Cardiac remodeling

Cardiac remodeling refers to the genomic, molecular, cellular, and structural changes that manifest clinically as alterations in the size, shape, and function of the heart following injury or chronic stress. It is primarily characterized by cardiomyocyte hypertrophy, loss of myocytes through apoptosis or necrosis, and the accumulation of collagen in the interstitial space (fibrosis) [1][2]. While initially an adaptive response to maintain cardiac output after events like myocardial infarction or chronic hypertension, the process eventually becomes maladaptive, leading to progressive ventricular dilation and heart failure [3]. Cardiac remodeling is not a single molecular target but a multifaceted pathological outcome influenced by various signaling pathways, including the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system [4]. Pharmacological interventions with ACE inhibitors, beta-blockers, and mineralocorticoid receptor antagonists aim to attenuate or reverse these structural changes, a process often referred to as 'reverse remodeling' [5]. Understanding this process is critical for developing disease-modifying therapies in cardiovascular medicine.

Other names

Ventricular remodelingMyocardial remodelingPathological cardiac remodelingLeft ventricular remodeling

Drugs targeting this process typically inhibit neurohumoral pathways (renin-angiotensin-aldosterone system and sympathetic nervous system) to reduce hemodynamic stress, inflammation, and fibrotic signaling.