Vitamin D deficiency has been associated with cardiovascular disease, diabetes, osteoporosis, chronic kidney disease, and cancer. But vitamin D deficiency can manifest as nebulous clinical symptoms such as musculoskeletal weakness and pain.

Dr. Ferdinand Schreuder conducted a randomized clinical trial of high-dose vitamin D₃ on nonspecific persistent musculoskeletal complaints in vitamin D–deficient non-Western immigrants (Ann. Fam. Med. 2012;10:547-55). The study was conducted in the Netherlands and enrolled non-Western immigrants and their children aged 18-60 years. People were eligible for enrollment if they visited their doctor for frequent, recurrent musculoskeletal pain or pain lasting longer than 3 months without an obvious cause.

Patients were predominantly from the Middle East, Turkey, northern Africa, and Somalia. They were tested for vitamin D, and a serum concentration of 25-hydroxyvitamin D of less than 50 nmol/L was defined as deficiency.

A total of 84 patients were randomized to receive 150,000 IU vitamin D₃ orally or matching placebo. At week 6, a second randomization was done for patients who received vitamin D; but all patients who received placebo for the first 6 weeks received a dose of vitamin D for the next 6 weeks. Outcomes were determined at weeks 6 and 12.

Patients in the vitamin D₃ group were significantly more likely than those on placebo to report pain relief 6 weeks after treatment (34.9% vs. 19.5%, P = .04). The vitamin D group was also significantly more likely to report improved ability to walk stairs (21.0% vs. 8.4%, P = .008). Serum concentrations of vitamin D were 20 nmol/L at baseline, 63.5 nmol/L at 6 weeks, and 40 nmol/L at 12 weeks.

The vitamin D in this study was given as a single dose, which improves clinical adherence greatly. However, we cannot adroitly translate the findings from this single-dose study to daily dosing of vitamin D.

Some practitioners recommend high daily doses of vitamin D. But we need to be cautious, because vitamin D toxicity can occur. The Institute of Medicine recommends an upper intake level of 4,000 IU/day for individuals older than 9 years, with a reasonable dose about 2,000 IU of vitamin D₃.

A reasonable approach may be to test and "treat to target" for vitamin D replacement. Clinical profiling of heavily clothed patients who spend a lot of time indoors from October to March may be wise.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

Having just passed the winter solstice, we are reminded that many of our patients may not see much of the sun this time of year. The sun that they do see is tangential – and patients in the northern climes in particular are typically covered from head to toe, tending not to linger outdoors "catching rays.

Available data suggest that people living north of the 37th parallel (north of a line from San Francisco to Richmond, Va.) see so little of the sun that it makes the manufacture of vitamin D nearly impossible.

Vitamin D deficiency has been associated with cardiovascular disease, diabetes, osteoporosis, chronic kidney disease, and cancer. But vitamin D deficiency can manifest as nebulous clinical symptoms such as musculoskeletal weakness and pain.

Dr. Ferdinand Schreuder conducted a randomized clinical trial of high-dose vitamin D₃ on nonspecific persistent musculoskeletal complaints in vitamin D–deficient non-Western immigrants (Ann. Fam. Med. 2012;10:547-55). The study was conducted in the Netherlands and enrolled non-Western immigrants and their children aged 18-60 years. People were eligible for enrollment if they visited their doctor for frequent, recurrent musculoskeletal pain or pain lasting longer than 3 months without an obvious cause.

Patients were predominantly from the Middle East, Turkey, northern Africa, and Somalia. They were tested for vitamin D, and a serum concentration of 25-hydroxyvitamin D of less than 50 nmol/L was defined as deficiency.

A total of 84 patients were randomized to receive 150,000 IU vitamin D₃ orally or matching placebo. At week 6, a second randomization was done for patients who received vitamin D; but all patients who received placebo for the first 6 weeks received a dose of vitamin D for the next 6 weeks. Outcomes were determined at weeks 6 and 12.

Patients in the vitamin D₃ group were significantly more likely than those on placebo to report pain relief 6 weeks after treatment (34.9% vs. 19.5%, P = .04). The vitamin D group was also significantly more likely to report improved ability to walk stairs (21.0% vs. 8.4%, P = .008). Serum concentrations of vitamin D were 20 nmol/L at baseline, 63.5 nmol/L at 6 weeks, and 40 nmol/L at 12 weeks.

