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CHICAGO – An investigational aldosterone synthase inhibitor could be an effective new treatment to reduce blood pressure in patients with treatment-resistant hypertension, reslts of a phase 2 study suggest.
The BrigHTN trial showed systolic blood pressure fell by an average of 20.3 mm Hg, 17.5 mm Hg, and 12.1 mm Hg with baxdrostat 2 mg, 1 mg, and 0.5 mg after 12 weeks follow-up in 248 patients unable to achieve target blood pressure on stable doses of at least three antihypertensive agents, including a diuretic.
After adjustment for the –9.4 mm Hg change observed in the placebo group, there was a statistically significant difference of 11.0 mm Hg in the 2-mg baxdrostat group (P = .0001) and of 8.1 mm Hg in the 1-mg baxdrostat group (P = .003).
The adjusted change in diastolic blood pressure was significant only for the 2-mg dose (–5.2 mm Hg; P = .004).
Once-daily oral baxdrostat had an acceptable side-effect profile and no patients died.
The study, which was stopped early after meeting criteria for overwhelming efficacy, was presented in the final late-breaking science session at the American Heart Association scientific sessions and published simultaneously in the New England Journal of Medicine.
Threading the needle
For at least 20 years, researchers have tried to create a drug that would lower aldosterone levels directly by inhibiting hormone synthesis rather than blocking the mineralocorticoid receptor.
What’s made this extraordinarily difficult is that the enzyme that makes aldosterone synthase and the enzyme required for cortisol synthase, 11-beta-hydroxylase, are 93% sequence similar. Baxdrostat, however, is able to selectively block aldosterone synthase, and thus the production of aldosterone, without also blocking the production of cortisol, explained Mason W. Freeman, MD, lead author of the study and executive vice president of clinical development at CinCor Pharma, which is developing the agent.
“We have beautiful biomarker evidence of not only blood pressure lowering but the mechanism by which that blood pressure reduction is occurring,” he said.
Over 12 weeks of follow-up in the new study, the use of baxdrostat led to decreases in serum aldosterone levels ranging from 3.0 ng/dL with the 0.5-mg dose to 4.9 ng/dL with the 2-mg dose. The 24-hour urinary aldosterone levels decreased with all three doses tested.
Baxdrostat increased plasma renin activity by 3.6, 5.0, and 13.8 mg/mL per hr with the 0.5, 1.0, and 2.0 mg doses, respectively, an indicator of its effect on lowering salt and fluid retention, Dr. Freeman said. Serum cortisol levels were not reduced in any of the baxdrostat groups throughout the study.
‘A bright future’
“It seems to have a bright future in the area of resistant hypertension, particularly in patients who are producing too much aldosterone,” said Suzanne Oparil, MD, invited discussant for the study and director of the Vascular Biology and Hypertension program at the University of Alabama at Birmingham.
She noted that aldosterone is a major contributor to the pathogenesis of resistant hypertension, which afflicts about 20% of the hypertensive population. Aldosterone antagonists are considered by many to be the best add-on treatment for resistant hypertension and do lower blood pressure.
“But they have major problems,” Dr. Oparil added. “Spironolactone, for example, causes hyperkalemia in many patients and adverse effects such as gynecomastia, erectile dysfunction, and feminization.”
Baxdrostat was well tolerated with no serious adverse events deemed related to treatment, Dr. Freeman reported. A total of 18 serious adverse events occurred in 10 patients, 6 of which were in a patient with urosepsis.
Ten adverse events of special interest occurred in eight patients, including one case of hypotension, three cases of hyponatremia, and six cases of hyperkalemia.
Potassium levels ranged from 6.0 to 6.3 mmol/L (6.0-6.3 mEq/L) in three patients and between 5.5 and 5.9 mmol/L (5.5-5.9 mEq/L) on at least two consecutive occasions in three others. Four of the patients were able to resume baxdrostat and complete the trial, whereas two patients discontinued treatment, one of whom was the patient with urosepsis.
Dr. Freeman pointed out that the study population was relatively diverse, with 33%-48% of participants of Hispanic or Latinx ethnicity and 23%-32% being Black.
At baseline, all patients had a seated blood pressure of at least 130/80 mm Hg (average 147.8/87.9 mm Hg) on a background therapy that included a diuretic in 100%, an agent targeting the renin-angiotensin-aldosterone system in 91%-96%, a beta-blocker in 52%-68%, and a calcium channel blocker in 64%-70%.
