CLINICAL RESEARCH: CORONARY ARTERY DISEASE
Angina pectoris prior to myocardial infarction protects against subsequent left ventricular remodeling
Scott D. Solomon, MD, FACC*,*,
Nagesh S. Anavekar, MBBS (Hons), FRACP*,
Sally Greaves, MD ,
Jean L. Rouleau, MD, FACC ,
Charles Hennekens, MD ,
Marc A. Pfeffer, MD, PhD, FACC* HEART Investigators
* Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
Green Lane Hospital, Auckland, New Zealand
Cardiovascular Division, University of Toronto Health Network, Toronto, Canada
University of Miami, Boca Raton, Florida, USA
Manuscript received July 18, 2003;
revised manuscript received September 12, 2003,
accepted September 23, 2003.
* Reprint requests and correspondence: Dr. Scott D. Solomon, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA.
ssolomon{at}rics.bwh.harvard.edu
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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Abbreviations and Acronyms
| | CK | = creatine kinase | | HEART | = Healing and Early Afterload Reducing Therapy trial | | LV | = left ventricle/ventricular | | MI | = myocardial infarction |
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