Cardiovascular disease (CVD) — including coronary artery disease, heart failure, and post-myocardial infarction cardiomyopathy — represents the leading cause of mortality worldwide. Inflammation drives atherosclerotic plaque development, ischemic injury, and adverse cardiac remodeling after MI. MSC therapy offers a multi-target approach to these mechanisms.
Post-MI and Heart Failure
Following myocardial infarction, MSCs delivered IV or directly into cardiac tissue reduce the inflammatory cascade that worsens infarct size, suppress fibrosis (scar formation) in the peri-infarct zone, and secrete factors promoting angiogenesis and cardiomyocyte survival. Phase II trials have demonstrated modest but consistent improvements in left ventricular ejection fraction (LVEF) and reduction in infarct scar size at 12 months.
Atherosclerosis and Systemic Inflammation
Systemic inflammatory burden — measured by CRP, IL-6, and oxidized LDL — contributes directly to atherosclerotic progression. MSC therapy consistently reduces systemic inflammatory markers, which may slow plaque progression over time. This is an adjunctive benefit to standard lipid and blood pressure management, not a replacement.
Patient Selection
Stable heart failure (NYHA Class II–III) and post-MI cardiomyopathy with LVEF 25–45% represent the best-evidenced indication. Unstable angina, active ischemia, or recent (within 30 days) MI require cardiac stabilization before MSC therapy is appropriate. All CVD patients are evaluated in coordination with their cardiologist.