The vitamin D in this study was given as a single dose, which improves clinical adherence greatly. However, we cannot adroitly translate the findings from this single-dose study to daily dosing of vitamin D.

Some practitioners recommend high daily doses of vitamin D. But we need to be cautious, because vitamin D toxicity can occur. The Institute of Medicine recommends an upper intake level of 4,000 IU/day for individuals older than 9 years, with a reasonable dose about 2,000 IU of vitamin D₃.

A reasonable approach may be to test and "treat to target" for vitamin D replacement. Clinical profiling of heavily clothed patients who spend a lot of time indoors from October to March may be wise.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

Having just passed the winter solstice, we are reminded that many of our patients may not see much of the sun this time of year. The sun that they do see is tangential – and patients in the northern climes in particular are typically covered from head to toe, tending not to linger outdoors "catching rays.

Available data suggest that people living north of the 37th parallel (north of a line from San Francisco to Richmond, Va.) see so little of the sun that it makes the manufacture of vitamin D nearly impossible.

Vitamin D deficiency has been associated with cardiovascular disease, diabetes, osteoporosis, chronic kidney disease, and cancer. But vitamin D deficiency can manifest as nebulous clinical symptoms such as musculoskeletal weakness and pain.

Dr. Ferdinand Schreuder conducted a randomized clinical trial of high-dose vitamin D₃ on nonspecific persistent musculoskeletal complaints in vitamin D–deficient non-Western immigrants (Ann. Fam. Med. 2012;10:547-55). The study was conducted in the Netherlands and enrolled non-Western immigrants and their children aged 18-60 years. People were eligible for enrollment if they visited their doctor for frequent, recurrent musculoskeletal pain or pain lasting longer than 3 months without an obvious cause.

Patients were predominantly from the Middle East, Turkey, northern Africa, and Somalia. They were tested for vitamin D, and a serum concentration of 25-hydroxyvitamin D of less than 50 nmol/L was defined as deficiency.

A total of 84 patients were randomized to receive 150,000 IU vitamin D₃ orally or matching placebo. At week 6, a second randomization was done for patients who received vitamin D; but all patients who received placebo for the first 6 weeks received a dose of vitamin D for the next 6 weeks. Outcomes were determined at weeks 6 and 12.

Patients in the vitamin D₃ group were significantly more likely than those on placebo to report pain relief 6 weeks after treatment (34.9% vs. 19.5%, P = .04). The vitamin D group was also significantly more likely to report improved ability to walk stairs (21.0% vs. 8.4%, P = .008). Serum concentrations of vitamin D were 20 nmol/L at baseline, 63.5 nmol/L at 6 weeks, and 40 nmol/L at 12 weeks.

The vitamin D in this study was given as a single dose, which improves clinical adherence greatly. However, we cannot adroitly translate the findings from this single-dose study to daily dosing of vitamin D.

Some practitioners recommend high daily doses of vitamin D. But we need to be cautious, because vitamin D toxicity can occur. The Institute of Medicine recommends an upper intake level of 4,000 IU/day for individuals older than 9 years, with a reasonable dose about 2,000 IU of vitamin D₃.

A reasonable approach may be to test and "treat to target" for vitamin D replacement. Clinical profiling of heavily clothed patients who spend a lot of time indoors from October to March may be wise.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

Perhaps like many primary care clinicians, I perseverate on diseases most prevalent or problematic. Overweight and obesity are both. So, at the risk of sounding like we’ve dedicated this column exclusively to this condition, let’s focus on new data about an intervention that can help people lose weight and maintain weight loss.

Technology as applied to clinical medicine is a complex phenomenon. For managing massive amounts of patient data accumulating over time, it is essential. But many of us have, and continue to hold onto, expectations that it will increase our clinical "batting average" by improving things like diabetes control, hypertension, and weight.

Sadly, successes in this arena have been few. Human behavior seems to undo all the well-laid plans for improving medical conditions by altering human behavior.

But this is the season of hope.

