Key result
Angina preceding MI is linked to less LV dilation at 90 days.
Why the study?
The extent to which ischemia occurring before myocardial infarction influences subsequent changes in ventricular size and function was unclear.
Does symptomatic angina prior to myocardial infarction prevent subsequent left ventricular remodeling in post-MI patients?
Cohort (n=283)
Does symptomatic angina prior to myocardial infarction prevent subsequent left ventricular remodeling in post-MI patients?
Absolute Event Rate: -0.73% vs 6.8%
p-value: p=0.017
Symptomatic angina prior to myocardial infarction is associated with reduced subsequent left ventricular remodeling, suggesting a protective effect possibly mediated by ischemic preconditioning or collateral recruitment.
Supports preconditioning hypothesis for reduced remodeling; leaves open prospective trials before practice change.
OBJECTIVES: To investigate the hypothesis that prior angina pectoris confers protection from remodeling occurring after myocardial infarction (MI), we analyzed echocardiograms from the Healing and Early Afterload Reducing Therapy (HEART) trial. BACKGROUND: Ischemia occurring before MI has been shown to reduce infarct size in experimental models and to improve outcomes in patients. The extent to which ischemia occurring before MI influences subsequent changes in ventricular size and function is unclear. METHODS: We studied 283 patients enrolled in the HEART trial who had echocardiograms at days 1 and 90 after MI. Left ventricular (LV) dilation from days 1 to 90 was used as a measure of LV remodeling. We explored the relationship between symptomatic angina occurring before infarction and subsequent LV remodeling. RESULTS: In patients who reported angina (n = 111) during the three months preceding MI, LV volume change was -0.73 +/- 2.6 ml over the 90-day post-MI period, compared with 6.8 +/- 2.6 ml for patients (n = 172) without angina (p = 0.017). In contrast, there were no differences in changes in ejection fraction based on prior angina. Maximal creatine kinase was significantly lower in patients with prior angina (2,119 +/- 1,729 vs. 2,701 +/- 2,088, p = 0.016). In a multivariate model, prior angina remained protective for ventricular remodeling after adjusting for age, gender, baseline ejection fraction, Killip class, baseline end-diastolic volume, and drug treatment group (p = 0.042). However, the protective effect of pre-infarction angina appeared to be attenuated in diabetic patients. CONCLUSIONS: Ischemic symptoms occurring before MI may protect against LV remodeling. These protective effects may be secondary to recruitment of collaterals or ischemic preconditioning of the myocardium, and they appear to be attenuated in diabetic patients.
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Solomon et al. (2004) conducted a cohort in Myocardial infarction (n=283). Angina pectoris prior to myocardial infarction vs. No prior angina pectoris was evaluated on Left ventricular (LV) volume change (dilation) from days 1 to 90 (p=0.017). Angina pectoris in the 3 months preceding myocardial infarction protected against left ventricular dilation at 90 days compared to no prior angina (-0.73 vs 6.8 ml; p=0.017).
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