The study was not designed to test the benefits and risks of aldosterone synthase inhibition beyond 12 weeks and baxdrostat was not compared to alternative antihypertensives, he said. Additional limitations are that medication adherence was based on pill counts rather than drug analysis and enrolling only patients with an estimated glomerular filtration rate over 45 mL/min per 1.73m2 reduced the likelihood of hyperkalemia and other adverse events.
Nevertheless, “we think that these data suggest that baxdrostat has the potential to treat disorders associated with aldosterone excess, including hypertension and primary hyperaldosteronism,” Dr. Freeman said.
The intention is to carry the drug forward into additional phase 2 studies in chronic kidney disease and to begin a phase 3 study in hypertension in 2023, he noted.
The study was funded by CinCor Pharma. Dr. Freeman and three coauthors are employees of CinCor and receive stock-based compensation. The remaining authors have a financial relationship with CinRx Pharma, which has an equity stake in CinCor. Dr. Oparil reports grant/research support from Bayer, Higi, and Novartis; and serving on the scientific advisory board/expert committee for CinCor Pharma and Preventric Diagnostics.
A version of this article first appeared on Medscape.com.
CHICAGO – An investigational aldosterone synthase inhibitor could be an effective new treatment to reduce blood pressure in patients with treatment-resistant hypertension, reslts of a phase 2 study suggest.
The BrigHTN trial showed systolic blood pressure fell by an average of 20.3 mm Hg, 17.5 mm Hg, and 12.1 mm Hg with baxdrostat 2 mg, 1 mg, and 0.5 mg after 12 weeks follow-up in 248 patients unable to achieve target blood pressure on stable doses of at least three antihypertensive agents, including a diuretic.
After adjustment for the –9.4 mm Hg change observed in the placebo group, there was a statistically significant difference of 11.0 mm Hg in the 2-mg baxdrostat group (P = .0001) and of 8.1 mm Hg in the 1-mg baxdrostat group (P = .003).
The adjusted change in diastolic blood pressure was significant only for the 2-mg dose (–5.2 mm Hg; P = .004).
Once-daily oral baxdrostat had an acceptable side-effect profile and no patients died.
The study, which was stopped early after meeting criteria for overwhelming efficacy, was presented in the final late-breaking science session at the American Heart Association scientific sessions and published simultaneously in the New England Journal of Medicine.
Threading the needle
For at least 20 years, researchers have tried to create a drug that would lower aldosterone levels directly by inhibiting hormone synthesis rather than blocking the mineralocorticoid receptor.
What’s made this extraordinarily difficult is that the enzyme that makes aldosterone synthase and the enzyme required for cortisol synthase, 11-beta-hydroxylase, are 93% sequence similar. Baxdrostat, however, is able to selectively block aldosterone synthase, and thus the production of aldosterone, without also blocking the production of cortisol, explained Mason W. Freeman, MD, lead author of the study and executive vice president of clinical development at CinCor Pharma, which is developing the agent.
“We have beautiful biomarker evidence of not only blood pressure lowering but the mechanism by which that blood pressure reduction is occurring,” he said.
Over 12 weeks of follow-up in the new study, the use of baxdrostat led to decreases in serum aldosterone levels ranging from 3.0 ng/dL with the 0.5-mg dose to 4.9 ng/dL with the 2-mg dose. The 24-hour urinary aldosterone levels decreased with all three doses tested.
Baxdrostat increased plasma renin activity by 3.6, 5.0, and 13.8 mg/mL per hr with the 0.5, 1.0, and 2.0 mg doses, respectively, an indicator of its effect on lowering salt and fluid retention, Dr. Freeman said. Serum cortisol levels were not reduced in any of the baxdrostat groups throughout the study.
‘A bright future’
“It seems to have a bright future in the area of resistant hypertension, particularly in patients who are producing too much aldosterone,” said Suzanne Oparil, MD, invited discussant for the study and director of the Vascular Biology and Hypertension program at the University of Alabama at Birmingham.
She noted that aldosterone is a major contributor to the pathogenesis of resistant hypertension, which afflicts about 20% of the hypertensive population. Aldosterone antagonists are considered by many to be the best add-on treatment for resistant hypertension and do lower blood pressure.
“But they have major problems,” Dr. Oparil added. “Spironolactone, for example, causes hyperkalemia in many patients and adverse effects such as gynecomastia, erectile dysfunction, and feminization.”