Bonnie Spring, Ph.D., and her colleagues published results from a randomized clinical trial evaluating the use of mobile technology (via a personal digital assistant, or PDA) to track food intake, weight, and physical activity, and then facilitate intervention based on the data (Arch. Intern. Med. 2012 [doi:10.1001/jamainternmed.2013.1221]).

Sixty-nine adults took part, 85.5% of whom were male, with a mean age of 57.7 years. Inclusion criteria included a body mass index between 25 and 40 kg/m², weight less than 181.4 kg, and the ability to participate in moderate-intensity physical activity. Patients were randomized to either a control group following the standard of care, or to an intervention group following the standard of care plus mobile technology and telephone coaching.

Participants were given a 5%-10% weight loss goal. The study had two phases: a weight loss phase (months 0-6) and a weight maintenance phase (months 7-12).

All patients received the standard intervention composed of the MOVE! group weight loss program offered at all Veterans Affairs medical centers. In the first 6 months, both arms of the study attended biweekly MOVE! sessions facilitated by dieticians, psychologists, or physicians. Each session lasted approximately 90 minutes, incorporating teachings on nutrition, physical activity, and behavior change.

The intervention group recorded daily food intake and used the PDA as a decision-support tool to assist in personal decisions about energy balance. The resulting data were used to guide a physical activity intervention, and a lifestyle coach provided telephone support every 2 weeks to review data and assist in data management issues. Physical activity recommendations and calorie intake were tailored to achieve weight loss goals. During the weight maintenance phase, data were collected but no behavioral counseling was provided.

The mobile technology group lost 3.9 kg more than the control group (95% CI: 2.2-5.5 kg). The mobile technology group members had significantly greater odds of losing 5% of their body weight.

The study shows that remote lifestyle coaching providing intervention based on data collected through mobile technology can be effective. The appeal of the intervention is the ability to use transmitted data to enhance the intervention without the need for face-to-face interactions. However, the MOVE! intervention used by both groups is itself an intense, resource-intensive intervention with 12 group sessions during a 6-month period.

We obviously need to accept the cold reality of clinical medicine and life: You get out what you put in. The more intense the intervention, the better patients will do. But this study definitely moves us closer to the vision of leveraging existing medical infrastructure and medical technology to remotely treat our patients and improve their lives by supporting them in weight loss.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

Perhaps like many primary care clinicians, I perseverate on diseases most prevalent or problematic. Overweight and obesity are both. So, at the risk of sounding like we’ve dedicated this column exclusively to this condition, let’s focus on new data about an intervention that can help people lose weight and maintain weight loss.

Technology as applied to clinical medicine is a complex phenomenon. For managing massive amounts of patient data accumulating over time, it is essential. But many of us have, and continue to hold onto, expectations that it will increase our clinical "batting average" by improving things like diabetes control, hypertension, and weight.

Sadly, successes in this arena have been few. Human behavior seems to undo all the well-laid plans for improving medical conditions by altering human behavior.

But this is the season of hope.

Bonnie Spring, Ph.D., and her colleagues published results from a randomized clinical trial evaluating the use of mobile technology (via a personal digital assistant, or PDA) to track food intake, weight, and physical activity, and then facilitate intervention based on the data (Arch. Intern. Med. 2012 [doi:10.1001/jamainternmed.2013.1221]).

Sixty-nine adults took part, 85.5% of whom were male, with a mean age of 57.7 years. Inclusion criteria included a body mass index between 25 and 40 kg/m², weight less than 181.4 kg, and the ability to participate in moderate-intensity physical activity. Patients were randomized to either a control group following the standard of care, or to an intervention group following the standard of care plus mobile technology and telephone coaching.

Participants were given a 5%-10% weight loss goal. The study had two phases: a weight loss phase (months 0-6) and a weight maintenance phase (months 7-12).

All patients received the standard intervention composed of the MOVE! group weight loss program offered at all Veterans Affairs medical centers. In the first 6 months, both arms of the study attended biweekly MOVE! sessions facilitated by dieticians, psychologists, or physicians. Each session lasted approximately 90 minutes, incorporating teachings on nutrition, physical activity, and behavior change.

