Regular exercise training reduces coronary restenosis after percutaneous coronary intervention in patients with acute myocardial infarction

BackgroundIt is well known that cardiac rehabilitation (CR) including regular exercise training (ET) is cardioprotective with respect to clinical events in patients with acute myocardial infarction (AMI). However, it is not known whether the regular ET may affect coronary restenosis after percutaneous coronary intervention (PCI) with stenting in AMI. The aim of this study was to evaluate the effect of regular ET on a stented coronary segment and its association with inflammatory markers in AMI.MethodsConsecutively 74 AMI patients who underwent PCI with implantation of a drug-eluting stent and 9 month follow-up angiography were included. Thirty seven patients who received CR with ET were assigned to the ET group. Another 37 patients who did not participate in ET, of similar age to those of participants, were assigned to the control group. At 9 months, angiographic restenosis measured as in-segment late luminal loss of the stented coronary artery was analyzed via quantitative coronary angiography using CAAS 5.9.ResultsThere were no significant differences in baseline characteristics including age, sex, body mass index, smoking, DM, hypertension, lipid profile, use of statin, and complete blood cell between two groups. On 9 month follow-up angiography, late luminal loss per stent was significantly smaller in the ET group compared to the control group (0.14 ± 0.57 vs. 0.54 ± 0.88 mm, p = 0.02). Maximal oxygen consumption (VO2max) significantly improved in the ET group after 9 months (27.9 ± 6.4 vs. 30.8 ± 5.2 mL/kg/min, p < 0.001). Increment in high density lipoprotein-cholesterol (HDL-C) was significantly larger in the ET group at 9 months (0.15 ± 0.12 vs. 0.04 ± 0.24 mg/dL, p = 0.03).ConclusionRegular ET contributes to a significant reduction in late luminal loss in the stented coronary segment in AMI patients. This effect was associated with increased exercise capacity and increased HDL-C.