Abstract 16210: Stratified Coronary Restenosis Risk by Aldehyde Dehydrogenase Polymorphism and Endotherial Function
Background: Endothelial dysfunction is considered as an independent factor that influences clinical outcome in coronary artery disease patients (CAD). Endothelial dysfunction is associated with increased oxidative stress, and recently mitochondrial aldehyde dehydrogenase 2 (ALDH2*2) polymorphism has been reported to cause decreased ALDH2 activity, increased reactive aldehydes, and increased reactive oxygen species. Thus in the present study, we examined the role and the interaction of endothelial function and ALDH2 variant in cardiovascular outcomes.
Methods: Consecutive 158 patients requiring percutaneous coronary intervention were enrolled. ALDH2 variant is defined having the ALDH2 *2 allele (*1/*2 or *2/*2). We assessed peripheral endothelial function by reactive hyperemia-peripheral arterial tonometry (RH-PAT) using the EndoPAT2000 system, and divided patients into low- and high- RHI groups using the median value of the natural logarithm of RH-PAT index (Ln-RHI). Clinical outcome in the present study was the target lesion revascularization (TLR).
Results: There were 88 (55.7%), 54 (34.2%) and 16 (10.1%) patients with regard to *1/*1, *1/*2 and *2/*2 ALDH2 genotypes. There was no significant difference in Ln-RHI among them (0.52 ± 0.21, 0.56 ± 0.22, and 0.62 ± 0.25; P = 0.26, respectively). A total of 30 patients suffered a cardiovascular event. Kaplan-Meyer analysis showed a significant higher probability of clinical outcome in low RHI patients than high RHI patients in the ALDH2 variant group (log-rank test: P=0.023), but there was no significant difference in the ALDH2 non-variant group (log-rank test: P=0.704). In the ALDH2 variant group, multivariate Cox hazard analysis among various clinical factors found low RHI as a significant and independent predictor of clinical outcome (hazard ratio, 5.34; 95% confidence interval, 1.41-20.2; P=0.014). The interaction between ALDH2 variant and low RHI was significant (P=0.051).
Conclusion: The present study demonstrated a possible contribution of ALDH2 polymorphism to the risk stratification of TLR in patients with endothelial dysfunction.
Author Disclosures: T. Yamashita: None. S. Hokimoto: None. D. Sueta: None. N. Tabata: None. T. Akasaka: None. Y. Arima: None.
- © 2016 by American Heart Association, Inc.