Baxdrostat was well tolerated with no serious adverse events deemed related to treatment, Dr. Freeman reported. A total of 18 serious adverse events occurred in 10 patients, 6 of which were in a patient with urosepsis.
Ten adverse events of special interest occurred in eight patients, including one case of hypotension, three cases of hyponatremia, and six cases of hyperkalemia.
Potassium levels ranged from 6.0 to 6.3 mmol/L (6.0-6.3 mEq/L) in three patients and between 5.5 and 5.9 mmol/L (5.5-5.9 mEq/L) on at least two consecutive occasions in three others. Four of the patients were able to resume baxdrostat and complete the trial, whereas two patients discontinued treatment, one of whom was the patient with urosepsis.
Dr. Freeman pointed out that the study population was relatively diverse, with 33%-48% of participants of Hispanic or Latinx ethnicity and 23%-32% being Black.
At baseline, all patients had a seated blood pressure of at least 130/80 mm Hg (average 147.8/87.9 mm Hg) on a background therapy that included a diuretic in 100%, an agent targeting the renin-angiotensin-aldosterone system in 91%-96%, a beta-blocker in 52%-68%, and a calcium channel blocker in 64%-70%.
The study was not designed to test the benefits and risks of aldosterone synthase inhibition beyond 12 weeks and baxdrostat was not compared to alternative antihypertensives, he said. Additional limitations are that medication adherence was based on pill counts rather than drug analysis and enrolling only patients with an estimated glomerular filtration rate over 45 mL/min per 1.73m2 reduced the likelihood of hyperkalemia and other adverse events.
Nevertheless, “we think that these data suggest that baxdrostat has the potential to treat disorders associated with aldosterone excess, including hypertension and primary hyperaldosteronism,” Dr. Freeman said.
The intention is to carry the drug forward into additional phase 2 studies in chronic kidney disease and to begin a phase 3 study in hypertension in 2023, he noted.
The study was funded by CinCor Pharma. Dr. Freeman and three coauthors are employees of CinCor and receive stock-based compensation. The remaining authors have a financial relationship with CinRx Pharma, which has an equity stake in CinCor. Dr. Oparil reports grant/research support from Bayer, Higi, and Novartis; and serving on the scientific advisory board/expert committee for CinCor Pharma and Preventric Diagnostics.
A version of this article first appeared on Medscape.com.
CHICAGO – An investigational aldosterone synthase inhibitor could be an effective new treatment to reduce blood pressure in patients with treatment-resistant hypertension, reslts of a phase 2 study suggest.
The BrigHTN trial showed systolic blood pressure fell by an average of 20.3 mm Hg, 17.5 mm Hg, and 12.1 mm Hg with baxdrostat 2 mg, 1 mg, and 0.5 mg after 12 weeks follow-up in 248 patients unable to achieve target blood pressure on stable doses of at least three antihypertensive agents, including a diuretic.
After adjustment for the –9.4 mm Hg change observed in the placebo group, there was a statistically significant difference of 11.0 mm Hg in the 2-mg baxdrostat group (P = .0001) and of 8.1 mm Hg in the 1-mg baxdrostat group (P = .003).
The adjusted change in diastolic blood pressure was significant only for the 2-mg dose (–5.2 mm Hg; P = .004).
Once-daily oral baxdrostat had an acceptable side-effect profile and no patients died.
The study, which was stopped early after meeting criteria for overwhelming efficacy, was presented in the final late-breaking science session at the American Heart Association scientific sessions and published simultaneously in the New England Journal of Medicine.
Threading the needle
For at least 20 years, researchers have tried to create a drug that would lower aldosterone levels directly by inhibiting hormone synthesis rather than blocking the mineralocorticoid receptor.
What’s made this extraordinarily difficult is that the enzyme that makes aldosterone synthase and the enzyme required for cortisol synthase, 11-beta-hydroxylase, are 93% sequence similar. Baxdrostat, however, is able to selectively block aldosterone synthase, and thus the production of aldosterone, without also blocking the production of cortisol, explained Mason W. Freeman, MD, lead author of the study and executive vice president of clinical development at CinCor Pharma, which is developing the agent.
“We have beautiful biomarker evidence of not only blood pressure lowering but the mechanism by which that blood pressure reduction is occurring,” he said.
