PARIS – How can the problem of poor treatment compliance in patients with hypertension be resolved? A new therapeutic approach could be a game-changer.

Many approaches have been explored in recent years to make life easier for patients living with chronic conditions that require them to take daily medication: subcutaneous implantable devices, nanogels, and, more specifically in the case of hypertension, renal denervation or small interfering RNA (siRNA) with a long half-life.

It’s siRNA that Michel Azizi, MD, PhD, head of the blood pressure clinic at Georges Pompidou European Hospital (HEGP) in Paris, discussed at the International Meeting of the French Society of Hypertension.

These small molecules have already shown their worth in treating rare diseases such as transthyretin amyloidosis. More recently, treating hypercholesterolemia with the PCSK9 inhibitor inclisiran has proven effective. “One subcutaneous injection of inclisiran reduces LDL cholesterol by 50% for a period of 210 days,” said Dr. Azizi.

The benefit of a new therapeutic siRNA – zilebesiran, administered subcutaneously – in treating hypertension is currently the subject of a phase II clinical trial.

This is a double-stranded RNA. One of the strands is linked to a sugar, N-acetylgalactosamine (GalNAc), which protects these highly fragile siRNA and binds with a very strong affinity in the liver. The second strand binds to a specific area of the RNA to prevent synthesis of the precursor peptide of angiotensin, angiotensinogen. The resulting effect is suppression of the production of angiotensin I and II, which leads to a long-lasting lowering of blood pressure.
 

Lasting efficacy

Phase I studies with zilebesiran have demonstrated a long-term effect, with a reduction of greater than 90% in circulating angiotensinogen over 6 months after a single subcutaneous dose (800 mg). The peak in reduction of circulating angiotensinogen occurs after approximately 3 weeks.

“It’s extremely powerful,” said Dr. Azizi.

Lasting reductions in blood pressure have also been observed, with 24-hour ambulatory blood pressure monitoring showing a reduction in systolic BP of greater than 15 mm Hg 8 weeks after administration of a single dose of zilebesiran (800 mg).

Zilebesiran was also well tolerated, with only mild to moderate reactions at the site of the injection (n = 5/56) and no serious treatment-related adverse events, hypotension, or significant changes in kidney or liver function.

“In terms of benefits, the effect is ongoing. Zilebesiran leads to reduced medication use and causes less variability in blood pressure response. Nevertheless, interfering RNA acts slowly, meaning that zilebesiran would not be suitable for people presenting with a hypertensive crisis. The fact that it blocks the renin-angiotensin system [RAS] for a very long period of time also poses the question of how to reverse its hypotensive effects,” said Dr. Azizi.
 

Unanswered questions

The lasting RAS antagonist and blood pressure–lowering effects pose a potential safety problem in circumstances involving patients in a state of hypovolemia and hypotension who require rapid blood pressure–raising interventions to prevent morbidity and mortality.

In recent studies, Estrellita Uijl et al. have thus examined strategies to counteract the blood pressure–lowering effect of siRNA in spontaneously hypertensive rats.

Fludrocortisone and a high-salt diet were both successful in gradually increasing blood pressure, which returned to its baseline levels on days 5 and 7, respectively. Yet this rate of response would be wholly inadequate in an urgent clinical situation.

However, midodrine could not reduce blood pressure to normal levels, whether administered subcutaneously or orally.

A rapid and short-lasting increase in blood pressure was observed with bolus doses of vasopressors, but clinically, these would need to be administered intravenously to achieve a lasting effect. Such administration would require hospitalization, close monitoring, and the use of human resources and additional health care provisions.

Encouragingly, the laboratory that created this molecule, Alnylam Pharmaceuticals, has come up with an antidote: Reversir. It is a GalNAc-conjugated, single-stranded, high-affinity oligonucleotide complementary to the zilebesiran strand that achieves effective reversal of siRNA activity in 24 hours.

In the future, after the phase 2 trials have been completed, whether or not zilebesiran reduces the incidence of cardiovascular events and mortality remains to be seen. But as for Dr. Azizi, the director of HEGP’s blood pressure clinic in Paris, he has no doubt that “this approach is about to shake up how we treat patients in the cardiovascular field.”
 

On the horizon

Zilebesiran is being studied in phase 2 trials in patients with mild to moderate hypertension not taking antihypertensive drugs (KARDIA-1: 375 patients; double-blind, placebo-controlled, five-arm trial; zilebesiran at 150, 300, and 600 mg twice per year and 300 mg once every 3 months) and in patients whose blood pressure is not controlled (KARDIA-2: 800 patients; initial open-label start-up period of 4 weeks with indapamide/amlodipine/olmesartan, followed by a double-blind, placebo-controlled study over 6 months, then an open-label extension study for up to 12 additional months; zilebesiran at 600 mg on the first day of the initial double-blind period, then every 6 months during the open-label extension period).

This article was translated from the Medscape French edition and a version appeared on Medscape.com.

PARIS – How can the problem of poor treatment compliance in patients with hypertension be resolved? A new therapeutic approach could be a game-changer.

Many approaches have been explored in recent years to make life easier for patients living with chronic conditions that require them to take daily medication: subcutaneous implantable devices, nanogels, and, more specifically in the case of hypertension, renal denervation or small interfering RNA (siRNA) with a long half-life.

It’s siRNA that Michel Azizi, MD, PhD, head of the blood pressure clinic at Georges Pompidou European Hospital (HEGP) in Paris, discussed at the International Meeting of the French Society of Hypertension.

These small molecules have already shown their worth in treating rare diseases such as transthyretin amyloidosis. More recently, treating hypercholesterolemia with the PCSK9 inhibitor inclisiran has proven effective. “One subcutaneous injection of inclisiran reduces LDL cholesterol by 50% for a period of 210 days,” said Dr. Azizi.

The benefit of a new therapeutic siRNA – zilebesiran, administered subcutaneously – in treating hypertension is currently the subject of a phase II clinical trial.

This is a double-stranded RNA. One of the strands is linked to a sugar, N-acetylgalactosamine (GalNAc), which protects these highly fragile siRNA and binds with a very strong affinity in the liver. The second strand binds to a specific area of the RNA to prevent synthesis of the precursor peptide of angiotensin, angiotensinogen. The resulting effect is suppression of the production of angiotensin I and II, which leads to a long-lasting lowering of blood pressure.
 

Lasting efficacy

Phase I studies with zilebesiran have demonstrated a long-term effect, with a reduction of greater than 90% in circulating angiotensinogen over 6 months after a single subcutaneous dose (800 mg). The peak in reduction of circulating angiotensinogen occurs after approximately 3 weeks.

“It’s extremely powerful,” said Dr. Azizi.

Lasting reductions in blood pressure have also been observed, with 24-hour ambulatory blood pressure monitoring showing a reduction in systolic BP of greater than 15 mm Hg 8 weeks after administration of a single dose of zilebesiran (800 mg).

Zilebesiran was also well tolerated, with only mild to moderate reactions at the site of the injection (n = 5/56) and no serious treatment-related adverse events, hypotension, or significant changes in kidney or liver function.

“In terms of benefits, the effect is ongoing. Zilebesiran leads to reduced medication use and causes less variability in blood pressure response. Nevertheless, interfering RNA acts slowly, meaning that zilebesiran would not be suitable for people presenting with a hypertensive crisis. The fact that it blocks the renin-angiotensin system [RAS] for a very long period of time also poses the question of how to reverse its hypotensive effects,” said Dr. Azizi.
 

Unanswered questions

The lasting RAS antagonist and blood pressure–lowering effects pose a potential safety problem in circumstances involving patients in a state of hypovolemia and hypotension who require rapid blood pressure–raising interventions to prevent morbidity and mortality.

In recent studies, Estrellita Uijl et al. have thus examined strategies to counteract the blood pressure–lowering effect of siRNA in spontaneously hypertensive rats.

Fludrocortisone and a high-salt diet were both successful in gradually increasing blood pressure, which returned to its baseline levels on days 5 and 7, respectively. Yet this rate of response would be wholly inadequate in an urgent clinical situation.

However, midodrine could not reduce blood pressure to normal levels, whether administered subcutaneously or orally.

A rapid and short-lasting increase in blood pressure was observed with bolus doses of vasopressors, but clinically, these would need to be administered intravenously to achieve a lasting effect. Such administration would require hospitalization, close monitoring, and the use of human resources and additional health care provisions.

Encouragingly, the laboratory that created this molecule, Alnylam Pharmaceuticals, has come up with an antidote: Reversir. It is a GalNAc-conjugated, single-stranded, high-affinity oligonucleotide complementary to the zilebesiran strand that achieves effective reversal of siRNA activity in 24 hours.

In the future, after the phase 2 trials have been completed, whether or not zilebesiran reduces the incidence of cardiovascular events and mortality remains to be seen. But as for Dr. Azizi, the director of HEGP’s blood pressure clinic in Paris, he has no doubt that “this approach is about to shake up how we treat patients in the cardiovascular field.”
 

On the horizon

Zilebesiran is being studied in phase 2 trials in patients with mild to moderate hypertension not taking antihypertensive drugs (KARDIA-1: 375 patients; double-blind, placebo-controlled, five-arm trial; zilebesiran at 150, 300, and 600 mg twice per year and 300 mg once every 3 months) and in patients whose blood pressure is not controlled (KARDIA-2: 800 patients; initial open-label start-up period of 4 weeks with indapamide/amlodipine/olmesartan, followed by a double-blind, placebo-controlled study over 6 months, then an open-label extension study for up to 12 additional months; zilebesiran at 600 mg on the first day of the initial double-blind period, then every 6 months during the open-label extension period).

This article was translated from the Medscape French edition and a version appeared on Medscape.com.

PARIS – How can the problem of poor treatment compliance in patients with hypertension be resolved? A new therapeutic approach could be a game-changer.

Many approaches have been explored in recent years to make life easier for patients living with chronic conditions that require them to take daily medication: subcutaneous implantable devices, nanogels, and, more specifically in the case of hypertension, renal denervation or small interfering RNA (siRNA) with a long half-life.

It’s siRNA that Michel Azizi, MD, PhD, head of the blood pressure clinic at Georges Pompidou European Hospital (HEGP) in Paris, discussed at the International Meeting of the French Society of Hypertension.

These small molecules have already shown their worth in treating rare diseases such as transthyretin amyloidosis. More recently, treating hypercholesterolemia with the PCSK9 inhibitor inclisiran has proven effective. “One subcutaneous injection of inclisiran reduces LDL cholesterol by 50% for a period of 210 days,” said Dr. Azizi.

The benefit of a new therapeutic siRNA – zilebesiran, administered subcutaneously – in treating hypertension is currently the subject of a phase II clinical trial.

This is a double-stranded RNA. One of the strands is linked to a sugar, N-acetylgalactosamine (GalNAc), which protects these highly fragile siRNA and binds with a very strong affinity in the liver. The second strand binds to a specific area of the RNA to prevent synthesis of the precursor peptide of angiotensin, angiotensinogen. The resulting effect is suppression of the production of angiotensin I and II, which leads to a long-lasting lowering of blood pressure.
 

