Abstract 17212: High Levels of LDL-C, apoB, and non-HDL-C in Patients With Coronary Microvascular Dysfunction
Introduction: Patients with coronary microvascular dysfunction (CMD) reportedly have high rates of major adverse outcomes, such as death, myocardial infarction, and congestive heart failure. However, the reason why these patients frequently develop major adverse cardiac events remains unknown.
Hypothesis: We assessed the hypothesis that CMD might precede coronary artery disease (CAD).
Methods: In 134 consecutive patients with angiographically normal coronary arteries (% diameter stenosis < 50%), a novel index of microcirculatory resistance (IMR) was measured using a pressure/temperature sensing coronary wire. After inducing maximal hyperemia using an intravenous infusion of adenosine triphosphate (180μg/kg/mL), room-temperature saline was injected into the coronary artery to calculate the IMR. Coronary risk factors, current medications, and blood biomarkers were assessed to evaluate their correlations with the IMR value.
Results: (1) In a multivariate analysis, hypercholesterolemia (hazard ratio [HR], 3.2; P = 0.036) and the use of statin (HR, 0.28; P = 0.025) were significant predictors of a higher IMR value. (2) Significant correlations were observed between the IMR value and the levels of low-density lipoprotein cholesterol (LDL-C) (r = 0.41, P < 0.0001), apolipoprotein B (apoB) (r = 0.38, P < 0.0001), and non-high-density lipoprotein cholesterol (non-HDL-C) (r = 0.32, P = 0.0005). (3) In a receiver operator characteristic analysis of the higher (median) IMR value, the C-statistics were 0.71 for LDL-C (cut-off value, 96 mg/dL), 0.72 for apoB (cut-off value, 80 mg/dL), and 0.69 for non-HDL-C (cut-off value, 125 mg/dL).
Conclusions: These findings suggest that lipid metabolism may have an important role in the development of CMD. Since high levels of LDL-C, apoB, and non-HDL-C increase the risk of CAD, CMD patients might have risk factors that are also seen in patients with CAD, suggesting that CMD might precede CAD.
Author Disclosures: H. Takahashi: None. S. Tani: None. K. Kikushima: None. S. Furuya: None. T. Washio: None. S. Niizuma: None. K. Kawauchi: None. M. Kobori: None. M. Matsuzaki: None. T. Ashida: None. N. Matsumoto: None.
- © 2016 by American Heart Association, Inc.