- Poster presentation
- Open Access
Diabetes remains an independent risk factor for adverse remodeling following acute myocardial infarction even with quantification of total infarct size and change in myocardial extracellular volume fraction by CMR
© Heydari et al; licensee BioMed Central Ltd. 2013
- Published: 30 January 2013
- Acute Myocardial Infarction
- Adverse Remodel
- National Heart Lung
- Diabetic Heart Disease
- Alberta Heritage Foundation
Diabetes (DM) has important implications on LV remodeling and prognosis following acute myocardial infarction (MI). We explored the impact of diabetic heart disease independent of traditional risk factors, infarct size, and myocardial extracellular volume fraction (MECVF).
We prospectively studied 105 patients with acute MI from the ongoing PROSPECT-CMR clinical trial. Subjects underwent CMR 2 to 4 weeks following MI with follow-up scan at 6-months. Presence of diabetes was determined by history and laboratory testing. Total infarct size was calculated according to previously described full width half-maximum method. MECVF was quantified by serial sampling of T1 ratios of myocardium remote from infarct and blood pool corrected for hematocrit. Sampling was performed in 5-minute intervals beginning 5 minutes and ending 30 minutes after contrast administration from 3 parallel short-axis slices of the heart. Adverse remodeling was defined as a positive change in left ventricular diastolic volume index of greater than 10% at follow-up.
Baseline Characteristics and Change in MECVF stratified by Presence of DM (n=105)
Hx Coronary Artery Disease
Total Infarct Size (g)
Change in mean segmental MECVF
Diabetics represent a particularly high risk cohort following acute MI. Our results revealed that presence of DM was an independent risk factor for adverse LV remodeling, including baseline clinical variables, LVEF, change in total infarct size and mean segmental MECVF. We postulate that there are independent mechanisms for adverse remodeling in diabetics, such as genetic predisposition and inflammation, that contribute to adverse remodeling following acute infarction.
National Heart Lung and Blood Institute, National Institutes of Health (RO1-HL091157).
Dr. Heydari's salary is supported by the Alberta Heritage Foundation for Medical Research.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.