Lasting efficacy

Phase I studies with zilebesiran have demonstrated a long-term effect, with a reduction of greater than 90% in circulating angiotensinogen over 6 months after a single subcutaneous dose (800 mg). The peak in reduction of circulating angiotensinogen occurs after approximately 3 weeks.

“It’s extremely powerful,” said Dr. Azizi.

Lasting reductions in blood pressure have also been observed, with 24-hour ambulatory blood pressure monitoring showing a reduction in systolic BP of greater than 15 mm Hg 8 weeks after administration of a single dose of zilebesiran (800 mg).

Zilebesiran was also well tolerated, with only mild to moderate reactions at the site of the injection (n = 5/56) and no serious treatment-related adverse events, hypotension, or significant changes in kidney or liver function.

“In terms of benefits, the effect is ongoing. Zilebesiran leads to reduced medication use and causes less variability in blood pressure response. Nevertheless, interfering RNA acts slowly, meaning that zilebesiran would not be suitable for people presenting with a hypertensive crisis. The fact that it blocks the renin-angiotensin system [RAS] for a very long period of time also poses the question of how to reverse its hypotensive effects,” said Dr. Azizi.
 

Unanswered questions

The lasting RAS antagonist and blood pressure–lowering effects pose a potential safety problem in circumstances involving patients in a state of hypovolemia and hypotension who require rapid blood pressure–raising interventions to prevent morbidity and mortality.

In recent studies, Estrellita Uijl et al. have thus examined strategies to counteract the blood pressure–lowering effect of siRNA in spontaneously hypertensive rats.

Fludrocortisone and a high-salt diet were both successful in gradually increasing blood pressure, which returned to its baseline levels on days 5 and 7, respectively. Yet this rate of response would be wholly inadequate in an urgent clinical situation.

However, midodrine could not reduce blood pressure to normal levels, whether administered subcutaneously or orally.

A rapid and short-lasting increase in blood pressure was observed with bolus doses of vasopressors, but clinically, these would need to be administered intravenously to achieve a lasting effect. Such administration would require hospitalization, close monitoring, and the use of human resources and additional health care provisions.

Encouragingly, the laboratory that created this molecule, Alnylam Pharmaceuticals, has come up with an antidote: Reversir. It is a GalNAc-conjugated, single-stranded, high-affinity oligonucleotide complementary to the zilebesiran strand that achieves effective reversal of siRNA activity in 24 hours.

In the future, after the phase 2 trials have been completed, whether or not zilebesiran reduces the incidence of cardiovascular events and mortality remains to be seen. But as for Dr. Azizi, the director of HEGP’s blood pressure clinic in Paris, he has no doubt that “this approach is about to shake up how we treat patients in the cardiovascular field.”
 

On the horizon

Zilebesiran is being studied in phase 2 trials in patients with mild to moderate hypertension not taking antihypertensive drugs (KARDIA-1: 375 patients; double-blind, placebo-controlled, five-arm trial; zilebesiran at 150, 300, and 600 mg twice per year and 300 mg once every 3 months) and in patients whose blood pressure is not controlled (KARDIA-2: 800 patients; initial open-label start-up period of 4 weeks with indapamide/amlodipine/olmesartan, followed by a double-blind, placebo-controlled study over 6 months, then an open-label extension study for up to 12 additional months; zilebesiran at 600 mg on the first day of the initial double-blind period, then every 6 months during the open-label extension period).

This article was translated from the Medscape French edition and a version appeared on Medscape.com.

Physicians and other clinicians could more easily exit contracts and change jobs under the Federal Trade Commission’s new proposed rule that would block companies from limiting employees’ ability to work for a rival.

The proposed rule seeks to ban companies from enforcing noncompete clauses in employment contracts, a practice that represents an “unfair method of competition” with “exploitative and widespread” impacts, including suppression of wages, innovation, and entrepreneurial spirit, the FTC said. The public has 60 days to submit comments on the proposal before the FTC issues the final rule.

Employers often include noncompete clauses in physician contracts because they want to avoid having patients leave their health care system and follow a doctor to a competitor. A 2018 survey of primary care physicians found that about half of office-based physicians and 37% of physicians employed at hospitals or freestanding care centers were bound by restrictive covenants.

“A federal ban on noncompete agreements will ensure that physicians nationwide can finally change jobs without fear of being sued,” Erik B. Smith, MD, JD, clinical assistant professor of anesthesiology at the University of Southern California, Los Angeles, said in an interview.

Many doctors would like to see noncompete agreements vanish, but some physicians still favor them.

“As a small-practice owner, I am personally against this. The noncompete helps me take a risk and hire a physician. It typically takes 2-3 years for me to break even. I think this will further consolidate employment with large hospital systems unfortunately,” Texas cardiologist Rishin Shah, MD, recently tweeted in response to the FTC announcement.

Dr. Smith, who has advocated for noncompete reform, said about half of states currently allow the controversial clauses.

However, several states have recently passed laws restricting their use. California, North Dakota, and Oklahoma ban noncompetes, although some narrowly defined exceptions, such as the sale of a business, remain.

Other states, like Colorado, Illinois, and Oregon, broadly ban noncompete clauses, except for workers earning above a certain threshold. For example, in Colorado, noncompete agreements are permitted for highly compensated employees earning more than $101,250.

Despite additional restrictions on noncompete agreements for workers in the District of Columbia, the new legislation does not apply to physicians earning total compensation of $250,000 or more. However, their employers must define the geographic parameters of the noncompete and limit postemployment restrictions to 2 years.

Restrictive covenants are “uniquely challenging to family medicine’s emphasis on longitudinal care and the patient-physician relationship,” said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians. The limitations imposed by noncompete agreements “potentially reduce patient choice, lower the quality of care for patients, and ultimately harm the foundation of family medicine – our relationships with our patients.”

Although the proposed rule aligns with President Biden’s executive order promoting economic competition, Dr. Smith said a national ban on noncompete agreements may push the limits of FTC authority.

“This new rule will certainly result in a ‘major questions doctrine’ Supreme Court challenge,” said Dr. Smith, and possibly be struck down if the court determines an administrative overstep into areas of “vast economic or political significance.”
 

A controversial policy

The American Medical Association’s code of ethics discourages covenants that “unreasonably restrict” the ability of physicians to practice following contract termination. And in 2022, the AMA cited “overly broad” noncompete language as a red flag young physicians should watch out for during contract negotiations.

But in 2020, the AMA asked the FTC not to use its rulemaking authority to regulate noncompete clauses in physician employment contracts, and instead, relegate enforcement of such agreements to each state. The American Hospital Association expressed similar views.

Still, the FTC said that eliminating noncompete clauses will increase annual wages by $300 billion, allow 30 million Americans to pursue better job opportunities, and encourage hiring competition among employers. It will also save consumers up to $148 billion in health care costs annually.

“Noncompetes block workers from freely switching jobs, depriving them of higher wages and better working conditions, and depriving businesses of a talent pool that they need to build and expand,” Lina M. Khan, FTC chair, said in a press release about the proposal.

A national ban on noncompetes would keep more physicians in the industry and practicing in their communities, a win for patients and providers, said Dr. Smith. It could also compel employers to offer more competitive employment packages, including fair wages, better work conditions, and a culture of well-being and patient safety.

“Whatever the final rule is, I’m certain it will be legally challenged,” said Dr. Smith, adding that the nation’s most prominent business lobbying group, the Chamber of Commerce, has already issued a statement calling the rule “blatantly unlawful."

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

Physicians and other clinicians could more easily exit contracts and change jobs under the Federal Trade Commission’s new proposed rule that would block companies from limiting employees’ ability to work for a rival.

The proposed rule seeks to ban companies from enforcing noncompete clauses in employment contracts, a practice that represents an “unfair method of competition” with “exploitative and widespread” impacts, including suppression of wages, innovation, and entrepreneurial spirit, the FTC said. The public has 60 days to submit comments on the proposal before the FTC issues the final rule.

Employers often include noncompete clauses in physician contracts because they want to avoid having patients leave their health care system and follow a doctor to a competitor. A 2018 survey of primary care physicians found that about half of office-based physicians and 37% of physicians employed at hospitals or freestanding care centers were bound by restrictive covenants.

“A federal ban on noncompete agreements will ensure that physicians nationwide can finally change jobs without fear of being sued,” Erik B. Smith, MD, JD, clinical assistant professor of anesthesiology at the University of Southern California, Los Angeles, said in an interview.

Many doctors would like to see noncompete agreements vanish, but some physicians still favor them.

“As a small-practice owner, I am personally against this. The noncompete helps me take a risk and hire a physician. It typically takes 2-3 years for me to break even. I think this will further consolidate employment with large hospital systems unfortunately,” Texas cardiologist Rishin Shah, MD, recently tweeted in response to the FTC announcement.

Dr. Smith, who has advocated for noncompete reform, said about half of states currently allow the controversial clauses.

However, several states have recently passed laws restricting their use. California, North Dakota, and Oklahoma ban noncompetes, although some narrowly defined exceptions, such as the sale of a business, remain.

Other states, like Colorado, Illinois, and Oregon, broadly ban noncompete clauses, except for workers earning above a certain threshold. For example, in Colorado, noncompete agreements are permitted for highly compensated employees earning more than $101,250.

Despite additional restrictions on noncompete agreements for workers in the District of Columbia, the new legislation does not apply to physicians earning total compensation of $250,000 or more. However, their employers must define the geographic parameters of the noncompete and limit postemployment restrictions to 2 years.

Restrictive covenants are “uniquely challenging to family medicine’s emphasis on longitudinal care and the patient-physician relationship,” said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians. The limitations imposed by noncompete agreements “potentially reduce patient choice, lower the quality of care for patients, and ultimately harm the foundation of family medicine – our relationships with our patients.”

Although the proposed rule aligns with President Biden’s executive order promoting economic competition, Dr. Smith said a national ban on noncompete agreements may push the limits of FTC authority.

“This new rule will certainly result in a ‘major questions doctrine’ Supreme Court challenge,” said Dr. Smith, and possibly be struck down if the court determines an administrative overstep into areas of “vast economic or political significance.”
 

A controversial policy

The American Medical Association’s code of ethics discourages covenants that “unreasonably restrict” the ability of physicians to practice following contract termination. And in 2022, the AMA cited “overly broad” noncompete language as a red flag young physicians should watch out for during contract negotiations.

But in 2020, the AMA asked the FTC not to use its rulemaking authority to regulate noncompete clauses in physician employment contracts, and instead, relegate enforcement of such agreements to each state. The American Hospital Association expressed similar views.

Still, the FTC said that eliminating noncompete clauses will increase annual wages by $300 billion, allow 30 million Americans to pursue better job opportunities, and encourage hiring competition among employers. It will also save consumers up to $148 billion in health care costs annually.

