Journal of CardioVascular Insights
Open Access • Peer Reviewed • Quarterly Publication
Adverse and Reverse Myocardial Remodeling in Hypertension: Mechanisms, Assessment, and Therapeutic Reversal
Abstract
Background: Hypertension is a leading driver of structural and functional change in the heart. Left ventricular hypertrophy (LVH), the best-known manifestation, begins as an adaptive response that normalizes wall stress but progresses, under sustained load, to maladaptive remodeling involving fibrosis, microvascular rarefaction, electrical instability and, ultimately, heart failure.
Scope: This narrative review summarizes current understanding of the cellular, hemodynamic and non-hemodynamic determinants of hypertensive myocardial remodeling; the imaging and electrocardiographic tools used to detect it; and the evidence that pharmacological and exercise-based interventions can slow or reverse it.
Key points: Cardiomyocyte hypertrophy, myofibroblast-driven fibrosis, inflammation, apoptosis, coronary microvascular remodeling and ion-channel and calcium-handling changes interact to produce the adverse phenotype. Systolic load is the principal determinant, but ethnicity, obesity, diabetes, dietary salt, neurohormonal activation and genetic background modify both the extent and the geometric pattern of remodeling. Echocardiography remains the principal clinical tool, with cardiac magnetic resonance serving as the reference for LV mass. Reverse remodeling, characterized by reduced chamber volume, normalized shape and improved function, is associated with better prognosis in heart failure; however, its definitions derive mainly from dilated cardiomyopathy and heart failure with reduced ejection fraction, and much of the supporting drug evidence comes from myocardial infarction and heart failure populations rather than from hypertension specifically. Renin–angiotensin–aldosterone system inhibitors and beta-blockers have the most consistent evidence, and aerobic exercise induces a physiological phenotype that is mechanistically distinct from pathological hypertrophy.
Conclusions: Reversal of remodeling is a clinically meaningful treatment target in hypertensive heart disease. Hypertension-specific trials using standardized, imaging-based definitions of reverse remodeling are needed.
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© 2026 The Author(s). Published by WM Journals.
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