Cardiac scar tissue

Cardiac scar tissue is a non-contractile, collagen-rich extracellular matrix that replaces functional cardiomyocytes following significant cardiac injury, such as a myocardial infarction [1]. This process, known as replacement fibrosis, is initially a critical survival mechanism that maintains the structural integrity of the ventricular wall and prevents cardiac rupture [2]. However, persistent activation of myofibroblasts leads to excessive deposition of Type I and Type III collagen, resulting in increased myocardial stiffness and impaired diastolic filling [1, 2]. Beyond mechanical dysfunction, the scar acts as an electrical insulator, disrupting normal conduction and creating a substrate for life-threatening re-entrant arrhythmias [4]. From a pharmacological perspective, cardiac scar tissue is not a single molecular target but a complex pathological environment; therapeutic strategies focus on modulating the signaling pathways that drive its formation, such as the TGF-beta and RAAS pathways [2, 3]. Recent advancements have also explored the use of CAR-T cells to target fibroblast activation protein (FAP) within the scar to actively regress existing fibrosis [3]. Clinical management currently relies on drugs like ACE inhibitors and mineralocorticoid receptor antagonists to limit scar expansion and improve patient outcomes [2].

Other names

Myocardial scarMyocardial fibrosisCardiac fibrosisPost-infarct scarFibrotic scar

Inhibition of the renin-angiotensin-aldosterone system (RAAS), antagonism of TGF-beta signaling, and targeted depletion of activated myofibroblasts.