Aging and Markers of Adverse Remodeling After Myocardial Infarction

Acute myocardial infarction (MI) is a catastrophic event in patients aged 18 years and above. While improved coronary reperfusion strategies and medical therapies over the last 2 decades have increased survival, hearts of survivors undergo progressive remodeling with changes in structure, size, shape, and systolic function that lead to heart failure. Morbidity from heart failure in post-MI survivors remains high, especially after ST-segment-elevation MI (STEMI) and in older compared to younger patients. Cumulative knowledge of the biology of cardiovascular aging suggests that the aging process is progressive and results in physiological, cellular, and molecular changes that can negatively impact post-MI remodeling. Emerging evidence suggests that aging may adversely influence key factors in post-MI remodeling, including the extent of damage to the cardiac muscle and extracellular matrix (ECM) on the one hand and adequacy of the healing/repair process (with inflammation, ECM remodeling, fibrosis, hypertrophy, and angiogenesis) on the other. These effects may result in differential outcomes of therapy between younger and older survivors of STEMI. Furthermore, reperfusion therapy that is delayed beyond several minutes of acute STEMI results in significant reperfusion damage and adverse remodeling that may be amplified with aging. Biomarkers, including emerging healing-specific proteins, can be used not only to noninvasively monitor the remodeling process and responses to therapy but also to predict adverse post-STEMI remodeling and clinical outcome. Novel biomarkers of adverse remodeling hold great promise for developing novel therapeutic strategies to limit adverse remodeling and improve outcome after STEMI in patients of different ages.