{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T22:50:43Z","timestamp":1788562243419,"version":"build-2803163510"},"reference-count":39,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,7,16]],"date-time":"2024-07-16T00:00:00Z","timestamp":1721088000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hypertrophic cardiomyopathy (HCM), the most common genetic heart disease, is classified into hypertrophic non-obstructive and hypertrophic obstructive cardiomyopathy (HOCM). Patients with HOCM and coexisting heart failure or arterial hypertension are often prescribed afterload-reducing drugs. Although recommended in current guidelines, data on the direct effect of discontinuing afterload-reducing medication are scarce. This study aims to demonstrate the benefit of discontinuing afterload-reducing medication in HOCM patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This monocentric retrospective analysis included 24 patients with HOCM with afterload-reducing medication, including angiotensin-converting enzyme inhibitors, angiotensin-1 receptor blocker and dihydropyridine-calcium channel blocker, at their first outpatient visit. Effects of discontinuing this medication on LVOTO were examined compared to patients with persistent use despite medical advice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      16 patients discontinued their afterload-reducing drugs, resulting in a significant decrease in median LVOT gradient from 86.5 [60.5\u2013109.3]\u2005mmHg to 61.5 [28.3\u201397.50]\u2005mmHg (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0004). In 6 patients, beta-blocker therapy was initiated simultaneously, or the dose was increased. Regardless, LVOT gradient reduction was also significant in the remaining 10 patients (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001). The gradient was not changed significantly in the 8 patients continuing their afterload-reducing medication.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Discontinuation of afterload-reducing drugs significantly decreases LVOTO. Our study underscores the significance of abstaining from afterload-reducing drugs in HOCM patients, particularly in patients with concomitant hypertension or heart failure. According to recently published European guidelines, HOCM patients should preferably be treated with beta-blockers or non-dihydropyridine-calcium channel blockers.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2024.1403422","type":"journal-article","created":{"date-parts":[[2024,7,16]],"date-time":"2024-07-16T00:31:04Z","timestamp":1721089864000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["Discontinuation of afterload-reducing drugs decreases left ventricular outflow tract obstruction in hypertrophic obstructive cardiomyopathy"],"prefix":"10.3389","volume":"11","author":[{"given":"Anselm A.","family":"Derda","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malin","family":"Abelmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina","family":"Sonnenschein","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan-Thorben","family":"Sieweke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Udo","family":"Bavendiek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johann","family":"Bauersachs","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Thum","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominik","family":"Berliner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2024,7,16]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1249","DOI":"10.1016\/j.jacc.2015.01.019","article-title":"New perspectives on the prevalence of hypertrophic cardiomyopathy","volume":"65","author":"Semsarian","year":"2015","journal-title":"J Am Coll Cardiol"},{"key":"B2","doi-asserted-by":"publisher","first-page":"749","DOI":"10.1161\/CIRCRESAHA.117.311059","article-title":"Hypertrophic cardiomyopathy: genetics, pathogenesis, clinical manifestations, diagnosis, and therapy","volume":"121","author":"Marian","year":"2017","journal-title":"Circ Res"},{"key":"B3","doi-asserted-by":"publisher","first-page":"655","DOI":"10.1056\/NEJMra1710575","article-title":"Clinical course and management of hypertrophic cardiomyopathy","volume":"379","author":"Maron","year":"2018","journal-title":"N Engl J Med"},{"key":"B4","doi-asserted-by":"publisher","first-page":"2232","DOI":"10.1161\/CIRCULATIONAHA.106.644682","article-title":"Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction","volume":"114","author":"Maron","year":"2006","journal-title":"Circulation"},{"key":"B5","doi-asserted-by":"publisher","first-page":"295","DOI":"10.1056\/NEJMoa021332","article-title":"Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy","volume":"348","author":"Maron","year":"2003","journal-title":"N Engl J Med"},{"key":"B6","doi-asserted-by":"publisher","first-page":"e533","DOI":"10.1161\/CIR.0000000000000938","article-title":"2020 AHA\/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: executive summary: a report of the American College of Cardiology\/American Heart Association joint committee on clinical practice guidelines","volume":"142","author":"Ommen","year":"2020","journal-title":"Circulation"},{"key":"B7","doi-asserted-by":"publisher","first-page":"2733","DOI":"10.1093\/eurheartj\/ehu284","article-title":"2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy: the task force for the diagnosis and management of hypertrophic cardiomyopathy of the European Society of Cardiology (ESC)","volume":"35","author":"Elliott","year":"2014","journal-title":"Eur Heart J"},{"key":"B8","doi-asserted-by":"publisher","first-page":"3503","DOI":"10.1093\/eurheartj\/ehad194","article-title":"2023 ESC guidelines for the management of cardiomyopathies","volume":"44","author":"Arbelo","year":"2023","journal-title":"Eur Heart J"},{"key":"B9","doi-asserted-by":"publisher","first-page":"567","DOI":"10.1007\/s40261-022-01166-2","article-title":"Pharmacological anti-remodelling effects of disease-modifying drugs in heart failure with reduced ejection fraction","volume":"42","author":"Correale","year":"2022","journal-title":"Clin Drug Investig"},{"key":"B10","doi-asserted-by":"publisher","first-page":"569","DOI":"10.1016\/s0735-1097(99)00630-0","article-title":"Cardiac remodeling\u2013concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. 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