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Cardiac structure and function, remodeling, and clinical outcomes among patients with diabetes after myocardial infarction complicated by left ventricular systolic dysfunction, heart failure, or both

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AMERICAN HEART JOURNAL
卷 162, 期 4, 页码 685-691

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MOSBY-ELSEVIER
DOI: 10.1016/j.ahj.2011.07.015

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  1. Novartis Pharmaceuticals

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Aims The mechanisms responsible for the increased risk of heart failure (HF) post-myocardial infarction (MI) may differ between patients with versus without diabetes. We hypothesized that after high-risk MI, patients with diabetes would demonstrate patterns of remodeling that are suggestive of reduced ventricular compliance and that are associated with an increased risk of death or HF. Methods and Results We performed quantitative echocardiographic analysis in 153 patients with diabetes and 451 patients without diabetes enrolled in the VALIANT Echo study. Diabetes was associated with a higher risk of death or HF in age-adjusted models (hazard ratio 1.44, 95% CI 1.04-2.00, P = .028). Diabetic patients were similar to nondiabetic patients with respect to left ventricular (LV) volume and ejection fraction but had higher LV mass index (104.1 +/- 27.5 vs 97.1 +/- 28.6 g/m(2), P = .009), relative wall thickness (0.41 +/- 0.08 vs 0.38 +/- 0.07, P < .0001), and left atrial volume index (LAVi) (26.2 +/- 8.1 vs 24.0 +/- 8.2 mL/m(2), P = .008)-all parameters that were significantly related to the risk of death or HF hospitalization. Changes in LV volume and ejection fraction from baseline to 20 months were not different, although diabetic patients demonstrated greater increase in LAVi (4.4 +/- 7.7 vs 2.2 +/- 6.7 mL/m(2), P = .01). Conclusions After high-risk MI, diabetic patients were at higher risk of death or HF and demonstrated greater baseline LV mass index, relative wall thickness, and LAVi as well as greater left atrial enlargement at 20-month follow-up. These findings suggest greater baseline concentric remodeling and long-term elevation in LV diastolic pressure post-MI among diabetic patients, which may partially mediate this risk. (Am Heart J 2011;162:685-91.)

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