title: Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial.
abstract: BACKGROUND
  We quantified cardiovascular death and/or left ventricular (LV) dilatation in patients from the SAVE trial to determine whether dilatation continued beyond 1 year, whether ACE inhibitor therapy attenuated late LV dilatation, and whether any baseline descriptors predicted late dilatation.
  
  
  RESULTS
  Two-dimensional echocardiograms were obtained in 512 patients at 11+/-3 days and 1 and 2 years postinfarction to assess LV size, percentage of the LV that was akinetic/dyskinetic (%AD), and LV shape index. LV function was assessed by radionuclide ejection fraction. Two hundred sixty-three patients (51.4%) sustained cardiovascular death and/or LV diastolic dilatation; 279 (54.5%) had cardiovascular death and/or systolic dilatation. In 373 patients with serial echocardiograms, LV end-diastolic and end-systolic sizes increased progressively from baseline to 2 years (both P<.01). More patients with LV dilatation had a decrease in ejection fraction: 24.8% versus 6.8% (P<.001) (diastole) and 25.7% versus 5.3% (P<.001) (systole). Captopril attenuated diastolic LV dilatation at 2 years (P=.048), but this effect was carried over from the first year of therapy because changes in LV size with captopril beyond 1 year were similar to those with placebo. Predictors of cardiovascular death and/or dilatation were age (P=.023), prior infarction (P<.001), lower ejection fraction (P<.001), angina (P=.007), heart failure (P=.002), LV size (P<.001), and infarct size (%AD) (P<.001).
  
  
  CONCLUSIONS
  Cardiovascular death and/or LV dilatation occurred in >50% of patients by 2 years. LV dilatation is progressive, associated with chamber distortion and deteriorating function that is unaffected by captopril beyond 1 year.
authors.affiliation: Brigham and Women's Hospital, Harvard Medical School, Boston, Mass, USA.
authors.forename: M
authors.initials: M
authors.lastname: St John Sutton
authors.forename: M A
authors.initials: MA
authors.lastname: Pfeffer
authors.forename: L
authors.initials: L
authors.lastname: Moye
authors.forename: T
authors.initials: T
authors.lastname: Plappert
authors.forename: J L
authors.initials: JL
authors.lastname: Rouleau
authors.forename: G
authors.initials: G
authors.lastname: Lamas
authors.forename: J
authors.initials: J
authors.lastname: Rouleau
authors.forename: J O
authors.initials: JO
authors.lastname: Parker
authors.forename: M O
authors.initials: MO
authors.lastname: Arnold
authors.forename: B
authors.initials: B
authors.lastname: Sussex
authors.forename: E
authors.initials: E
authors.lastname: Braunwald
mesh_terms: D002216:Captopril / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000401:mortality*; D004452:Echocardiography; D005544:Forecasting; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D016019:Survival Analysis; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D002216:Captopril