Age-Related Patterns of Myocardial Recovery After Primary PCI for Acute Myocardial Infarction: A Prospective 12-Month...

Background/Objectives: Age may influence myocardial recovery after acute myocardial infarction (AMI) beyond changes in left ventricular ejection fraction (LVEF). We investigated age-related patterns in ischemic delay, admission biomarkers, biventricular function, myocardial deformation, and exploratory patterns of prescribed heart failure guideline-directed medical therapy (HF-GDMT) classes after primary percutaneous coronary intervention (PCI). Methods: This prospective frequency-matched cohort study included 90 AMI patients treated with primary PCI, stratified into younger (25-44 years; n = 30) and older (≥45 years; n = 60) groups. Clinical data, ischemic time, cardiac biomarkers, serial echocardiography at baseline, 6, and 12 months, and HF-GDMT intensity were analyzed. Results: Older patients had longer pain-to-balloon time (720 [480-1230] vs. 540 [420-660] min; p = 0.021), higher hs-cTnI (p = 0.045), and higher NT-proBNP (4776 [3013-5952] vs. 833.5 [95.7-1939.5] pg/mL; p < 0.001). Baseline and 12-month LVEF were similar between groups. Younger patients showed greater 12-month global longitudinal strain (GLS) improvement (-3.7 [-5.1 to -1.9] vs. -2.3 [-3.0 to -1.3] percentage points; p = 0.002), despite comparable absolute GLS. In exploratory post hoc analyses, prescribed HF-GDMT drug-class count showed an association with LVEF change primarily in older patients, who also had significantly lower baseline LVEF (ρ = 0.59; p < 0.001). Conclusions: In this prospective exploratory cohort, 12-month conventional systolic recovery assessed by LVEF and absolute GLS was comparable between age groups after primary PCI. However, the older comparator group had longer ischemic delay and higher admission biomarkers reflecting cardiomyocyte injury and myocardial wall stress, while younger patients showed greater longitudinal GLS improvement over time. These findings suggest that age-stratified recovery after AMI is better characterized by ischemic timing, baseline biomarker profile, and deformation trajectory than by LVEF alone. Because infarct size was not directly quantified, admission biomarker differences should not be interpreted as evidence of larger infarcts.