Congestive Heart Failure & Angina

Myocardial Fibrosis: Mechanisms and Clinical Implications

Myocardial fibrosis is a hallmark of adverse remodeling in both ischemic and non-ischemic heart disease. It results from an imbalance between extracellular matrix synthesis and degradation, driven by fibroblast activation, transforming growth factor-beta (TGF-β) signaling, and chronic neurohormonal and inflammatory stimuli. Fibrosis stiffens the myocardium, impairs diastolic function, disrupts electrical conduction, and predisposes patients to arrhythmias. Importantly, the extent of fibrosis correlates with prognosis across the spectrum of cardiomyopathies.

Cardiac MRI with late gadolinium enhancement and T1 mapping has revolutionized fibrosis detection, enabling precise quantification and risk stratification. Therapeutic efforts are shifting toward anti-fibrotic strategies, including mineralocorticoid receptor antagonists, TGF-β pathway inhibitors, and emerging molecular therapies. This track will highlight the mechanistic underpinnings of fibrosis, diagnostic advances, and translational therapies that aim not only to halt but potentially reverse fibrotic remodeling. Attendees will gain insights into how targeting fibrosis could reshape outcomes in heart failure and angina populations.