Abstract 561: Ultrasonic Evaluated Endothelial Dysfunction Highly Predicts Future Diabetic Evolution and Development of Adverse Cardiovascular Events or Fatal Events
Background and hypothesis: Although diabetes mellitus (DM) and endothelial dysfunction (ED) are thought to affect atherogenic processes, we know little about the clinical impact of ED on evolutional mechanisms of DM and the related cardiovascular events. This study assessed hypothesis that ED accelerates diabetic evolution (DME).
Methods: ED was graded by reactive changes in lumen diameter of right brachial artery following transient forearm occlusion (FMD; flow-mediated endothelium-dependent vasodilation) in consecutive 518 patients with suspected coronary artery disease using high-resolution ultrasonography. The enrolled patients were categorized into 3 groups according to the values of FMD, and their glucose tolerance and adverse clinical events were followed-up for 36 months or more. We prospectively followed up DME, which was defined as newly diagnosed DM by 75g-OGTT or new administration of an antidiabetic agent.
Results: For a mean follow-up period of 60 months with 100% follow-up, the patients with severe ED (FMD<4%; Group-L, n=174), more frequently manifested DME, cardiovascular events (CVE), and any fatal events, compared to those in Group-M with mild ED (4%≤FMD<8%, n=171) or Group-H with preserved endothelial function (FMD 8% or more, n=173), [p<0.001, by Kaplan-Meier analysis]. HbA1c significantly elevated in Group-L (p=0.009) but not in Group-M or Group-H. Cox proportional hazard model analysis including clinical variables showed that severe ED was a significant predictor for future DME (hazard ratio=2.69, 95%confidential interval; 1.73– 4.77, p=0.011), CVE (hazard ratio=3.75, 95%confidential interval; 2.07– 6.78, p<0.001), and all-causal death (hazard ratio=5.87, 95%confidential interval; 1.26 –72.25, p=0.009).
Conclusion: This is the first clinical ultrasonic vascular investigation demonstrating endothelial dysfunction accelerates diabetic evolution and causes excess of adverse cardiovascular events or fatal events.