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September 8, 2026Journal of Cardiovascular Development and DiseaseOpen Access

MRAs and SGLT2 inhibitors show potential as substrate-modifying therapies for stretch-induced arrhythmic MVP.

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Why the study?

A small subset of MVP patients develops complex ventricular arrhythmias and sudden cardiac death disproportionate to hemodynamic burden, prompting the need to reframe aMVP pathogenesis and explore substrate-directed prevention.

Design

Narrative review

Key result

Arrhythmic mitral valve prolapse is reframed as a regional, stretch-induced cardiomyopathy, with MRAs and SGLT2 inhibitors identified as potential substrate-modifying preventive therapies.

Authors

MDMili DaveSAShaaf AhmadKAKirkwood Adams

Discussion

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Overview

Hypothesis-generating for substrate-directed prevention in aMVP; extends mechanistic framework but leaves open efficacy pending randomized trials.

Key Points

  • To conceptualize arrhythmic mitral valve prolapse (aMVP) as a regional stretch-induced cardiomyopathy with a fibro-inflammatory signature and identify potential substrate-modifying medical therapies.
  • Synthesized current literature across multimodal cardiac imaging, clinical electrophysiology, surgical series, mechanotransduction biology, and cardiovascular pharmacology.
  • Evaluated candidate substrate-directed drug therapies based on mechanistic plausibility, human myocardial evidence, and feasibility in randomized trials.
  • Characterized a two-hit pathogenesis whereby excessive valvular traction generates regional mechanical stress that interacts with individual susceptibility to trigger inflammation, fibrosis, and complex ventricular arrhythmias.
  • Proposed shifting the therapeutic paradigm in intermediate-risk aMVP from reactive device-based rescue toward early, substrate-directed prevention.
  • Identified mineralocorticoid receptor antagonists and sodium–glucose cotransporter 2 inhibitors as the most promising pharmacotherapies based on antifibrotic efficacy and clinical trial readiness.

Structured PICO

P
Population
Patients with arrhythmic mitral valve prolapse (aMVP), defined as MVP with complex ventricular arrhythmias in the absence of another defined arrhythmic substrate
I
Intervention
Substrate-modifying pharmacotherapies (specifically mineralocorticoid receptor antagonists [MRAs] and sodium-glucose cotransporter 2 [SGLT2] inhibitors)

This conceptual review reframes arrhythmic mitral valve prolapse as a stretch-induced cardiomyopathy and proposes MRAs and SGLT2 inhibitors as potential substrate-modifying therapies for prevention.

Cite This Study

Dave et al. (2026) conducted a review in Arrhythmic Mitral Valve Prolapse. Mineralocorticoid receptor antagonists and SGLT2 inhibitors was evaluated. Arrhythmic mitral valve prolapse is reframed as a regional, stretch-induced cardiomyopathy, with MRAs and SGLT2 inhibitors identified as potential substrate-modifying preventive therapies.

synapsesocial.com/papers/6a9fd7c658e84d0ff5b46c03https://doi.org/10.3390/jcdd13090437
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Mitral Valve Prolapse Associated with Mitral Annular Disjunction: Diagnosis, Prognosis, and Arrhythmic Risk2026
  2. 2Current understanding of mitral valve prolapse syndrome and related arrhythmia: State-of-the-Art Review2026 · 2 citations
  3. 3Mitral Valve Prolapse Induces Regionalized Myocardial Fibrosis2021 · 51 citations
  4. 4The Arrhythmogenic Spectrum of Mitral Valve Disease: Pathophysiology, Risk Stratification, and Surgical Management2026
  5. 5Mitral valve prolapse—arrhythmic faces of the valve disease2023 · 1 citations