Basal and ischemia-induced transcardiac troponin release into the coronary circulation in patients with suspected coronary artery disease

PLoS One. 2013;8(4):e60163. doi: 10.1371/journal.pone.0060163. Epub 2013 Apr 2.

Abstract

Background: Cardiac 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 results: The 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 (25(th), 75(th) 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.

Conclusion: Basal 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology
  • Aged
  • Biomarkers / blood
  • Coronary Artery Disease / blood*
  • Coronary Artery Disease / complications
  • Coronary Circulation*
  • Coronary Vessels / drug effects
  • Female
  • Humans
  • Male
  • Middle Aged
  • Myocardial Ischemia / blood*
  • Myocardial Ischemia / etiology
  • Risk Factors
  • Troponin T / blood*

Substances

  • Biomarkers
  • Troponin T
  • Acetylcholine

Grants and funding

This study was supported in part by a grant-in-aid for scientific research (grant number C22590786 for S. Sugiyama) from the Ministry of Education, Science, and Culture in Japan, and a grant for clinical vascular function (for M. Konishi) from the Kimura Memorial Heart Foundation-Bayer. The Ministry of Education, Science, and Culture in Japan and the Kimura Memorial Heart Foundation-Bayer had no role in the design, implementation, and reporting of the study and drafting of the manuscript (apart from their financial contributions).