Published online Aug 6, 2021. doi: 10.12998/wjcc.v9.i22.6308
Peer-review started: April 8, 2021
First decision: April 28, 2021
Revised: May 12, 2021
Accepted: June 7, 2021
Article in press: June 7, 2021
Published online: August 6, 2021
Processing time: 110 Days and 17.3 Hours
A growing amount of evidence provides support for the hypothesis that acute myocardial infarction (AMI) patients should go through cardiopulmonary exercise testing about 3-5 d after AMI is diagnosed, make reasonable exercising prescription, and conduct exercise training under guidance.
To investigate the effect of exercise training on left ventricular systolic function and left ventricular remodeling and to study the possible mechanisms of left ventricular remodeling (LVRM) by the changes of matrix metallopeptidase 9 (MMP-9) and tissue inhibitor of metalloproteinases 1 (TIMP-1) in patients with acute ST-segment elevation myocardial infarction (STEMI).
To investigate the effect of exercise training on left ventricular systolic function and left ventricular remodeling and to study the possible mechanisms of LVRM.
Sixty patients with first STEMI undergoing direct percutaneous coronary intervention from February 2008 to October 2008 were randomly assigned to an exercise group (n = 30) or a control group (n = 30). The levels of MMP-9 and TIMP-1 were measured in all patients at 1 d, 10-14 d, 30 d, and 6 mo after admission. Two-dimensional echocardiography and cardiopulmonary exercise testing were done in patients at 10-14 d and 6 mo after admission.
In cardiopulmonary exercise testing of the two group, at 6 mo, the time of exercise, peak and anaerobic threshold values of O2 uptake, and metabolic equivalents increased in both groups, but markedly increased in the exercise group than in the control group. There was no significant differences in LVESV, LVEDV, or left ventricular ejection fraction (LVEF) between the two groups. At 6 mo, LVEF increased in the exercise group, but not in the control group. Change in LVEF in the exercise group was significantly higher than that of the control group. At 6 mo, the percentage of patients with positive result of LVRM was 26.6% in the exercise group and 52.6% in the control group (P < 0.05). The levels of plasma MMP-9 and TIMP-1 and the ratio of MMP-9 to TIMP-1 in both groups had no significant difference at 1 d and 10-14 d after AMI, but at 30 d and 6 mo, the levels of plasma MMP-9 and TIMP-1 in the exercise group were significantly lower than those in the control group; the ratio of MMP-9 to TIMP-1 in the exercise group was significantly higher than that in the control group.
Exercise training under supervision based on home condition in early and recovery stage of AMI can improve exercise cardiopulmonary function and prevent the LVRM. Therefore, it may reduce unfavorable remodeling response by decreasing the levels of plasma MMP-9 and TIMP-1 and adjusting the ratio of MMP-9 to TIMP-1 hereafter.
Randomized controlled trials are needed to investigate the effect of exercise training on left ventricular systolic function and LVRM and to study the possible mechanisms of LVRM in patients with acute STEMI.