Angina pectoris prior to myocardial infarction protects against subsequent left ventricular remodeling

• Published in: Journal of the American College of Cardiology 2004-05, Vol.43 (9), p.1511-1514
• Main Authors: Solomon, Scott D, Anavekar, Nagesh S, Greaves, Sally, Rouleau, Jean L, Hennekens, Charles, Pfeffer, Marc A
• Format: Article
• Language: English
• Subjects: Aged; Angina pectoris; Angina Pectoris - drug therapy; Angina Pectoris - epidemiology; Angina Pectoris - physiopathology; Angioplasty; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Biomarkers - blood; Cardiology; Creatine Kinase - blood; Diabetes; Diabetes Mellitus - epidemiology; Diabetes Mellitus - physiopathology; Double-Blind Method; Echocardiography; Female; Heart; Heart attacks; Humans; Hypotheses; Ischemia; Male; Middle Aged; Mortality; Multivariate Analysis; Myocardial Infarction - drug therapy; Myocardial Infarction - epidemiology; Myocardial Infarction - physiopathology; Predictive Value of Tests; Prevalence; Ramipril - therapeutic use; Stroke Volume - physiology; Variance analysis; Ventricular Remodeling - physiology
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/j.jacc.2003.09.069

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. 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. 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. 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. 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.