Abstract 18400: Distinct Endothelial Function in Patients With Chronic Total Occlusion With Preserved Myocardial Viability
Backgrounds: Coronary collateral vessels work as a detour and ameliorate ischemic myocardial damage. Induction or enhancement of the collateral growth is a novel therapeutic strategy for the ischemic heart disease, however their mechanisms are almost unknown. Patients with chronic total occlusion (CTO) who keep the intact myocardium maintain rich collateral sources, which perfuse the area of the occluded artery. We tried to assess the characteristics of patients with CTO compared with non-occlusive patients with ischemic heart disease and those with old myocardial infarction (OMI).
Methods: Consecutive 264 patients from January 2010 to February 2014 were enrolled this study. First we assessed the myocardial viability using summed rest score (SRS) of thallium perfusion scintigraphy and divided into OMI patients (SRS greater than or equal to 4, OMI group, n=99) and the others with almost normal myocardial viabilities (n=165). Next we divided into CTO group (n=51) and Stenosis group (n=114) from the coronary angiographic findings. We also measured their peripheral endothelial function by reactive hyperemia peripheral arterial tonometry index (RHI).
Results: There were no significant differences between CTO group and Stenosis group in clinical characteristics. Ln-RHI was lowest in the OMI group (OMI 0.53±0.21), furthermore, CTO group showed higher endothelial function than Stenosis group (CTO 0.71±0.21 vs Stenosis 0.63±0.23, p<0.05). Multivariate logistic regression analysis identified high Ln-RHI as an independent factor associated with the presence of CTO (OR 2.523, 95% CI 1.119-5.687, p<0.05) among preserved myocardial patients. Other factors did not show the statistical significance.
Conclusion: Patient with CTO showed paradoxically high Ln-RHI values in spite of the existence of the total occlusion vessel. Enhanced endothelial function might promote the collateral vessel growth and protect myocardium from the irreversible damage.
Author Disclosures: Y. Arima: None. S. Hokimoto: None. S. Tayama: None. S. Iwashita: None. T. Akasaka: None. N. Tabata: None. K. Sakamoto: None. K. Tsujita: None. E. Yamamoto: None. T. Tanaka: None. S. Kojima: None. K. Kaikita: None. H. Ogawa: Honoraria; Modest; AstraZeneca, Bayer, Pfizer, Sanofi, Takeda. Honoraria; Significant; Daiichi Sankyo, MSD. Other; Modest; AstraZeneca, Astellas, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Dainippon Sumitomo Pharma, Kowa, MSD, Novartis, Pfizer, Sanofi, Takeda. Other; Significant; Bayer, Chugai, Otsuka.
- © 2014 by American Heart Association, Inc.