Basal and Ischemia-Induced Transcardiac Troponin Release into the Coronary Circulation in Patients with Suspected Coronary Artery Disease |
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| Authors: | Masaaki Konishi Seigo Sugiyama Koichi Sugamura Toshimitsu Nozaki Keisuke Ohba Junichi Matsubara Kenji Sakamoto Yasuhiro Nagayoshi Hitoshi Sumida Eiichi Akiyama Yasushi Matsuzawa Kentaro Sakamaki Satoshi Morita Kazuo Kimura Satoshi Umemura Hisao Ogawa |
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| Institution: | 1. Departments of Cardiovascular Medicine, Faculty of Life Sciences, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.; 2. Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.; 3. Department of Biostatistics and Epidemiology, Yokohama City University Medical Center, Yokohama, Japan.; 4. Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.; S.G.Battista Hospital, Italy, |
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| Abstract: | BackgroundCardiac troponin is a specific biomarker for cardiomyocyte necrosis in acute coronary syndromes. Troponin release from the coronary circulation remains to be determined because of the lower sensitivity of the conventional assay. We sought to determine basal and angina-induced troponin release using a highly sensitive troponin assay.Methods and ResultsThe cardiac troponin T levels in serum sampled from the peripheral vein (PV), the aortic root (AO), and the coronary sinus (CS) were measured in 105 consecutive stable patients with coronary risk factor(s) and suspected coronary artery disease (CAD) and in 33 patients without CAD who underwent an acetylcholine provocation test. At baseline, there was a significant increase in the troponin levels from AO 9.0 (6.4, 13.1) pg/mL for median (25th, 75th percentiles)] to CS 10.3 (7.3, 15.5) pg/mL, p<0.001] in 96 (91.4%) patients and the difference was 1.1 (0.4, 2.1) pg/mL, which reflected basal transcardiac troponin release (TTR). TTR was positively correlated with PV levels (r = 0.22, p = 0.03). Male sex, left ventricular hypertrophy determined by echocardiography, T-wave inversion, and CAD correlated with elevated TTR defined as above: median, 1.1 pg/mL. A significant increase in TTR was noted in 17 patients with coronary spasms 0.6 (0.2, 1.2) pg/mL, p<0.01] but not in 16 patients without spasms 0.0 (−0.5, 0.9) pg/mL, p = 0.73] after the acetylcholine provocation.ConclusionBasal TTR in the coronary circulation was observed in most of the patients with suspected CAD and risk factor(s). This sensitive assay detected myocardial ischemia-induced increases in TTR caused by coronary spasms. |
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