Diabetes Care · 2013 · 12 citations · 22 references
MedicineCardiologyInternal MedicineClinical CardiologyDiabetologyPreventive CardiologyAcute Coronary SyndromesCardiac BiomarkersCardiac Risk AssessmentCardiovascular DiseaseCardiovascular RiskMyocardial Infarction ComplicationsCardiovascular Risk DetectionCoronary Ct AngiographyDiabetes-associated Cardiac RiskDiagnostic Cut-off ThresholdsDiagnostic Cut-offsMyocardial Injury DetectionTroponin ElevationTroponin Release
OBJECTIVE: To investigate the relationship between different degrees of subclinical myocardial necrosis, glycemic control, and long-term adverse clinical outcomes within a stable patient population with diabetes mellitus. RESEARCH DESIGN AND METHODS: We examined 1,275 stable patients with diabetes mellitus undergoing elective diagnostic coronary angiography with cardiac troponin I (cTnI) levels below the diagnostic cut-off for defining myocardial infarction (MI) (<0.03 ng/mL). The relationship of subclinical myocardial necrosis (cTnI 0.009-0.029 ng/mL) with incident major adverse cardiovascular events (MACE; defined as any death, MI, or stroke) over 3 years of follow-up was examined. RESULTS: Subclinical myocardial necrosis was observed in 22% of patients. A strong association was observed between the magnitude of subclinical myocardial necrosis and risk of 3-year incident MACE (hazard ratio, 1.98; 95% confidence interval, 1.48-2.65; P < 0.001) and remained statistically significant even after adjustment for traditional risk factors, high-sensitivity C-reactive protein, and creatinine clearance. Only a weak correlation was observed between the presence of subclinical myocardial necrosis and either glycemic control (r = 0.06; P = 0.044 for hemoglobin A1c versus cTnI) or insulin resistance (r = 0.04; P = 0.094 for glucose-to-insulin ratio versus cTnI). CONCLUSIONS: The presence of detectable subclinical myocardial necrosis in stable patients with diabetes mellitus is associated with heightened long-term risk for MACE, independent of traditional risk factors and glycemic control.
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