Cardiac ventricular remodeling (VR)

Cardiac ventricular remodeling refers to the structural and functional changes in the heart's ventricles, such as changes in size, shape, and wall thickness, typically occurring after a myocardial infarction or in response to chronic pressure or volume overload [2, 4, 17]. This complex process is driven by molecular and cellular events including cardiomyocyte hypertrophy, apoptosis, and excessive collagen deposition leading to fibrosis [15, 18]. While initially adaptive to maintain cardiac output, progressive remodeling is a hallmark of heart failure and is strongly associated with increased morbidity and mortality [2, 6]. Therapeutic strategies aim to achieve 'reverse remodeling'—the partial or full restoration of normal cardiac geometry and function—primarily through pharmacological blockade of maladaptive neurohormonal pathways [8, 14]. Common drug classes used for this purpose include ACE inhibitors, beta-blockers, mineralocorticoid receptor antagonists (MRAs), and angiotensin receptor-neprilysin inhibitors (ARNIs), all of which help halt or reverse the structural decline of the failing heart [1, 9, 12].

Other names

Ventricular remodelingCardiac remodelingMyocardial remodelingLeft ventricular remodelingReverse remodeling

Intervention usually involves neurohormonal blockade of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, alongside enhancement of the natriuretic peptide system and inhibition of SGLT2 transporters to reduce cardiac workload and wall stress [1, 8, 12].