Discontinuation of afterload-reducing drugs decreases left ventricular outflow tract obstruction in hypertrophic obstructive cardiomyopathy.

HCM LVOT cardiomyopathy heart failure mavacamten pharmacotherapy

Journal

Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388

Informations de publication

Date de publication:
2024
Historique:
received: 19 03 2024
accepted: 02 07 2024
medline: 31 7 2024
pubmed: 31 7 2024
entrez: 31 7 2024
Statut: epublish

Résumé

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. 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. 16 patients discontinued their afterload-reducing drugs, resulting in a significant decrease in median LVOT gradient from 86.5 [60.5-109.3] mmHg to 61.5 [28.3-97.50] mmHg ( 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.

Sections du résumé

Background UNASSIGNED
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.
Methods UNASSIGNED
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.
Results UNASSIGNED
16 patients discontinued their afterload-reducing drugs, resulting in a significant decrease in median LVOT gradient from 86.5 [60.5-109.3] mmHg to 61.5 [28.3-97.50] mmHg (
Conclusions UNASSIGNED
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.

Identifiants

pubmed: 39081367
doi: 10.3389/fcvm.2024.1403422
pmc: PMC11286422
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1403422

Informations de copyright

© 2024 Derda, Abelmann, Sonnenschein, Sieweke, Bavendiek, Bauersachs, Thum and Berliner.

Déclaration de conflit d'intérêts

AD received honoraria for lectures by AstraZeneca, BMS, Boehringer Ingelheim and Bayer not related to this article. KS received presentation honoraria and travel grants from medi, Novartis, BMS, Chiesi and Amicus. JB received honoraria for lectures/consulting from Novartis, Vifor, Bayer, Pfizer, Boehringer Ingelheim, AstraZeneca, Cardior, CVRx, BMS, Amgen, Corvia, Norgine, Edwards, Roche not related to this article; and research support for the department from Zoll, CVRx, Abiomed, Norgine, Roche, not related to this article. DB received honoraria for lectures/consulting from Abbott Vascular, AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Edwards Lifesciences, Pfizer. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Anselm A Derda (AA)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany.

Malin Abelmann (M)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany.

Kristina Sonnenschein (K)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany.

Jan-Thorben Sieweke (JT)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.

Udo Bavendiek (U)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.

Johann Bauersachs (J)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.

Thomas Thum (T)

Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany.

Dominik Berliner (D)

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.

Classifications MeSH