“Noncompetes block workers from freely switching jobs, depriving them of higher wages and better working conditions, and depriving businesses of a talent pool that they need to build and expand,” Lina M. Khan, FTC chair, said in a press release about the proposal.

A national ban on noncompetes would keep more physicians in the industry and practicing in their communities, a win for patients and providers, said Dr. Smith. It could also compel employers to offer more competitive employment packages, including fair wages, better work conditions, and a culture of well-being and patient safety.

“Whatever the final rule is, I’m certain it will be legally challenged,” said Dr. Smith, adding that the nation’s most prominent business lobbying group, the Chamber of Commerce, has already issued a statement calling the rule “blatantly unlawful."

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

Physicians and other clinicians could more easily exit contracts and change jobs under the Federal Trade Commission’s new proposed rule that would block companies from limiting employees’ ability to work for a rival.

The proposed rule seeks to ban companies from enforcing noncompete clauses in employment contracts, a practice that represents an “unfair method of competition” with “exploitative and widespread” impacts, including suppression of wages, innovation, and entrepreneurial spirit, the FTC said. The public has 60 days to submit comments on the proposal before the FTC issues the final rule.

Employers often include noncompete clauses in physician contracts because they want to avoid having patients leave their health care system and follow a doctor to a competitor. A 2018 survey of primary care physicians found that about half of office-based physicians and 37% of physicians employed at hospitals or freestanding care centers were bound by restrictive covenants.

“A federal ban on noncompete agreements will ensure that physicians nationwide can finally change jobs without fear of being sued,” Erik B. Smith, MD, JD, clinical assistant professor of anesthesiology at the University of Southern California, Los Angeles, said in an interview.

Many doctors would like to see noncompete agreements vanish, but some physicians still favor them.

“As a small-practice owner, I am personally against this. The noncompete helps me take a risk and hire a physician. It typically takes 2-3 years for me to break even. I think this will further consolidate employment with large hospital systems unfortunately,” Texas cardiologist Rishin Shah, MD, recently tweeted in response to the FTC announcement.

Dr. Smith, who has advocated for noncompete reform, said about half of states currently allow the controversial clauses.

However, several states have recently passed laws restricting their use. California, North Dakota, and Oklahoma ban noncompetes, although some narrowly defined exceptions, such as the sale of a business, remain.

Other states, like Colorado, Illinois, and Oregon, broadly ban noncompete clauses, except for workers earning above a certain threshold. For example, in Colorado, noncompete agreements are permitted for highly compensated employees earning more than $101,250.

Despite additional restrictions on noncompete agreements for workers in the District of Columbia, the new legislation does not apply to physicians earning total compensation of $250,000 or more. However, their employers must define the geographic parameters of the noncompete and limit postemployment restrictions to 2 years.

Restrictive covenants are “uniquely challenging to family medicine’s emphasis on longitudinal care and the patient-physician relationship,” said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians. The limitations imposed by noncompete agreements “potentially reduce patient choice, lower the quality of care for patients, and ultimately harm the foundation of family medicine – our relationships with our patients.”

Although the proposed rule aligns with President Biden’s executive order promoting economic competition, Dr. Smith said a national ban on noncompete agreements may push the limits of FTC authority.

“This new rule will certainly result in a ‘major questions doctrine’ Supreme Court challenge,” said Dr. Smith, and possibly be struck down if the court determines an administrative overstep into areas of “vast economic or political significance.”
 

A controversial policy

The American Medical Association’s code of ethics discourages covenants that “unreasonably restrict” the ability of physicians to practice following contract termination. And in 2022, the AMA cited “overly broad” noncompete language as a red flag young physicians should watch out for during contract negotiations.

But in 2020, the AMA asked the FTC not to use its rulemaking authority to regulate noncompete clauses in physician employment contracts, and instead, relegate enforcement of such agreements to each state. The American Hospital Association expressed similar views.

Still, the FTC said that eliminating noncompete clauses will increase annual wages by $300 billion, allow 30 million Americans to pursue better job opportunities, and encourage hiring competition among employers. It will also save consumers up to $148 billion in health care costs annually.

“Noncompetes block workers from freely switching jobs, depriving them of higher wages and better working conditions, and depriving businesses of a talent pool that they need to build and expand,” Lina M. Khan, FTC chair, said in a press release about the proposal.

A national ban on noncompetes would keep more physicians in the industry and practicing in their communities, a win for patients and providers, said Dr. Smith. It could also compel employers to offer more competitive employment packages, including fair wages, better work conditions, and a culture of well-being and patient safety.

“Whatever the final rule is, I’m certain it will be legally challenged,” said Dr. Smith, adding that the nation’s most prominent business lobbying group, the Chamber of Commerce, has already issued a statement calling the rule “blatantly unlawful."

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

New research suggests that coffee’s benefits for reducing severity of nonalcoholic fatty liver disease (NAFLD) stem from more than just caffeine.

Increased intake of both regular and decaffeinated coffee was significantly associated with a reduced severity of NAFLD in the study, published in Nutrients. The study participants included 156 overweight adults, most of whom had type 2 diabetes.

A confluence of factors including diet and lifestyle changes and increased obesity have contributed to a rise in type 2 diabetes and of NAFLD, Margarida Coelho, of the Center for Neuroscience and Cell Biology at the University of Coimbra (Portugal), and colleagues wrote.

Previous studies support an association between coffee and protection against NAFLD, but the roles of the caffeine and noncaffeine components of coffee have not been examined, corresponding author John Griffith Jones, PhD, also of the Center for Neuroscience and Cell Biology at the University of Coimbra, said in an interview.

“There have been previous studies indicating a link between coffee intake and NAFLD amelioration, but these were entirely based on self-reporting questionnaire data, but the main limitation of this approach is that it does not provide any information on which components of coffee confer the beneficial effects,” Dr. Jones said. “The development of new analytical techniques allowing reliable profiling of coffee metabolites in urine allowed this limitation to be addressed.”

Dr. Jones and associates examined the relationship between consumption of regular and decaffeinated coffee on the fatty liver index (FLI), a validated predictor of NAFLD. They measured coffee intake of 156 overweight adults, 135 of whom had type 2 diabetes. The study population included 76 women and 80 men with a mean age of 59 years and a mean body mass index of 29 kg/m².

The participants reported coffee intake via questionnaires, and 98 participants (all with type 2 diabetes) also provided urine samples for measurement of caffeine and noncaffeine metabolites (the products of the body breaking down coffee). NAFLD was assessed using the FLI and a scanning measure of fibrosis.

Overall, no associations appeared between self-reported coffee intake and NAFLD measures. However, urine caffeine metabolite levels were significantly higher among individuals with no liver fibrosis, compared with those with fibrosis, and noncaffeine metabolites showed a significant negative association with FLI measures.

In a multiple regression analysis of 89 individuals with type 2 diabetes, both caffeine and noncaffeine metabolites were negatively associated with FLI, which suggests less severe NAFLD, the researchers noted.

Although the mechanism of action remains unclear, the findings suggest that other noncaffeine coffee components such as polyphenols may reduce the risk of fibrosis by reducing oxidative stress on the liver, they said.
 

Benefits beyond caffeine

“The main surprise of the study was that both caffeine and noncaffeine metabolites had beneficial effects,” Dr. Jones said. “We had anticipated caffeine, based on its well-known effects on inhibiting liver fibrosis, but the effects of other components were less well described.”

Clinicians can encourage their patients with type 2 diabetes who drink coffee to continue to do so within a normal range (up to three to four cups per day) including decaffeinated coffee; however, “they should be strongly encouraged to drink coffee without added fats and sugars, otherwise the protective benefits [against more severe NAFLD] will not be realized,” Dr. Jones said.

Additional research is needed to extend the analysis to include more coffee compounds, especially those truly unique to coffee, since caffeine can be found in many other foods and beverages, Dr. Jones added.
 

Limitations include 24-hour time frame

The findings were limited by several factors, including the use of 24-hour urine sample, which may not represent an individual’s habitual coffee consumption, the researchers noted. The urine metabolites measured also may be derived from foods and beverages other than coffee. In addition, the assessment of NAFLD was based on serum markers and ultrasound/elastography, which are less precise than liver biopsy and magnetic resonance spectroscopy.

However, the study is the first known to use urine data to examine coffee’s protective effect against NAFLD and suggests that both caffeine and noncaffeine metabolites are associated with less severe disease, they concluded.
 

Findings intriguing but not ready for prime time

“The bottom line is that we have a major epidemic of NAFLD in the United States,” Victor L. Roberts, MD, professor of internal medicine at the University of Central Florida, Orlando, said in an interview. NAFLD has become the most common cause of chronic liver disease worldwide, and will become one of the leading causes of cirrhosis – surpassing infections as the main driver of end-stage liver disease.

“In this country, the epidemic of obesity compounds the problem, and risks for NAFLD include obesity and type 2 diabetes,” said Dr. Roberts.

The concept of coffee as beneficial is not new, but data suggest that the effects vary with insulin resistance, he said. If liver disease is advanced, coffee and its components may not have much benefit, but early on, it might have a role.

The likely mechanism of action for the benefits of coffee on the reduction in liver fibrosis is through a complex set of metabolic steps that interrupt the promotion of collagen production and reduce liver stiffness, said Dr. Roberts.

The current study authors were up front about the limitations, mainly the use of self-reports, although including the urine collection provided more scientific data, he said. More studies are needed in other populations, but the findings are interesting enough to merit additional research.

The take-home message for primary care, however, is that drinking coffee – regular or decaf – does not replace standard of care, Dr. Roberts emphasized.

“If a patient is a coffee drinker and they have NAFLD or are at risk, they could be encouraged to continue drinking coffee,” in reasonable amounts, said Dr. Roberts. “Anywhere from 1-3 cups a day is unlikely to be a problem, and there is some hope and interest in this area,” but the findings of the current study “should not be taken as gospel or advocacy as a solution for people with NAFLD.”

Instead, clinicians should focus on the standard of care for management of patients at risk for NAFLD, promoting lifestyle changes such as weight loss, diet, and exercise (challenging as that may be), and prescribing appropriate medications, he said.

The study was supported by the Institute for Scientific Information on Coffee, and the researchers received funding from the ISIC to conduct the study. Dr. Roberts had no financial conflicts to disclose, but he serves on the editorial advisory board of Internal Medicine News.

New research suggests that coffee’s benefits for reducing severity of nonalcoholic fatty liver disease (NAFLD) stem from more than just caffeine.

Increased intake of both regular and decaffeinated coffee was significantly associated with a reduced severity of NAFLD in the study, published in Nutrients. The study participants included 156 overweight adults, most of whom had type 2 diabetes.

A confluence of factors including diet and lifestyle changes and increased obesity have contributed to a rise in type 2 diabetes and of NAFLD, Margarida Coelho, of the Center for Neuroscience and Cell Biology at the University of Coimbra (Portugal), and colleagues wrote.

