title: Angina pectoris prior to myocardial infarction protects against subsequent left ventricular remodeling.
abstract: OBJECTIVE
  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.
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ssolomon@rics.bwh.harvard.edu
authors.forename: Scott D
authors.initials: SD
authors.lastname: Solomon
authors.forename: Nagesh S
authors.initials: NS
authors.lastname: Anavekar
authors.forename: Sally
authors.initials: S
authors.lastname: Greaves
authors.forename: Jean L
authors.initials: JL
authors.lastname: Rouleau
authors.forename: Charles
authors.initials: C
authors.lastname: Hennekens
authors.forename: Marc A
authors.initials: MA
authors.lastname: Pfeffer
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D003920:Diabetes Mellitus / Q000453:epidemiology / Q000503:physiopathology; D004311:Double-Blind Method; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D011237:Predictive Value of Tests; D015995:Prevalence; D017257:Ramipril / Q000627:therapeutic use; D013318:Stroke Volume / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D003402:Creatine Kinase; D017257:Ramipril