Prevention of ventricular remodeling

Prevention of ventricular remodeling is a clinical therapeutic objective rather than a single molecular target. It refers to the efforts to halt or reverse the structural and functional changes in the heart's ventricles—such as alterations in size, shape, and mass—that occur following myocardial injury or chronic pressure and volume overload [1]. This remodeling process is driven by a complex interplay of neurohormonal activation, inflammatory signaling, and extracellular matrix deposition, which eventually leads to progressive heart failure and increased mortality [2]. Pharmacological management aimed at preventing or reversing this process involves several classes of drugs, including ACE inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and ARNI (angiotensin receptor-neprilysin inhibitors) [3]. These therapies work by reducing wall stress and inhibiting the maladaptive biological pathways, such as the renin-angiotensin-aldosterone system (RAAS), that promote hypertrophy and fibrosis [4]. Successful prevention of remodeling is clinically evidenced by stabilized or improved left ventricular ejection fraction and reduced cardiac volumes, which are strongly correlated with better patient outcomes [5]. [1] StatPearls, 'Ventricular Remodeling', https://www.ncbi.nlm.nih.gov/books/NBK553100/ [2] PubMed, 'Pathophysiology of Cardiac Remodeling', https://pubmed.ncbi.nlm.nih.gov/10903340/ [3] American Heart Association, 'Guidelines for the Management of Heart Failure', https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063 [4] NIH, 'Mechanisms of Cardiac Remodeling', https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181930/ [5] European Society of Cardiology, 'Guidelines on Heart Failure', https://academic.oup.com/eurheartj/article/42/36/3599/6358045

Other names

Cardiac remodelingLeft ventricular remodelingPost-infarct remodelingReverse remodelingVentricular restructuring

Inhibition of the renin-angiotensin-aldosterone system (RAAS), antagonism of sympathetic nervous system activity, inhibition of neprilysin to increase natriuretic peptides, and modulation of sodium-glucose cotransporter 2 (SGLT2) activity to reduce preload and afterload while improving myocardial energetics.