ABSTRACT & COMMENTARY
Synopsis: Exercise training post-MI can prevent LV remodeling and dysfunction.
Source: Giannuzzi P, et al. Circulation 1997;96: 1790-1797.
Although cardiac rehabilitation post-mi is generally regarded as beneficial, the role of exercise training after large Q-wave MI associated with reduced left ventricular function has been questioned. Thus, the results of the Exercise in LV Dysfunction (ELVD) trial is of interest. This multicentered trial randomized 80 asymptomatic patients, 3-5 weeks post first Q-wave MI with LV ejection fraction (EF) less than 40%, to a systematic six-month exercise program or a control group. Exercise consisted of 30 minutes of bicycle ergometry at least three times per week. All patients had a pre-randomization multistage symptom limited bicycle ergometric test, an echocardiogram, and a quality of life assessment. Only 77 patients completed the study; 39 in the training group and 38 in the control group. When the tests were repeated at six months, exercise capacity increased significantly only in the training group from 4.5 to 5.8 kpm (P < 0.01). LV volumes increased only in the control group; diastolic from 94 to 99 mL/m2 (P < 0.01); end-systolic volume from 62 to 67 mL/m2 (P < 0.01). LVEF improved only in the training group from 34% to 38% (P < 0.01). Some measures of quality of life improved significantly only in the training group. Giannuzzi and colleagues conclude that in patients after first Q-wave MI with LV dysfunction, systematic supervised exercise training may prevent LV remodeling and improve LV function.
COMMENT BY MICHAEL H. CRAWFORD, MD
This study suggests that a third intervention can reduce LV remodeling post-MI. ACE inhibitors and an open infarct artery have both been shown to abrogate post-MI LV function deterioration, and, now perhaps, exercise training needs to be added to the list. Also, it is noteworthy that about three-fourths of the patients in both groups were on ACEI, and two-thirds had open infarct arteries. Thus, exercise training seems additive to these interventions.
Exercise training improves exercise performance and patient well-being in post-MI and in heart failure patients. In the latter group, it is believed to be because of enhanced skeletal muscle blood flow or metabolism. The mechanism in post-MI patients has not been elucidated, but this study suggests it is due to the abrogation of LV remodeling. How exercise accomplishes this is unknown, but Giannuzzi et al suggest that it may be related to reduced wall tension secondary to decreased peripheral resistance. It is probably not related to improvement in myocardial ischemia, since patients with overt ischemia were excluded and most patients had a patent infarct artery.
Beta blockers improve survival post-MI especially in patients with large MIs and LV dysfunction, but the mechanism of the effect has not been established. About half the patients in both groups were on beta blockers in this study, which is better than the rate in many studies. It would be interesting to know the relative importance of these interventions. As each new intervention is shown to be beneficial, when given in addition to previously demonstrated beneficial therapy, there is a tendency to diminish the use of the older intervention. Thus, beta-blocker use post-MI has declined in favor of ACE and the open artery hypothesis. Should we forsake these for exercise training?