Previous studies support an association between coffee and protection against NAFLD, but the roles of the caffeine and noncaffeine components of coffee have not been examined, corresponding author John Griffith Jones, PhD, also of the Center for Neuroscience and Cell Biology at the University of Coimbra, said in an interview.

“There have been previous studies indicating a link between coffee intake and NAFLD amelioration, but these were entirely based on self-reporting questionnaire data, but the main limitation of this approach is that it does not provide any information on which components of coffee confer the beneficial effects,” Dr. Jones said. “The development of new analytical techniques allowing reliable profiling of coffee metabolites in urine allowed this limitation to be addressed.”

Dr. Jones and associates examined the relationship between consumption of regular and decaffeinated coffee on the fatty liver index (FLI), a validated predictor of NAFLD. They measured coffee intake of 156 overweight adults, 135 of whom had type 2 diabetes. The study population included 76 women and 80 men with a mean age of 59 years and a mean body mass index of 29 kg/m².

The participants reported coffee intake via questionnaires, and 98 participants (all with type 2 diabetes) also provided urine samples for measurement of caffeine and noncaffeine metabolites (the products of the body breaking down coffee). NAFLD was assessed using the FLI and a scanning measure of fibrosis.

Overall, no associations appeared between self-reported coffee intake and NAFLD measures. However, urine caffeine metabolite levels were significantly higher among individuals with no liver fibrosis, compared with those with fibrosis, and noncaffeine metabolites showed a significant negative association with FLI measures.

In a multiple regression analysis of 89 individuals with type 2 diabetes, both caffeine and noncaffeine metabolites were negatively associated with FLI, which suggests less severe NAFLD, the researchers noted.

Although the mechanism of action remains unclear, the findings suggest that other noncaffeine coffee components such as polyphenols may reduce the risk of fibrosis by reducing oxidative stress on the liver, they said.
 

Benefits beyond caffeine

“The main surprise of the study was that both caffeine and noncaffeine metabolites had beneficial effects,” Dr. Jones said. “We had anticipated caffeine, based on its well-known effects on inhibiting liver fibrosis, but the effects of other components were less well described.”

Clinicians can encourage their patients with type 2 diabetes who drink coffee to continue to do so within a normal range (up to three to four cups per day) including decaffeinated coffee; however, “they should be strongly encouraged to drink coffee without added fats and sugars, otherwise the protective benefits [against more severe NAFLD] will not be realized,” Dr. Jones said.

Additional research is needed to extend the analysis to include more coffee compounds, especially those truly unique to coffee, since caffeine can be found in many other foods and beverages, Dr. Jones added.
 

Limitations include 24-hour time frame

The findings were limited by several factors, including the use of 24-hour urine sample, which may not represent an individual’s habitual coffee consumption, the researchers noted. The urine metabolites measured also may be derived from foods and beverages other than coffee. In addition, the assessment of NAFLD was based on serum markers and ultrasound/elastography, which are less precise than liver biopsy and magnetic resonance spectroscopy.

However, the study is the first known to use urine data to examine coffee’s protective effect against NAFLD and suggests that both caffeine and noncaffeine metabolites are associated with less severe disease, they concluded.
 

Findings intriguing but not ready for prime time

“The bottom line is that we have a major epidemic of NAFLD in the United States,” Victor L. Roberts, MD, professor of internal medicine at the University of Central Florida, Orlando, said in an interview. NAFLD has become the most common cause of chronic liver disease worldwide, and will become one of the leading causes of cirrhosis – surpassing infections as the main driver of end-stage liver disease.

“In this country, the epidemic of obesity compounds the problem, and risks for NAFLD include obesity and type 2 diabetes,” said Dr. Roberts.

The concept of coffee as beneficial is not new, but data suggest that the effects vary with insulin resistance, he said. If liver disease is advanced, coffee and its components may not have much benefit, but early on, it might have a role.

The likely mechanism of action for the benefits of coffee on the reduction in liver fibrosis is through a complex set of metabolic steps that interrupt the promotion of collagen production and reduce liver stiffness, said Dr. Roberts.

The current study authors were up front about the limitations, mainly the use of self-reports, although including the urine collection provided more scientific data, he said. More studies are needed in other populations, but the findings are interesting enough to merit additional research.

The take-home message for primary care, however, is that drinking coffee – regular or decaf – does not replace standard of care, Dr. Roberts emphasized.

“If a patient is a coffee drinker and they have NAFLD or are at risk, they could be encouraged to continue drinking coffee,” in reasonable amounts, said Dr. Roberts. “Anywhere from 1-3 cups a day is unlikely to be a problem, and there is some hope and interest in this area,” but the findings of the current study “should not be taken as gospel or advocacy as a solution for people with NAFLD.”

Instead, clinicians should focus on the standard of care for management of patients at risk for NAFLD, promoting lifestyle changes such as weight loss, diet, and exercise (challenging as that may be), and prescribing appropriate medications, he said.

The study was supported by the Institute for Scientific Information on Coffee, and the researchers received funding from the ISIC to conduct the study. Dr. Roberts had no financial conflicts to disclose, but he serves on the editorial advisory board of Internal Medicine News.

New research suggests that coffee’s benefits for reducing severity of nonalcoholic fatty liver disease (NAFLD) stem from more than just caffeine.

Increased intake of both regular and decaffeinated coffee was significantly associated with a reduced severity of NAFLD in the study, published in Nutrients. The study participants included 156 overweight adults, most of whom had type 2 diabetes.

A confluence of factors including diet and lifestyle changes and increased obesity have contributed to a rise in type 2 diabetes and of NAFLD, Margarida Coelho, of the Center for Neuroscience and Cell Biology at the University of Coimbra (Portugal), and colleagues wrote.

Previous studies support an association between coffee and protection against NAFLD, but the roles of the caffeine and noncaffeine components of coffee have not been examined, corresponding author John Griffith Jones, PhD, also of the Center for Neuroscience and Cell Biology at the University of Coimbra, said in an interview.

“There have been previous studies indicating a link between coffee intake and NAFLD amelioration, but these were entirely based on self-reporting questionnaire data, but the main limitation of this approach is that it does not provide any information on which components of coffee confer the beneficial effects,” Dr. Jones said. “The development of new analytical techniques allowing reliable profiling of coffee metabolites in urine allowed this limitation to be addressed.”

Dr. Jones and associates examined the relationship between consumption of regular and decaffeinated coffee on the fatty liver index (FLI), a validated predictor of NAFLD. They measured coffee intake of 156 overweight adults, 135 of whom had type 2 diabetes. The study population included 76 women and 80 men with a mean age of 59 years and a mean body mass index of 29 kg/m².

The participants reported coffee intake via questionnaires, and 98 participants (all with type 2 diabetes) also provided urine samples for measurement of caffeine and noncaffeine metabolites (the products of the body breaking down coffee). NAFLD was assessed using the FLI and a scanning measure of fibrosis.

Overall, no associations appeared between self-reported coffee intake and NAFLD measures. However, urine caffeine metabolite levels were significantly higher among individuals with no liver fibrosis, compared with those with fibrosis, and noncaffeine metabolites showed a significant negative association with FLI measures.

In a multiple regression analysis of 89 individuals with type 2 diabetes, both caffeine and noncaffeine metabolites were negatively associated with FLI, which suggests less severe NAFLD, the researchers noted.

Although the mechanism of action remains unclear, the findings suggest that other noncaffeine coffee components such as polyphenols may reduce the risk of fibrosis by reducing oxidative stress on the liver, they said.
 

Benefits beyond caffeine

“The main surprise of the study was that both caffeine and noncaffeine metabolites had beneficial effects,” Dr. Jones said. “We had anticipated caffeine, based on its well-known effects on inhibiting liver fibrosis, but the effects of other components were less well described.”

Clinicians can encourage their patients with type 2 diabetes who drink coffee to continue to do so within a normal range (up to three to four cups per day) including decaffeinated coffee; however, “they should be strongly encouraged to drink coffee without added fats and sugars, otherwise the protective benefits [against more severe NAFLD] will not be realized,” Dr. Jones said.

Additional research is needed to extend the analysis to include more coffee compounds, especially those truly unique to coffee, since caffeine can be found in many other foods and beverages, Dr. Jones added.
 

Limitations include 24-hour time frame

The findings were limited by several factors, including the use of 24-hour urine sample, which may not represent an individual’s habitual coffee consumption, the researchers noted. The urine metabolites measured also may be derived from foods and beverages other than coffee. In addition, the assessment of NAFLD was based on serum markers and ultrasound/elastography, which are less precise than liver biopsy and magnetic resonance spectroscopy.

However, the study is the first known to use urine data to examine coffee’s protective effect against NAFLD and suggests that both caffeine and noncaffeine metabolites are associated with less severe disease, they concluded.
 

Findings intriguing but not ready for prime time

“The bottom line is that we have a major epidemic of NAFLD in the United States,” Victor L. Roberts, MD, professor of internal medicine at the University of Central Florida, Orlando, said in an interview. NAFLD has become the most common cause of chronic liver disease worldwide, and will become one of the leading causes of cirrhosis – surpassing infections as the main driver of end-stage liver disease.

“In this country, the epidemic of obesity compounds the problem, and risks for NAFLD include obesity and type 2 diabetes,” said Dr. Roberts.

The concept of coffee as beneficial is not new, but data suggest that the effects vary with insulin resistance, he said. If liver disease is advanced, coffee and its components may not have much benefit, but early on, it might have a role.

The likely mechanism of action for the benefits of coffee on the reduction in liver fibrosis is through a complex set of metabolic steps that interrupt the promotion of collagen production and reduce liver stiffness, said Dr. Roberts.

The current study authors were up front about the limitations, mainly the use of self-reports, although including the urine collection provided more scientific data, he said. More studies are needed in other populations, but the findings are interesting enough to merit additional research.

The take-home message for primary care, however, is that drinking coffee – regular or decaf – does not replace standard of care, Dr. Roberts emphasized.

“If a patient is a coffee drinker and they have NAFLD or are at risk, they could be encouraged to continue drinking coffee,” in reasonable amounts, said Dr. Roberts. “Anywhere from 1-3 cups a day is unlikely to be a problem, and there is some hope and interest in this area,” but the findings of the current study “should not be taken as gospel or advocacy as a solution for people with NAFLD.”

Instead, clinicians should focus on the standard of care for management of patients at risk for NAFLD, promoting lifestyle changes such as weight loss, diet, and exercise (challenging as that may be), and prescribing appropriate medications, he said.

The study was supported by the Institute for Scientific Information on Coffee, and the researchers received funding from the ISIC to conduct the study. Dr. Roberts had no financial conflicts to disclose, but he serves on the editorial advisory board of Internal Medicine News.

When I was a resident (back in the Cretaceous era), the idea of autoimmune encephalitis was just beginning to take hold. It was kind of like Bigfoot. A few reports, vague articles, the occasional sighting of what may or may not be a case. …

Unlike Bigfoot, however, the evidence quickly added up until there was no question that such a disorder existed. Then disorder became disorders, and now it seems a few more types are added to the list each year.