Over 12 weeks of follow-up in the new study, the use of baxdrostat led to decreases in serum aldosterone levels ranging from 3.0 ng/dL with the 0.5-mg dose to 4.9 ng/dL with the 2-mg dose. The 24-hour urinary aldosterone levels decreased with all three doses tested.
Baxdrostat increased plasma renin activity by 3.6, 5.0, and 13.8 mg/mL per hr with the 0.5, 1.0, and 2.0 mg doses, respectively, an indicator of its effect on lowering salt and fluid retention, Dr. Freeman said. Serum cortisol levels were not reduced in any of the baxdrostat groups throughout the study.
‘A bright future’
“It seems to have a bright future in the area of resistant hypertension, particularly in patients who are producing too much aldosterone,” said Suzanne Oparil, MD, invited discussant for the study and director of the Vascular Biology and Hypertension program at the University of Alabama at Birmingham.
She noted that aldosterone is a major contributor to the pathogenesis of resistant hypertension, which afflicts about 20% of the hypertensive population. Aldosterone antagonists are considered by many to be the best add-on treatment for resistant hypertension and do lower blood pressure.
“But they have major problems,” Dr. Oparil added. “Spironolactone, for example, causes hyperkalemia in many patients and adverse effects such as gynecomastia, erectile dysfunction, and feminization.”
Baxdrostat was well tolerated with no serious adverse events deemed related to treatment, Dr. Freeman reported. A total of 18 serious adverse events occurred in 10 patients, 6 of which were in a patient with urosepsis.
Ten adverse events of special interest occurred in eight patients, including one case of hypotension, three cases of hyponatremia, and six cases of hyperkalemia.
Potassium levels ranged from 6.0 to 6.3 mmol/L (6.0-6.3 mEq/L) in three patients and between 5.5 and 5.9 mmol/L (5.5-5.9 mEq/L) on at least two consecutive occasions in three others. Four of the patients were able to resume baxdrostat and complete the trial, whereas two patients discontinued treatment, one of whom was the patient with urosepsis.
Dr. Freeman pointed out that the study population was relatively diverse, with 33%-48% of participants of Hispanic or Latinx ethnicity and 23%-32% being Black.
At baseline, all patients had a seated blood pressure of at least 130/80 mm Hg (average 147.8/87.9 mm Hg) on a background therapy that included a diuretic in 100%, an agent targeting the renin-angiotensin-aldosterone system in 91%-96%, a beta-blocker in 52%-68%, and a calcium channel blocker in 64%-70%.
The study was not designed to test the benefits and risks of aldosterone synthase inhibition beyond 12 weeks and baxdrostat was not compared to alternative antihypertensives, he said. Additional limitations are that medication adherence was based on pill counts rather than drug analysis and enrolling only patients with an estimated glomerular filtration rate over 45 mL/min per 1.73m2 reduced the likelihood of hyperkalemia and other adverse events.
Nevertheless, “we think that these data suggest that baxdrostat has the potential to treat disorders associated with aldosterone excess, including hypertension and primary hyperaldosteronism,” Dr. Freeman said.
The intention is to carry the drug forward into additional phase 2 studies in chronic kidney disease and to begin a phase 3 study in hypertension in 2023, he noted.
The study was funded by CinCor Pharma. Dr. Freeman and three coauthors are employees of CinCor and receive stock-based compensation. The remaining authors have a financial relationship with CinRx Pharma, which has an equity stake in CinCor. Dr. Oparil reports grant/research support from Bayer, Higi, and Novartis; and serving on the scientific advisory board/expert committee for CinCor Pharma and Preventric Diagnostics.
A version of this article first appeared on Medscape.com.