The intervention group recorded daily food intake and used the PDA as a decision-support tool to assist in personal decisions about energy balance. The resulting data were used to guide a physical activity intervention, and a lifestyle coach provided telephone support every 2 weeks to review data and assist in data management issues. Physical activity recommendations and calorie intake were tailored to achieve weight loss goals. During the weight maintenance phase, data were collected but no behavioral counseling was provided.

The mobile technology group lost 3.9 kg more than the control group (95% CI: 2.2-5.5 kg). The mobile technology group members had significantly greater odds of losing 5% of their body weight.

The study shows that remote lifestyle coaching providing intervention based on data collected through mobile technology can be effective. The appeal of the intervention is the ability to use transmitted data to enhance the intervention without the need for face-to-face interactions. However, the MOVE! intervention used by both groups is itself an intense, resource-intensive intervention with 12 group sessions during a 6-month period.

We obviously need to accept the cold reality of clinical medicine and life: You get out what you put in. The more intense the intervention, the better patients will do. But this study definitely moves us closer to the vision of leveraging existing medical infrastructure and medical technology to remotely treat our patients and improve their lives by supporting them in weight loss.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.

Perhaps like many primary care clinicians, I perseverate on diseases most prevalent or problematic. Overweight and obesity are both. So, at the risk of sounding like we’ve dedicated this column exclusively to this condition, let’s focus on new data about an intervention that can help people lose weight and maintain weight loss.

Technology as applied to clinical medicine is a complex phenomenon. For managing massive amounts of patient data accumulating over time, it is essential. But many of us have, and continue to hold onto, expectations that it will increase our clinical "batting average" by improving things like diabetes control, hypertension, and weight.

Sadly, successes in this arena have been few. Human behavior seems to undo all the well-laid plans for improving medical conditions by altering human behavior.

But this is the season of hope.

Bonnie Spring, Ph.D., and her colleagues published results from a randomized clinical trial evaluating the use of mobile technology (via a personal digital assistant, or PDA) to track food intake, weight, and physical activity, and then facilitate intervention based on the data (Arch. Intern. Med. 2012 [doi:10.1001/jamainternmed.2013.1221]).

Sixty-nine adults took part, 85.5% of whom were male, with a mean age of 57.7 years. Inclusion criteria included a body mass index between 25 and 40 kg/m², weight less than 181.4 kg, and the ability to participate in moderate-intensity physical activity. Patients were randomized to either a control group following the standard of care, or to an intervention group following the standard of care plus mobile technology and telephone coaching.

Participants were given a 5%-10% weight loss goal. The study had two phases: a weight loss phase (months 0-6) and a weight maintenance phase (months 7-12).

All patients received the standard intervention composed of the MOVE! group weight loss program offered at all Veterans Affairs medical centers. In the first 6 months, both arms of the study attended biweekly MOVE! sessions facilitated by dieticians, psychologists, or physicians. Each session lasted approximately 90 minutes, incorporating teachings on nutrition, physical activity, and behavior change.

The intervention group recorded daily food intake and used the PDA as a decision-support tool to assist in personal decisions about energy balance. The resulting data were used to guide a physical activity intervention, and a lifestyle coach provided telephone support every 2 weeks to review data and assist in data management issues. Physical activity recommendations and calorie intake were tailored to achieve weight loss goals. During the weight maintenance phase, data were collected but no behavioral counseling was provided.

The mobile technology group lost 3.9 kg more than the control group (95% CI: 2.2-5.5 kg). The mobile technology group members had significantly greater odds of losing 5% of their body weight.

The study shows that remote lifestyle coaching providing intervention based on data collected through mobile technology can be effective. The appeal of the intervention is the ability to use transmitted data to enhance the intervention without the need for face-to-face interactions. However, the MOVE! intervention used by both groups is itself an intense, resource-intensive intervention with 12 group sessions during a 6-month period.

We obviously need to accept the cold reality of clinical medicine and life: You get out what you put in. The more intense the intervention, the better patients will do. But this study definitely moves us closer to the vision of leveraging existing medical infrastructure and medical technology to remotely treat our patients and improve their lives by supporting them in weight loss.

Dr. Ebbert is professor of medicine and primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author.