This doesn’t change the fact that they’re still, in the grand scheme of general neurology, relatively rare, though no one questions that they exist.

Today people still wishfully take pictures of Bigfoot, but they turn out to be images of bears or other animals, or tricks of light and shadow.

This is an issue with human thought. Many times we see what we want to see, especially if it’s more interesting than a mundane alternative.

An autoimmune encephalitis article in the January 2023 issue of JAMA Neurology looked into this. On reviewing 393 patients diagnosed with the disorder, the researchers found that 27% of them actually didn’t have it at all. Such things as functional disorders, neurodegenerative diseases, and primary psychiatric diagnoses were, instead, the culprits.

I’m not criticizing those who made an incorrect diagnosis. We all do. That’s the nature of medicine.

Which is worse? Missing the diagnosis entirely and not treating, or diagnosing a patient with something else and treating incorrectly? I guess it depends on the disease and nature of treatment.

Certainly, finding a case of autoimmune encephalitis is more interesting than, say toxic-metabolic encephalopathy from a bladder infection, just as getting a picture of Bigfoot is way more cool than one of a bear with mange.

But we need to be careful when faced with equivocal labs and data lest we read too much into them. There are too many gray zones in medicine to lead you astray. Not to say we won’t be. Even well-intentioned physicians (which I assume is pretty much all of us) are going to make mistakes.

But it’s not just rare diseases. In the early 1990s two different studies found that 24% of patients diagnosed with Parkinson’s disease were found to have something else on autopsy.

That was 30 years ago. Now we have DaT scans to help. Maybe our abilities as neurologists have also gotten better (though I don’t think the neurological exam has changed much since Charcot).

Our gadgets, labs, and treatments get better every year. We have tools available to us now that were unthinkable a generation ago. For that matter, they were unthinkable when I began my career.

But they don’t change the fact that human error never goes away. All of us are susceptible to it, and all of us make mistakes.

Such is the way of medicine now, and likely always. All we can do is our best and keep moving forward.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

When I was a resident (back in the Cretaceous era), the idea of autoimmune encephalitis was just beginning to take hold. It was kind of like Bigfoot. A few reports, vague articles, the occasional sighting of what may or may not be a case. …

Unlike Bigfoot, however, the evidence quickly added up until there was no question that such a disorder existed. Then disorder became disorders, and now it seems a few more types are added to the list each year.

This doesn’t change the fact that they’re still, in the grand scheme of general neurology, relatively rare, though no one questions that they exist.

Today people still wishfully take pictures of Bigfoot, but they turn out to be images of bears or other animals, or tricks of light and shadow.

This is an issue with human thought. Many times we see what we want to see, especially if it’s more interesting than a mundane alternative.

An autoimmune encephalitis article in the January 2023 issue of JAMA Neurology looked into this. On reviewing 393 patients diagnosed with the disorder, the researchers found that 27% of them actually didn’t have it at all. Such things as functional disorders, neurodegenerative diseases, and primary psychiatric diagnoses were, instead, the culprits.

I’m not criticizing those who made an incorrect diagnosis. We all do. That’s the nature of medicine.

Which is worse? Missing the diagnosis entirely and not treating, or diagnosing a patient with something else and treating incorrectly? I guess it depends on the disease and nature of treatment.

Certainly, finding a case of autoimmune encephalitis is more interesting than, say toxic-metabolic encephalopathy from a bladder infection, just as getting a picture of Bigfoot is way more cool than one of a bear with mange.

But we need to be careful when faced with equivocal labs and data lest we read too much into them. There are too many gray zones in medicine to lead you astray. Not to say we won’t be. Even well-intentioned physicians (which I assume is pretty much all of us) are going to make mistakes.

But it’s not just rare diseases. In the early 1990s two different studies found that 24% of patients diagnosed with Parkinson’s disease were found to have something else on autopsy.

That was 30 years ago. Now we have DaT scans to help. Maybe our abilities as neurologists have also gotten better (though I don’t think the neurological exam has changed much since Charcot).

Our gadgets, labs, and treatments get better every year. We have tools available to us now that were unthinkable a generation ago. For that matter, they were unthinkable when I began my career.

But they don’t change the fact that human error never goes away. All of us are susceptible to it, and all of us make mistakes.

Such is the way of medicine now, and likely always. All we can do is our best and keep moving forward.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

When I was a resident (back in the Cretaceous era), the idea of autoimmune encephalitis was just beginning to take hold. It was kind of like Bigfoot. A few reports, vague articles, the occasional sighting of what may or may not be a case. …

Unlike Bigfoot, however, the evidence quickly added up until there was no question that such a disorder existed. Then disorder became disorders, and now it seems a few more types are added to the list each year.

This doesn’t change the fact that they’re still, in the grand scheme of general neurology, relatively rare, though no one questions that they exist.

Today people still wishfully take pictures of Bigfoot, but they turn out to be images of bears or other animals, or tricks of light and shadow.

This is an issue with human thought. Many times we see what we want to see, especially if it’s more interesting than a mundane alternative.

An autoimmune encephalitis article in the January 2023 issue of JAMA Neurology looked into this. On reviewing 393 patients diagnosed with the disorder, the researchers found that 27% of them actually didn’t have it at all. Such things as functional disorders, neurodegenerative diseases, and primary psychiatric diagnoses were, instead, the culprits.

I’m not criticizing those who made an incorrect diagnosis. We all do. That’s the nature of medicine.

Which is worse? Missing the diagnosis entirely and not treating, or diagnosing a patient with something else and treating incorrectly? I guess it depends on the disease and nature of treatment.

Certainly, finding a case of autoimmune encephalitis is more interesting than, say toxic-metabolic encephalopathy from a bladder infection, just as getting a picture of Bigfoot is way more cool than one of a bear with mange.

But we need to be careful when faced with equivocal labs and data lest we read too much into them. There are too many gray zones in medicine to lead you astray. Not to say we won’t be. Even well-intentioned physicians (which I assume is pretty much all of us) are going to make mistakes.

But it’s not just rare diseases. In the early 1990s two different studies found that 24% of patients diagnosed with Parkinson’s disease were found to have something else on autopsy.

That was 30 years ago. Now we have DaT scans to help. Maybe our abilities as neurologists have also gotten better (though I don’t think the neurological exam has changed much since Charcot).

Our gadgets, labs, and treatments get better every year. We have tools available to us now that were unthinkable a generation ago. For that matter, they were unthinkable when I began my career.

But they don’t change the fact that human error never goes away. All of us are susceptible to it, and all of us make mistakes.

Such is the way of medicine now, and likely always. All we can do is our best and keep moving forward.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

How effective are the COVID-19 vaccines, third time around? Researchers compared 2 large groups of veterans to find out how well a third dose protected against documented infection, symptomatic COVID-19, and COVID-19–related hospitalization, intensive care unit (ICU) admission, and death.

The research, published in Nature, used electronic health records of 65,196 veterans who received BNT162b2 (Pfizer-BioNTech) and 65,196 who received mRNA-1273 (Moderna). They chose to study the 16 weeks between October 20, 2021 and February 8, 2022, which included both Delta- and Omicron-variant waves.

During the follow-up (median, 77 days), 2994 COVID-19 infections were documented, of which 200 were detected as symptomatic, 194 required hospitalization, and 52 required ICU admission. Twenty-two patients died.

In a previous head-to-head trial comparing breakthrough COVID-19 outcomes after the first doses of the 2 vaccines (given when the Alpha and Delta variants were predominant), the researchers had found a low risk of documented infection and severe outcomes, but lower for the Moderna vaccine. They note that few head-to-head comparisons have been made of third-dose effectiveness.

As expected, in this trial, the researchers found a “nearly identical” pattern for the risk of the 2 vaccine groups. Although the risks for all of the measured outcomes over 16 weeks were low for both vaccines ≤ 4% for documented infection and < 0.03% for death in each group—those veterans who received the Pfizer-BioNTech vaccine had an excess of 45 documented infections and 11 hospitalizations per 10,000 persons, compared with the Moderna group.  The Pfizer-BioNTech group also had a higher risk of documented infection over 9 weeks of follow-up, during which an Omicron-variant predominated.

Given the high effectiveness of a third dose of both vaccines, either vaccine is strongly recommended, the researchers conclude. They point to “evidence of clear and comparable benefits” for the most severe outcomes: The difference in estimated 16-week risk of death between the 2 groups was two-thousandths of 1 %.

They add that, while the differences in estimated risk for less severe outcomes between the 2 groups were small on the absolute scale, they may be meaningful when considering the population scale at which these vaccines are deployed.

How effective are the COVID-19 vaccines, third time around? Researchers compared 2 large groups of veterans to find out how well a third dose protected against documented infection, symptomatic COVID-19, and COVID-19–related hospitalization, intensive care unit (ICU) admission, and death.

The research, published in Nature, used electronic health records of 65,196 veterans who received BNT162b2 (Pfizer-BioNTech) and 65,196 who received mRNA-1273 (Moderna). They chose to study the 16 weeks between October 20, 2021 and February 8, 2022, which included both Delta- and Omicron-variant waves.

During the follow-up (median, 77 days), 2994 COVID-19 infections were documented, of which 200 were detected as symptomatic, 194 required hospitalization, and 52 required ICU admission. Twenty-two patients died.

In a previous head-to-head trial comparing breakthrough COVID-19 outcomes after the first doses of the 2 vaccines (given when the Alpha and Delta variants were predominant), the researchers had found a low risk of documented infection and severe outcomes, but lower for the Moderna vaccine. They note that few head-to-head comparisons have been made of third-dose effectiveness.

As expected, in this trial, the researchers found a “nearly identical” pattern for the risk of the 2 vaccine groups. Although the risks for all of the measured outcomes over 16 weeks were low for both vaccines ≤ 4% for documented infection and < 0.03% for death in each group—those veterans who received the Pfizer-BioNTech vaccine had an excess of 45 documented infections and 11 hospitalizations per 10,000 persons, compared with the Moderna group.  The Pfizer-BioNTech group also had a higher risk of documented infection over 9 weeks of follow-up, during which an Omicron-variant predominated.

Given the high effectiveness of a third dose of both vaccines, either vaccine is strongly recommended, the researchers conclude. They point to “evidence of clear and comparable benefits” for the most severe outcomes: The difference in estimated 16-week risk of death between the 2 groups was two-thousandths of 1 %.

They add that, while the differences in estimated risk for less severe outcomes between the 2 groups were small on the absolute scale, they may be meaningful when considering the population scale at which these vaccines are deployed.

How effective are the COVID-19 vaccines, third time around? Researchers compared 2 large groups of veterans to find out how well a third dose protected against documented infection, symptomatic COVID-19, and COVID-19–related hospitalization, intensive care unit (ICU) admission, and death.

The research, published in Nature, used electronic health records of 65,196 veterans who received BNT162b2 (Pfizer-BioNTech) and 65,196 who received mRNA-1273 (Moderna). They chose to study the 16 weeks between October 20, 2021 and February 8, 2022, which included both Delta- and Omicron-variant waves.