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All rights reserved. This material may not be published, broadcast, copied, or otherwise reproduced or distributed without the prior written permission of Frontline Medical Communications Inc.</copyrightNotice> </rightsInfo> </provider> <abstract/> <metaDescription>CHICAGO – An investigational aldosterone synthase inhibitor could be an effective new treatment to reduce blood pressure in patients with treatment-resistant hy</metaDescription> <articlePDF/> <teaserImage/> <teaser>The novel agent lowers aldosterone activity without the off-target inhibition of cortisol synthesis that has thwarted previous drug candidates, the researchers say.</teaser> <title>Baxdrostat slashes BP in resistant hypertension: BrigHTN</title> <deck/> <disclaimer/> <AuthorList/> <articleURL/> <doi/> <pubMedID/> <publishXMLStatus/> <publishXMLVersion>1</publishXMLVersion> <useEISSN>0</useEISSN> <urgency/> <pubPubdateYear/> <pubPubdateMonth/> <pubPubdateDay/> <pubVolume/> <pubNumber/> <wireChannels/> <primaryCMSID/> <CMSIDs/> <keywords/> <seeAlsos/> <publications_g> <publicationData> <publicationCode>card</publicationCode> <pubIssueName/> <pubArticleType/> <pubTopics/> <pubCategories/> <pubSections/> </publicationData> <publicationData> <publicationCode>endo</publicationCode> <pubIssueName/> <pubArticleType/> <pubTopics/> <pubCategories/> <pubSections/> </publicationData> <publicationData> <publicationCode>fp</publicationCode> <pubIssueName/> <pubArticleType/> <pubTopics/> <pubCategories/> <pubSections/> </publicationData> <publicationData> <publicationCode>im</publicationCode> <pubIssueName/> <pubArticleType/> <pubTopics/> <pubCategories/> <pubSections/> </publicationData> </publications_g> <publications> <term canonical="true">5</term> <term>34</term> <term>15</term> <term>21</term> </publications> <sections> <term canonical="true">53</term> <term>39313</term> </sections> <topics> <term canonical="true">229</term> <term>194</term> </topics> <links/> </header> <itemSet> <newsItem> <itemMeta> <itemRole>Main</itemRole> <itemClass>text</itemClass> <title>Baxdrostat slashes BP in resistant hypertension: BrigHTN</title> <deck/> </itemMeta> <itemContent> <p>CHICAGO – An investigational aldosterone synthase inhibitor could be an effective new treatment to reduce blood pressure in patients with treatment-resistant hypertension, reslts of a phase 2 study suggest.</p> <p>The <a href="https://clinicaltrials.gov/ct2/show/NCT04519658">BrigHTN trial</a> showed systolic blood pressure fell by an average of 20.3 mm Hg, 17.5 mm Hg, and 12.1 mm Hg with baxdrostat 2 mg, 1 mg, and 0.5 mg after 12 weeks follow-up in 248 patients unable to achieve target blood pressure on stable doses of at least three antihypertensive agents, including a diuretic.<br/><br/>After adjustment for the –9.4 mm Hg change observed in the placebo group, there was a statistically significant difference of 11.0 mm Hg in the 2-mg baxdrostat group (<em>P</em> = .0001) and of 8.1 mm Hg in the 1-mg baxdrostat group (<em>P</em> = .003).<br/><br/>The adjusted change in diastolic blood pressure was significant only for the 2-mg dose (–5.2 mm Hg; <em>P</em> = .004).<br/><br/>Once-daily oral baxdrostat had an acceptable side-effect profile and no patients died.<br/><br/>The study, which was stopped early after meeting criteria for overwhelming efficacy, was presented in the final late-breaking science session at the American Heart Association scientific sessions and <a href="https://www.nejm.org/doi/pdf/10.1056/NEJMoa2213169">published simultaneously</a> in the New England Journal of Medicine.<br/><br/></p> <h2>Threading the needle </h2> <p>For at least 20 years, researchers have tried to create a drug that would lower aldosterone levels directly by inhibiting hormone synthesis rather than blocking the mineralocorticoid receptor.</p> <p>What’s made this extraordinarily difficult is that the enzyme that makes aldosterone synthase and the enzyme required for cortisol synthase, 11-beta-hydroxylase, are 93% sequence similar. Baxdrostat, however, is able to selectively block aldosterone synthase, and thus the production of aldosterone, without also blocking the production of cortisol, explained Mason W. Freeman, MD, lead author of the study and executive vice president of clinical development at CinCor Pharma, which is developing the agent.<br/><br/>“We have beautiful biomarker evidence of not only blood pressure lowering but the mechanism by which that blood pressure reduction is occurring,” he said.<br/><br/>Over 12 weeks of follow-up in the new study, the use of baxdrostat led to decreases in serum aldosterone levels ranging from 3.0 ng/dL with the 0.5-mg dose to 4.9 ng/dL with the 2-mg dose. The 24-hour urinary aldosterone levels decreased with all three doses tested.