Published online before print August 19, 2002, doi: 10.1161/01.CIR.0000032313.82552.E3
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(Circulation. 2002;106:1251.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
Ventricular Remodeling Does Not Accompany the Development of Heart Failure in Diabetic Patients After Myocardial Infarction
From the Cardiovascular Division (S.S., H.S., E.B., M.P.), Department of Medicine, Brigham and Women’s Hospital, Boston, Mass; Cardiovascular Division (M.S., T.P.), University of Pennsylvania, Philadelphia, Pa; School of Public Health (L.M.), University of Texas, Houston, Tex; Cardiovascular Division (J.R.), University of Toronto Health Network, Toronto, Ontario; and Division of Cardiology (G.A.L.), Mt Sinai Medial Center, Miami Beach, Fla.
Correspondence to Scott D. Solomon, MD, Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail ssolomon{at}rics.bwh.harvard.edu
Background— Diabetic patients are at increased risk for heart failure (HF) and other adverse events after myocardial infarction (MI). Left ventricular (LV) enlargement after MI is also associated with the same increased risk. We used data from the Survival and Ventricular Enlargement (SAVE) echocardiographic substudy to test the hypothesis that diabetes was associated with increased LV enlargement after MI.
Methods and Results— Four hundred twelve nondiabetic and 100 diabetic patients underwent echocardiographic assessment at baseline and 3 months, 1 year, and 2 years after MI. HF developed in 30% of diabetic and 17% of nondiabetic patients during follow-up (P<0.001). Baseline LV diastolic size, ejection fraction, and infarct segment length were similar between diabetic and nondiabetic patients. Diabetic patients demonstrated less LV enlargement between baseline and 2 years than nondiabetic patients (0.9±11.1 cm2 versus 3.8±10.9 cm2, P=0.047). In patients who developed HF, LV diastolic dilatation (10.0±12.4 cm2 versus 3.7±13.1 cm2, P=0.06) and systolic dilatation (4.6±11.8 versus 0.91±12.1, P=0.017) were greater in nondiabetic than in diabetic patients. LV dilatation between baseline and 2 years was a predictor of HF in nondiabetic patients, but not in diabetic patients, even after excluding patients with recurrent MI and adjusting for history of hypertension, prior MI, age, treatment group, and smoking. Diabetes modified the relationship between ventricular enlargement and the risk of HF (P=0.011).
Conclusions— The increased incidence of HF after MI in diabetic patients is not explained by a greater propensity for LV remodeling.
Key Words: diabetes mellitus • heart failure • remodeling • myocardial infarction
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