During the follow-up (median, 77 days), 2994 COVID-19 infections were documented, of which 200 were detected as symptomatic, 194 required hospitalization, and 52 required ICU admission. Twenty-two patients died.

In a previous head-to-head trial comparing breakthrough COVID-19 outcomes after the first doses of the 2 vaccines (given when the Alpha and Delta variants were predominant), the researchers had found a low risk of documented infection and severe outcomes, but lower for the Moderna vaccine. They note that few head-to-head comparisons have been made of third-dose effectiveness.

As expected, in this trial, the researchers found a “nearly identical” pattern for the risk of the 2 vaccine groups. Although the risks for all of the measured outcomes over 16 weeks were low for both vaccines ≤ 4% for documented infection and < 0.03% for death in each group—those veterans who received the Pfizer-BioNTech vaccine had an excess of 45 documented infections and 11 hospitalizations per 10,000 persons, compared with the Moderna group.  The Pfizer-BioNTech group also had a higher risk of documented infection over 9 weeks of follow-up, during which an Omicron-variant predominated.

Given the high effectiveness of a third dose of both vaccines, either vaccine is strongly recommended, the researchers conclude. They point to “evidence of clear and comparable benefits” for the most severe outcomes: The difference in estimated 16-week risk of death between the 2 groups was two-thousandths of 1 %.

They add that, while the differences in estimated risk for less severe outcomes between the 2 groups were small on the absolute scale, they may be meaningful when considering the population scale at which these vaccines are deployed.

Every year, during the relatively slow winter-months period, I like to take a tour of my office from the paradigm of a patient visiting our facility for the first time. When was the last time you did a comprehensive inspection, looking for problems that your patients might see?

We tend not to notice gradual deterioration in the workplace we inhabit every day: Carpets fade and dull with constant traffic and cleaning; wallpaper and paint accumulate dirt, stains, and damage; furniture gets dirty and dented, fabric rips, hardware goes missing; laminate peels off the edges of desks and cabinets.

When did you last take a good look at your waiting room? How clean is it? Patients expect cleanliness in doctor’s offices, and they expect the reception area to be neat. How are the carpeting and upholstery holding up? Sit in your chairs; how do they feel? Patients don’t appreciate a sore back or bottom from any chairs, especially in a medical office. Consider investing in new furniture that will be attractive and comfortable for your patients.

Look at the decor itself; is it dated or just plain “old-looking?” Any interior designer will tell you they can determine quite accurately when a space was last decorated, simply by the color and style of the materials used. If your office is stuck in the ‘90s, it’s probably time for a change. Even if you don’t find anything obvious, it’s wise to check periodically for subtle evidence of age: Find some patches of protected carpeting and flooring under stationary furniture and compare them to exposed floors.

If your color scheme is hopelessly out of date and style, or if you are just tired of it, change it. Wallpaper and carpeting should be long-wearing industrial quality; paint should be high-quality “eggshell” finish to facilitate cleaning, and everything should be professionally applied. (This is neither the time nor place for do-it-yourself experiments.) Consider updating your overhead lighting. The harsh glow of fluorescent lights amid an uninspired decor creates a sterile, uninviting atmosphere.

During renovation, get your building’s maintenance crew to fix any nagging plumbing, electrical, or heating/air conditioning problems while pipes, ducts, and wires are more readily accessible. This is also a good time to clear out old textbooks, journals, and files that you will never open again, in this digital age.

If your wall decorations are dated and unattractive, now would be a good time to replace at least some of them. This need not be an expensive proposition; a few years ago, I redecorated my exam room walls with framed photos from my travel adventures – to very positive responses from patients and staff alike. If you’re not an artist or photographer, invite a family member, or local artists or talented patients, to display some of their creations on your walls. If you get too many contributions, you can rotate them on a periodic basis.

Plants are great aesthetic accents, yet many offices have little or no plant life. Plants naturally aerate an office suite and help make it feel less stuffy. Also, multiple studies have found that plants promote productivity among office staff and create a sense of calm for apprehensive patients. Improvements like this can make a big difference. They show an attention to detail and a willingness to make your practice as inviting as possible for patients and employees alike.

Spruce-up time is also an excellent opportunity to inventory your medical equipment. We’ve all seen “vintage” offices full of gadgets that were state-of-the-art decades ago. Nostalgia is nice; but would you want to be treated by a physician whose office could be a Smithsonian exhibit titled, “Doctor’s Office Circa 1975?” Neither would your patients, for the most part; many – particularly younger ones – assume that doctors who don’t keep up with technological innovations don’t keep up with anything else, either.

If you’re planning a vacation this year (and I hope you are), that would be the perfect time for a re-do. Your patients will be spared the dust and turmoil, tradespeople won’t have to work around your office hours, and you won’t have to cancel any hours that weren’t already canceled. Best of all, you’ll come back to a clean, fresh environment.

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

Every year, during the relatively slow winter-months period, I like to take a tour of my office from the paradigm of a patient visiting our facility for the first time. When was the last time you did a comprehensive inspection, looking for problems that your patients might see?

We tend not to notice gradual deterioration in the workplace we inhabit every day: Carpets fade and dull with constant traffic and cleaning; wallpaper and paint accumulate dirt, stains, and damage; furniture gets dirty and dented, fabric rips, hardware goes missing; laminate peels off the edges of desks and cabinets.

When did you last take a good look at your waiting room? How clean is it? Patients expect cleanliness in doctor’s offices, and they expect the reception area to be neat. How are the carpeting and upholstery holding up? Sit in your chairs; how do they feel? Patients don’t appreciate a sore back or bottom from any chairs, especially in a medical office. Consider investing in new furniture that will be attractive and comfortable for your patients.

Look at the decor itself; is it dated or just plain “old-looking?” Any interior designer will tell you they can determine quite accurately when a space was last decorated, simply by the color and style of the materials used. If your office is stuck in the ‘90s, it’s probably time for a change. Even if you don’t find anything obvious, it’s wise to check periodically for subtle evidence of age: Find some patches of protected carpeting and flooring under stationary furniture and compare them to exposed floors.

If your color scheme is hopelessly out of date and style, or if you are just tired of it, change it. Wallpaper and carpeting should be long-wearing industrial quality; paint should be high-quality “eggshell” finish to facilitate cleaning, and everything should be professionally applied. (This is neither the time nor place for do-it-yourself experiments.) Consider updating your overhead lighting. The harsh glow of fluorescent lights amid an uninspired decor creates a sterile, uninviting atmosphere.

During renovation, get your building’s maintenance crew to fix any nagging plumbing, electrical, or heating/air conditioning problems while pipes, ducts, and wires are more readily accessible. This is also a good time to clear out old textbooks, journals, and files that you will never open again, in this digital age.

If your wall decorations are dated and unattractive, now would be a good time to replace at least some of them. This need not be an expensive proposition; a few years ago, I redecorated my exam room walls with framed photos from my travel adventures – to very positive responses from patients and staff alike. If you’re not an artist or photographer, invite a family member, or local artists or talented patients, to display some of their creations on your walls. If you get too many contributions, you can rotate them on a periodic basis.

Plants are great aesthetic accents, yet many offices have little or no plant life. Plants naturally aerate an office suite and help make it feel less stuffy. Also, multiple studies have found that plants promote productivity among office staff and create a sense of calm for apprehensive patients. Improvements like this can make a big difference. They show an attention to detail and a willingness to make your practice as inviting as possible for patients and employees alike.

Spruce-up time is also an excellent opportunity to inventory your medical equipment. We’ve all seen “vintage” offices full of gadgets that were state-of-the-art decades ago. Nostalgia is nice; but would you want to be treated by a physician whose office could be a Smithsonian exhibit titled, “Doctor’s Office Circa 1975?” Neither would your patients, for the most part; many – particularly younger ones – assume that doctors who don’t keep up with technological innovations don’t keep up with anything else, either.

If you’re planning a vacation this year (and I hope you are), that would be the perfect time for a re-do. Your patients will be spared the dust and turmoil, tradespeople won’t have to work around your office hours, and you won’t have to cancel any hours that weren’t already canceled. Best of all, you’ll come back to a clean, fresh environment.

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

Every year, during the relatively slow winter-months period, I like to take a tour of my office from the paradigm of a patient visiting our facility for the first time. When was the last time you did a comprehensive inspection, looking for problems that your patients might see?

We tend not to notice gradual deterioration in the workplace we inhabit every day: Carpets fade and dull with constant traffic and cleaning; wallpaper and paint accumulate dirt, stains, and damage; furniture gets dirty and dented, fabric rips, hardware goes missing; laminate peels off the edges of desks and cabinets.

When did you last take a good look at your waiting room? How clean is it? Patients expect cleanliness in doctor’s offices, and they expect the reception area to be neat. How are the carpeting and upholstery holding up? Sit in your chairs; how do they feel? Patients don’t appreciate a sore back or bottom from any chairs, especially in a medical office. Consider investing in new furniture that will be attractive and comfortable for your patients.

Look at the decor itself; is it dated or just plain “old-looking?” Any interior designer will tell you they can determine quite accurately when a space was last decorated, simply by the color and style of the materials used. If your office is stuck in the ‘90s, it’s probably time for a change. Even if you don’t find anything obvious, it’s wise to check periodically for subtle evidence of age: Find some patches of protected carpeting and flooring under stationary furniture and compare them to exposed floors.

If your color scheme is hopelessly out of date and style, or if you are just tired of it, change it. Wallpaper and carpeting should be long-wearing industrial quality; paint should be high-quality “eggshell” finish to facilitate cleaning, and everything should be professionally applied. (This is neither the time nor place for do-it-yourself experiments.) Consider updating your overhead lighting. The harsh glow of fluorescent lights amid an uninspired decor creates a sterile, uninviting atmosphere.

During renovation, get your building’s maintenance crew to fix any nagging plumbing, electrical, or heating/air conditioning problems while pipes, ducts, and wires are more readily accessible. This is also a good time to clear out old textbooks, journals, and files that you will never open again, in this digital age.

If your wall decorations are dated and unattractive, now would be a good time to replace at least some of them. This need not be an expensive proposition; a few years ago, I redecorated my exam room walls with framed photos from my travel adventures – to very positive responses from patients and staff alike. If you’re not an artist or photographer, invite a family member, or local artists or talented patients, to display some of their creations on your walls. If you get too many contributions, you can rotate them on a periodic basis.

Plants are great aesthetic accents, yet many offices have little or no plant life. Plants naturally aerate an office suite and help make it feel less stuffy. Also, multiple studies have found that plants promote productivity among office staff and create a sense of calm for apprehensive patients. Improvements like this can make a big difference. They show an attention to detail and a willingness to make your practice as inviting as possible for patients and employees alike.

