Heart Attack Damage: Scar Tissue Replaces Lost Cardiomyocytes
Adult mammalian cardiomyocytes have minimal regenerative capacity. After myocardial infarction (MI), necrotic myocytes are replaced by fibrotic scar tissue composed of fibroblasts, collagen (types I and III), and extracellular matrix.
Consequences of Scar Formation
- Loss of contractile function: Scar does not shorten or generate force.
- Ventricular remodeling: Dilatation, wall thinning, spherical distortion → increased wall stress (Laplace's law) → progressive heart failure.
- Arrhythmogenic substrate: Scar border zones have heterogeneous conduction → reentrant ventricular tachycardia.
- Aneurysm formation: Dyskinetic bulge in akinetic segment.
Regenerative Research
- Cell therapy: MSCs, cardiac progenitor cells, iPSC-derived cardiomyocytes—modest benefit in trials; engraftment/electromechanical integration remain challenges.
- Direct reprogramming: Fibroblasts → induced cardiomyocytes (GMT, Hand2 transcription factors) in vivo.
- Mitogenic stimuli: Neuregulin, periostin, miR-199a/590 to induce cardiomyocyte proliferation.
- Tissue engineering: Epicardial patches, bioartificial myocardium.
Clinical Implications
Early reperfusion (PCI, thrombolysis) limits infarct size. Guideline-directed medical therapy (GDMT: ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2i) attenuates remodeling. ICD for primary prevention if LVEF ≤35% after 3 mo GDMT.
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