<br/><br/>Baxdrostat increased plasma renin activity by 3.6, 5.0, and 13.8 mg/mL per hr with the 0.5, 1.0, and 2.0 mg doses, respectively, an indicator of its effect on lowering salt and fluid retention, Dr. Freeman said. Serum cortisol levels were not reduced in any of the baxdrostat groups throughout the study.<br/><br/></p> <h2>‘A bright future’ </h2> <p>“It seems to have a bright future in the area of <a href="https://emedicine.medscape.com/article/241381-overview">resistant hypertension</a>, particularly in patients who are producing too much aldosterone,” said Suzanne Oparil, MD, invited discussant for the study and director of the Vascular Biology and Hypertension program at the University of Alabama at Birmingham.</p> <p>She noted that aldosterone is a major contributor to the pathogenesis of resistant hypertension, which afflicts about 20% of the hypertensive population. Aldosterone antagonists are considered by many to be the best add-on treatment for resistant hypertension and do lower blood pressure.<br/><br/>“But they have major problems,” Dr. Oparil added. “<a href="https://reference.medscape.com/drug/carospir-aldactone-spironolactone-342407">Spironolactone</a>, for example, causes <a href="https://emedicine.medscape.com/article/240903-overview">hyperkalemia</a> in many patients and adverse effects such as <a href="https://emedicine.medscape.com/article/120858-overview">gynecomastia</a>, <a href="https://emedicine.medscape.com/article/444220-overview">erectile dysfunction</a>, and feminization.”<br/><br/>Baxdrostat was well tolerated with no serious adverse events deemed related to treatment, Dr. Freeman reported. A total of 18 serious adverse events occurred in 10 patients, 6 of which were in a patient with urosepsis.<br/><br/>Ten adverse events of special interest occurred in eight patients, including one case of hypotension, three cases of <a href="https://emedicine.medscape.com/article/242166-overview">hyponatremia</a>, and six cases of hyperkalemia.<br/><br/>Potassium levels ranged from 6.0 to 6.3 mmol/L (6.0-6.3 mEq/L) in three patients and between 5.5 and 5.9 mmol/L (5.5-5.9 mEq/L) on at least two consecutive occasions in three others. Four of the patients were able to resume baxdrostat and complete the trial, whereas two patients discontinued treatment, one of whom was the patient with urosepsis.<br/><br/>Dr. Freeman pointed out that the study population was relatively diverse, with 33%-48% of participants of Hispanic or Latinx ethnicity and 23%-32% being Black.<br/><br/>At baseline, all patients had a seated blood pressure of at least 130/80 mm Hg (average 147.8/87.9 mm Hg) on a background therapy that included a diuretic in 100%, an agent targeting the renin-angiotensin-aldosterone system in 91%-96%, a beta-blocker in 52%-68%, and a calcium channel blocker in 64%-70%.<br/><br/>The study was not designed to test the benefits and risks of aldosterone synthase inhibition beyond 12 weeks and baxdrostat was not compared to alternative antihypertensives, he said. Additional limitations are that medication adherence was based on pill counts rather than drug analysis and enrolling only patients with an estimated glomerular filtration rate over 45 mL/min per 1.73m<sup>2</sup> reduced the likelihood of hyperkalemia and other adverse events.<br/><br/>Nevertheless, “we think that these data suggest that baxdrostat has the potential to treat disorders associated with aldosterone excess, including hypertension and primary hyperaldosteronism,” Dr. Freeman said.<br/><br/>The intention is to carry the drug forward into additional phase 2 studies in <a href="https://emedicine.medscape.com/article/238798-overview">chronic kidney disease</a> and to begin a phase 3 study in hypertension in 2023, he noted.<br/><br/>The study was funded by CinCor Pharma. Dr. Freeman and three coauthors are employees of CinCor and receive stock-based compensation. The remaining authors have a financial relationship with CinRx Pharma, which has an equity stake in CinCor. Dr. Oparil reports grant/research support from Bayer, Higi, and Novartis; and serving on the scientific advisory board/expert committee for CinCor Pharma and Preventric Diagnostics.<span class="end"/> </p> <p> <em>A version of this article first appeared on <span class="Hyperlink"><a href="https://www.medscape.com/viewarticle/984011">Medscape.com</a></span>.</em> </p> </itemContent> </newsItem> <newsItem> <itemMeta> <itemRole>teaser</itemRole> <itemClass>text</itemClass> <title/> <deck/> </itemMeta> <itemContent> </itemContent> </newsItem> </itemSet></root>
AT AHA 2022