Spruce-up time is also an excellent opportunity to inventory your medical equipment. We’ve all seen “vintage” offices full of gadgets that were state-of-the-art decades ago. Nostalgia is nice; but would you want to be treated by a physician whose office could be a Smithsonian exhibit titled, “Doctor’s Office Circa 1975?” Neither would your patients, for the most part; many – particularly younger ones – assume that doctors who don’t keep up with technological innovations don’t keep up with anything else, either.

If you’re planning a vacation this year (and I hope you are), that would be the perfect time for a re-do. Your patients will be spared the dust and turmoil, tradespeople won’t have to work around your office hours, and you won’t have to cancel any hours that weren’t already canceled. Best of all, you’ll come back to a clean, fresh environment.

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

Black veterans are less likely to have their benefits claims processed and paid than are their White peers because of systemic problems within the US Department of Veterans Affairs, according to a lawsuit filed against the agency.

“A Black veteran who served honorably can walk into the VA, file a disability claim, and be at a significantly higher likelihood of having that claim denied,” said Adam Henderson, a student working with the Yale Law School Veterans Legal Services Clinic, one of several groups connected to the lawsuit.

“The VA has denied countless meritorious applications of Black veterans and thus deprived them and their families of the support that they are entitled to.”

The suit, filed in federal court by the clinic on behalf of Vietnam War veteran Conley Monk Jr., asks for “redress for the harms caused by the failure of VA staff and leaders to administer these benefits programs in a manner free from racial discrimination against Black veterans.”

In a press conference announcing the lawsuit, the effort received backing from Sen. Richard Blumenthal (D, Connecticut) who called it an “unacceptable” situation.

“Black veterans are denied benefits at a very significantly disproportionate rate,” he said. “We know the results. We want to know the reason why.”

The suit stems from an analysis of VA claims records released by the department following an earlier legal action. Between 2001 and 2020, the average denial rate for disability claims filed for Black veterans was 29.5%, significantly above the 24.2% for White veterans.

Attorneys allege the problems date back even further and that VA officials should have known about the racial disparities in the system from previous complaints.

“The negligence of VA leadership, and their failure to train, supervise, monitor and instruct agency officials to take steps to identify and correct racial disparities, led to systematic benefits obstruction for Black veterans,” the suit states.

Monk is a Black disabled Marine Corps veteran who previously sued the military to overturn his less-than-honorable military discharge due to complications from undiagnosed posttraumatic stress disorder.

He was subsequently granted access to a host of veterans benefits but not to retroactive payouts for claims he was denied in the 1970s.

“They didn’t fully compensate me or my family,” he said. “I wasn’t able to give my kids my educational benefits. We should have been receiving checks while they were growing up.”

Along with potential past benefits for Monk, individuals involved with the lawsuit said the move could force the VA to reassess thousands of other unfairly dismissed cases. “For decades [the US government] has allowed racially discriminatory practices to obstruct Black veterans from easily accessing veterans housing, education, and health care benefits with wide-reaching economic consequences for Black veterans and their families,” said Richard Brookshire, executive director of the Black Veterans Project.

“This lawsuit reckons with the shameful history of racism by the Department of Veteran Affairs and seeks to redress long-standing improprieties reverberating across generations of Black military service.”

In a statement, VA press secretary Terrence Hayes did not directly respond to the lawsuit but noted that “throughout history, there have been unacceptable disparities in both VA benefits decisions and military discharge status due to racism, which have wrongly left Black veterans without access to VA care and benefits.”

“We are actively working to right these wrongs, and we will stop at nothing to ensure that all Black veterans get the VA services they have earned and deserve,” he said. “We are currently studying racial disparities in benefits claims decisions, and we will publish the results of that study as soon as they are available.”

Hayes said the department has already begun targeted outreach to Black veterans to help them with claims and is “taking steps to ensure that our claims process combats institutional racism, rather than perpetuating it.”

Black veterans are less likely to have their benefits claims processed and paid than are their White peers because of systemic problems within the US Department of Veterans Affairs, according to a lawsuit filed against the agency.

“A Black veteran who served honorably can walk into the VA, file a disability claim, and be at a significantly higher likelihood of having that claim denied,” said Adam Henderson, a student working with the Yale Law School Veterans Legal Services Clinic, one of several groups connected to the lawsuit.

“The VA has denied countless meritorious applications of Black veterans and thus deprived them and their families of the support that they are entitled to.”

The suit, filed in federal court by the clinic on behalf of Vietnam War veteran Conley Monk Jr., asks for “redress for the harms caused by the failure of VA staff and leaders to administer these benefits programs in a manner free from racial discrimination against Black veterans.”

In a press conference announcing the lawsuit, the effort received backing from Sen. Richard Blumenthal (D, Connecticut) who called it an “unacceptable” situation.

“Black veterans are denied benefits at a very significantly disproportionate rate,” he said. “We know the results. We want to know the reason why.”

The suit stems from an analysis of VA claims records released by the department following an earlier legal action. Between 2001 and 2020, the average denial rate for disability claims filed for Black veterans was 29.5%, significantly above the 24.2% for White veterans.

Attorneys allege the problems date back even further and that VA officials should have known about the racial disparities in the system from previous complaints.

“The negligence of VA leadership, and their failure to train, supervise, monitor and instruct agency officials to take steps to identify and correct racial disparities, led to systematic benefits obstruction for Black veterans,” the suit states.

Monk is a Black disabled Marine Corps veteran who previously sued the military to overturn his less-than-honorable military discharge due to complications from undiagnosed posttraumatic stress disorder.

He was subsequently granted access to a host of veterans benefits but not to retroactive payouts for claims he was denied in the 1970s.

“They didn’t fully compensate me or my family,” he said. “I wasn’t able to give my kids my educational benefits. We should have been receiving checks while they were growing up.”

Along with potential past benefits for Monk, individuals involved with the lawsuit said the move could force the VA to reassess thousands of other unfairly dismissed cases. “For decades [the US government] has allowed racially discriminatory practices to obstruct Black veterans from easily accessing veterans housing, education, and health care benefits with wide-reaching economic consequences for Black veterans and their families,” said Richard Brookshire, executive director of the Black Veterans Project.

“This lawsuit reckons with the shameful history of racism by the Department of Veteran Affairs and seeks to redress long-standing improprieties reverberating across generations of Black military service.”

In a statement, VA press secretary Terrence Hayes did not directly respond to the lawsuit but noted that “throughout history, there have been unacceptable disparities in both VA benefits decisions and military discharge status due to racism, which have wrongly left Black veterans without access to VA care and benefits.”

“We are actively working to right these wrongs, and we will stop at nothing to ensure that all Black veterans get the VA services they have earned and deserve,” he said. “We are currently studying racial disparities in benefits claims decisions, and we will publish the results of that study as soon as they are available.”

Hayes said the department has already begun targeted outreach to Black veterans to help them with claims and is “taking steps to ensure that our claims process combats institutional racism, rather than perpetuating it.”

Black veterans are less likely to have their benefits claims processed and paid than are their White peers because of systemic problems within the US Department of Veterans Affairs, according to a lawsuit filed against the agency.

“A Black veteran who served honorably can walk into the VA, file a disability claim, and be at a significantly higher likelihood of having that claim denied,” said Adam Henderson, a student working with the Yale Law School Veterans Legal Services Clinic, one of several groups connected to the lawsuit.

“The VA has denied countless meritorious applications of Black veterans and thus deprived them and their families of the support that they are entitled to.”

The suit, filed in federal court by the clinic on behalf of Vietnam War veteran Conley Monk Jr., asks for “redress for the harms caused by the failure of VA staff and leaders to administer these benefits programs in a manner free from racial discrimination against Black veterans.”

In a press conference announcing the lawsuit, the effort received backing from Sen. Richard Blumenthal (D, Connecticut) who called it an “unacceptable” situation.

“Black veterans are denied benefits at a very significantly disproportionate rate,” he said. “We know the results. We want to know the reason why.”

The suit stems from an analysis of VA claims records released by the department following an earlier legal action. Between 2001 and 2020, the average denial rate for disability claims filed for Black veterans was 29.5%, significantly above the 24.2% for White veterans.

Attorneys allege the problems date back even further and that VA officials should have known about the racial disparities in the system from previous complaints.

“The negligence of VA leadership, and their failure to train, supervise, monitor and instruct agency officials to take steps to identify and correct racial disparities, led to systematic benefits obstruction for Black veterans,” the suit states.

Monk is a Black disabled Marine Corps veteran who previously sued the military to overturn his less-than-honorable military discharge due to complications from undiagnosed posttraumatic stress disorder.

He was subsequently granted access to a host of veterans benefits but not to retroactive payouts for claims he was denied in the 1970s.

“They didn’t fully compensate me or my family,” he said. “I wasn’t able to give my kids my educational benefits. We should have been receiving checks while they were growing up.”

Along with potential past benefits for Monk, individuals involved with the lawsuit said the move could force the VA to reassess thousands of other unfairly dismissed cases. “For decades [the US government] has allowed racially discriminatory practices to obstruct Black veterans from easily accessing veterans housing, education, and health care benefits with wide-reaching economic consequences for Black veterans and their families,” said Richard Brookshire, executive director of the Black Veterans Project.

“This lawsuit reckons with the shameful history of racism by the Department of Veteran Affairs and seeks to redress long-standing improprieties reverberating across generations of Black military service.”

In a statement, VA press secretary Terrence Hayes did not directly respond to the lawsuit but noted that “throughout history, there have been unacceptable disparities in both VA benefits decisions and military discharge status due to racism, which have wrongly left Black veterans without access to VA care and benefits.”

“We are actively working to right these wrongs, and we will stop at nothing to ensure that all Black veterans get the VA services they have earned and deserve,” he said. “We are currently studying racial disparities in benefits claims decisions, and we will publish the results of that study as soon as they are available.”

Hayes said the department has already begun targeted outreach to Black veterans to help them with claims and is “taking steps to ensure that our claims process combats institutional racism, rather than perpetuating it.”

Metformin failure in people with type 2 diabetes is very common, particularly among those with high hemoglobin A1c levels at the time of diagnosis, new findings suggest.

An analysis of electronic health record data for more than 22,000 patients starting metformin at three U.S. clinical sites found that over 40% experienced metformin failure.

This was defined as either failure to achieve or maintain A1c less than 7% within 18 months or the use of additional glucose-lowering medications.

Other predictors that metformin use wouldn’t be successful included increasing age, male sex, and race/ethnicity. However, the latter ceased to be linked after adjustment for other clinical risk factors.

“Our study results suggest increased monitoring with potentially earlier treatment intensification to achieve glycemic control may be appropriate in patients with clinical parameters described in this paper,” Suzette J. Bielinski, PhD, and colleagues wrote.

“Further, these results call into question the ubiquitous use of metformin as the first-line therapy and suggest a more individualized approach may be needed to optimize therapy,” they added in their article, published online in the Journal of Clinical Endocrinology and Metabolism.

The study is also noteworthy in that it demonstrated the feasibility of using EHR data with a machine-learning approach to discover risk biomarkers, Dr. Bielinski, professor of epidemiology at the Mayo Clinic, Rochester, Minn., said in an interview.

