BACKGROUND: The aim of the prospective Homburg Cream and Sugar study was to analyze the role of fasting and postprandial serum triglycerides (TG) as risk modifiers in patients with coronary artery disease (CAD). METHODS AND RESULTS: A sequential oral triglyceride and glucose tolerance test was developed to obtain standardized measurements of postprandial TG kinetics and glucose in 514 consecutive patients with stable CAD confirmed by angiography (95% were treated with a statin). Fasting and postprandial TG predicted the primary outcome measure of cardiovascular death and hospitalizations after 48 months follow-up (fasting TG >150 vs. <106 mg/dl: Hazard ratio (HR) 1.79, 95% confidence interval (CI) 1.31-2.45, p = 0.0001; area under the curve >1120 vs. <750 mg/dl/5 hr: HR 1.78, 95% CI 1.29-2.45, p = 0.0003). Parameters of the postprandial TG increase did not improve risk prediction compared to fasting TG. The number of cardiovascular deaths and myocardial infarctions was higher in the upper tertile of fasting TG (HR 1.79, 95%-CI 1.04-3.09, p = 0.03). Risk prediction by TG was independent of traditional risk factors, medication, glucose metabolism, LDL- and HDL-cholesterol. Total cholesterol, LDL- and HDL-cholesterol concentrations were not associated with the primary outcome. CONCLUSIONS:Fasting serum triglycerides >150 mg/dl independently predict cardiovascular events in patients with coronary artery disease on guideline-recommended medication. Assessment of postprandial TG does not improve risk prediction compared to fasting TG in these patients.
RCT Entities:
BACKGROUND: The aim of the prospective Homburg Cream and Sugar study was to analyze the role of fasting and postprandial serum triglycerides (TG) as risk modifiers in patients with coronary artery disease (CAD). METHODS AND RESULTS: A sequential oral triglyceride and glucose tolerance test was developed to obtain standardized measurements of postprandial TG kinetics and glucose in 514 consecutive patients with stable CAD confirmed by angiography (95% were treated with a statin). Fasting and postprandial TG predicted the primary outcome measure of cardiovascular death and hospitalizations after 48 months follow-up (fasting TG >150 vs. <106 mg/dl: Hazard ratio (HR) 1.79, 95% confidence interval (CI) 1.31-2.45, p = 0.0001; area under the curve >1120 vs. <750 mg/dl/5 hr: HR 1.78, 95% CI 1.29-2.45, p = 0.0003). Parameters of the postprandial TG increase did not improve risk prediction compared to fasting TG. The number of cardiovascular deaths and myocardial infarctions was higher in the upper tertile of fasting TG (HR 1.79, 95%-CI 1.04-3.09, p = 0.03). Risk prediction by TG was independent of traditional risk factors, medication, glucose metabolism, LDL- and HDL-cholesterol. Total cholesterol, LDL- and HDL-cholesterol concentrations were not associated with the primary outcome. CONCLUSIONS: Fasting serum triglycerides >150 mg/dl independently predict cardiovascular events in patients with coronary artery disease on guideline-recommended medication. Assessment of postprandial TG does not improve risk prediction compared to fasting TG in these patients.
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