“We wanted to repurpose clinical data to answer questions ... I think more studies using these types of techniques repurposing data meant for one thing could potentially impact care in other domains. ... If we can get the bang for the buck from all these data that we generate on people I just think it will improve health care and maybe save health care dollars.”
 

Baseline A1c strongest predictor of metformin failure

The investigators identified a total of 22,047 metformin initiators from three clinical primary care sites: the University of Mississippi’s Jackson centers, which serves a mostly African American population, the Mountain Park Health Center in Arizona, a seven-clinic federally qualified community health center in Phoenix that serves a mostly Latino population, and the Rochester Epidemiology Project, which includes the Mayo Clinic and serves a primarily White population.  

Overall, a total of 43% (9,407) of patients met one of two criteria for metformin failure by 18 months. Among those, median time to failure on metformin was 3.9 months.

Unadjusted failure rates were higher among African Americans, Hispanics, and other racial groups, compared with non-Hispanic White patients.

However, the racial groups also differed by baseline characteristics. Mean A1c was 7.7% overall, 8.1% for the African American group, 7.9% for Asians, and 8.2% for Hispanics, compared with 7.6% for non-Hispanic Whites.

Of 150 clinical factors examined, higher A1c was the strongest predictor of metformin failure, with a rapid increase in risk appearing between 7.5% and 8.0%.

“The slope is steep. It gives us some clinical guidance,” Dr. Bielinski said.

Other variables positively correlated with metformin failure included “diabetes with complications,” increased age, and higher levels of potassium, triglycerides, heart rate, and mean cell hemoglobin.

Factors inversely correlated with metformin failure were having received screening for other suspected conditions and medical examination/evaluation, and lower levels of sodium, albumin, and HDL cholesterol.  

Three variables – body mass index, LDL cholesterol, and creatinine – had a U-shaped relationship with metformin failure, so that both high and low values were associated with increased risk.

“The racial/ethnic differences disappeared once other clinical factors were considered suggesting that the biological response to metformin is similar regardless of race/ethnicity,” Dr. Bielinski and colleagues wrote.

They also noted that the abnormal lab results which correlated with metformin failure “likely represent biomarkers for chronic illnesses. However, the effect size for lab abnormalities was small compared with that of baseline A1c.”

Dr. Bielinski urged caution in interpreting the findings. “Electronic health records data have limitations. We have evidence that these people were prescribed metformin. We have no idea if they took it. ... I would really be hesitant to be too strong in making clinical recommendations.”

However, she said that the data are “suggestive to say maybe we need to have some kind of threshold where if someone comes in with an A1c of X that they go on dual therapy right away. I think this is opening the door to that.” 

The authors reported no relevant financial relationships.

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

Metformin failure in people with type 2 diabetes is very common, particularly among those with high hemoglobin A1c levels at the time of diagnosis, new findings suggest.

An analysis of electronic health record data for more than 22,000 patients starting metformin at three U.S. clinical sites found that over 40% experienced metformin failure.

This was defined as either failure to achieve or maintain A1c less than 7% within 18 months or the use of additional glucose-lowering medications.

Other predictors that metformin use wouldn’t be successful included increasing age, male sex, and race/ethnicity. However, the latter ceased to be linked after adjustment for other clinical risk factors.

“Our study results suggest increased monitoring with potentially earlier treatment intensification to achieve glycemic control may be appropriate in patients with clinical parameters described in this paper,” Suzette J. Bielinski, PhD, and colleagues wrote.

“Further, these results call into question the ubiquitous use of metformin as the first-line therapy and suggest a more individualized approach may be needed to optimize therapy,” they added in their article, published online in the Journal of Clinical Endocrinology and Metabolism.

The study is also noteworthy in that it demonstrated the feasibility of using EHR data with a machine-learning approach to discover risk biomarkers, Dr. Bielinski, professor of epidemiology at the Mayo Clinic, Rochester, Minn., said in an interview.

“We wanted to repurpose clinical data to answer questions ... I think more studies using these types of techniques repurposing data meant for one thing could potentially impact care in other domains. ... If we can get the bang for the buck from all these data that we generate on people I just think it will improve health care and maybe save health care dollars.”
 

Baseline A1c strongest predictor of metformin failure

The investigators identified a total of 22,047 metformin initiators from three clinical primary care sites: the University of Mississippi’s Jackson centers, which serves a mostly African American population, the Mountain Park Health Center in Arizona, a seven-clinic federally qualified community health center in Phoenix that serves a mostly Latino population, and the Rochester Epidemiology Project, which includes the Mayo Clinic and serves a primarily White population.  

Overall, a total of 43% (9,407) of patients met one of two criteria for metformin failure by 18 months. Among those, median time to failure on metformin was 3.9 months.

Unadjusted failure rates were higher among African Americans, Hispanics, and other racial groups, compared with non-Hispanic White patients.

However, the racial groups also differed by baseline characteristics. Mean A1c was 7.7% overall, 8.1% for the African American group, 7.9% for Asians, and 8.2% for Hispanics, compared with 7.6% for non-Hispanic Whites.

Of 150 clinical factors examined, higher A1c was the strongest predictor of metformin failure, with a rapid increase in risk appearing between 7.5% and 8.0%.

“The slope is steep. It gives us some clinical guidance,” Dr. Bielinski said.

Other variables positively correlated with metformin failure included “diabetes with complications,” increased age, and higher levels of potassium, triglycerides, heart rate, and mean cell hemoglobin.

Factors inversely correlated with metformin failure were having received screening for other suspected conditions and medical examination/evaluation, and lower levels of sodium, albumin, and HDL cholesterol.  

Three variables – body mass index, LDL cholesterol, and creatinine – had a U-shaped relationship with metformin failure, so that both high and low values were associated with increased risk.

“The racial/ethnic differences disappeared once other clinical factors were considered suggesting that the biological response to metformin is similar regardless of race/ethnicity,” Dr. Bielinski and colleagues wrote.

They also noted that the abnormal lab results which correlated with metformin failure “likely represent biomarkers for chronic illnesses. However, the effect size for lab abnormalities was small compared with that of baseline A1c.”

Dr. Bielinski urged caution in interpreting the findings. “Electronic health records data have limitations. We have evidence that these people were prescribed metformin. We have no idea if they took it. ... I would really be hesitant to be too strong in making clinical recommendations.”

However, she said that the data are “suggestive to say maybe we need to have some kind of threshold where if someone comes in with an A1c of X that they go on dual therapy right away. I think this is opening the door to that.” 

The authors reported no relevant financial relationships.

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

Metformin failure in people with type 2 diabetes is very common, particularly among those with high hemoglobin A1c levels at the time of diagnosis, new findings suggest.

An analysis of electronic health record data for more than 22,000 patients starting metformin at three U.S. clinical sites found that over 40% experienced metformin failure.

This was defined as either failure to achieve or maintain A1c less than 7% within 18 months or the use of additional glucose-lowering medications.

Other predictors that metformin use wouldn’t be successful included increasing age, male sex, and race/ethnicity. However, the latter ceased to be linked after adjustment for other clinical risk factors.

“Our study results suggest increased monitoring with potentially earlier treatment intensification to achieve glycemic control may be appropriate in patients with clinical parameters described in this paper,” Suzette J. Bielinski, PhD, and colleagues wrote.

“Further, these results call into question the ubiquitous use of metformin as the first-line therapy and suggest a more individualized approach may be needed to optimize therapy,” they added in their article, published online in the Journal of Clinical Endocrinology and Metabolism.

The study is also noteworthy in that it demonstrated the feasibility of using EHR data with a machine-learning approach to discover risk biomarkers, Dr. Bielinski, professor of epidemiology at the Mayo Clinic, Rochester, Minn., said in an interview.

“We wanted to repurpose clinical data to answer questions ... I think more studies using these types of techniques repurposing data meant for one thing could potentially impact care in other domains. ... If we can get the bang for the buck from all these data that we generate on people I just think it will improve health care and maybe save health care dollars.”
 

Baseline A1c strongest predictor of metformin failure

The investigators identified a total of 22,047 metformin initiators from three clinical primary care sites: the University of Mississippi’s Jackson centers, which serves a mostly African American population, the Mountain Park Health Center in Arizona, a seven-clinic federally qualified community health center in Phoenix that serves a mostly Latino population, and the Rochester Epidemiology Project, which includes the Mayo Clinic and serves a primarily White population.  

Overall, a total of 43% (9,407) of patients met one of two criteria for metformin failure by 18 months. Among those, median time to failure on metformin was 3.9 months.

Unadjusted failure rates were higher among African Americans, Hispanics, and other racial groups, compared with non-Hispanic White patients.

However, the racial groups also differed by baseline characteristics. Mean A1c was 7.7% overall, 8.1% for the African American group, 7.9% for Asians, and 8.2% for Hispanics, compared with 7.6% for non-Hispanic Whites.

Of 150 clinical factors examined, higher A1c was the strongest predictor of metformin failure, with a rapid increase in risk appearing between 7.5% and 8.0%.

“The slope is steep. It gives us some clinical guidance,” Dr. Bielinski said.

Other variables positively correlated with metformin failure included “diabetes with complications,” increased age, and higher levels of potassium, triglycerides, heart rate, and mean cell hemoglobin.

Factors inversely correlated with metformin failure were having received screening for other suspected conditions and medical examination/evaluation, and lower levels of sodium, albumin, and HDL cholesterol.  

Three variables – body mass index, LDL cholesterol, and creatinine – had a U-shaped relationship with metformin failure, so that both high and low values were associated with increased risk.

“The racial/ethnic differences disappeared once other clinical factors were considered suggesting that the biological response to metformin is similar regardless of race/ethnicity,” Dr. Bielinski and colleagues wrote.

They also noted that the abnormal lab results which correlated with metformin failure “likely represent biomarkers for chronic illnesses. However, the effect size for lab abnormalities was small compared with that of baseline A1c.”

Dr. Bielinski urged caution in interpreting the findings. “Electronic health records data have limitations. We have evidence that these people were prescribed metformin. We have no idea if they took it. ... I would really be hesitant to be too strong in making clinical recommendations.”

However, she said that the data are “suggestive to say maybe we need to have some kind of threshold where if someone comes in with an A1c of X that they go on dual therapy right away. I think this is opening the door to that.” 

The authors reported no relevant financial relationships.

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

Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.

“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.

The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
 

Pathology despite function

“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.

He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.

In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.

“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
 

New entity necessary?

Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.

One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.

“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.

Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.

The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.

For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”

“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.

“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.

Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.

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

Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.

“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.

The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
 

Pathology despite function

“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.

He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.

In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.

“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
 

New entity necessary?

Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.

One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.

“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.

Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.

The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.

For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”

“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.

“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.

Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.

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

Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.

“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.

The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
 

Pathology despite function

“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.

He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.

In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.

“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
 

New entity necessary?

Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.

One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.

“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.

Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.

The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.

For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”

“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.

“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.

Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.

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