The Clinical Significance of Serial Measurement of Cardiac Troponin-T after Percutaneous Transluminal Coronary Angioplasty(PTCA).
10.4070/kcj.1995.25.2.434
- Author:
Young Cheoul DOO
;
Young Il SEO
;
Jae Myung LEE
;
Rok Yun LEE
;
Soon Hee KOH
;
Chong Yun RIM
;
Young Bahk KOH
;
Young LEE
- Publication Type:Original Article
- Keywords:
PTCA;
Myocardial injury;
Cardiac Troponin-T
- MeSH:
Angina, Unstable;
Discrimination (Psychology);
Electrocardiography;
Humans;
Immunoenzyme Techniques;
Inflation, Economic;
Myocardial Infarction;
Troponin T*;
Ventricular Dysfunction, Left
- From:Korean Circulation Journal
1995;25(2):434-438
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: During and immediately after percutaneous transluminal coronary angioplasty(PTCA), reversible ischemic electrocardiographic change and/of left ventricular dysfunction are developed. But it is not investigated whether there are potential myocardial cell damages following PTCA or not, and the clinical Significance of myocardial cell damage following PTCA. Recently cardiac Troponin-T has been developed as a new myocardial specific marker, especially myocardial damage. The object of this study is to investigate whether potential Myocardial damage following PTCA was occurred and the utility of cardiac Tropoin-T for predicting the complications during and immediately after PTCA. METHODS: The study group comprised 12 patients(M/F;8/4mean age;60 +/- 4year,AMI in 6) undergoing PTCA, Samples for Troponin-T were obtained before, directly after, after 2 hours, 6 hours, and after 12 hours and was determined by enzyme immunoassay on an ES 300 analyzer(Boehringer Mannheim). Discrimination limit for myocardial cell damage is 0.1 ng/ml in normal baseline level but if the baseline level is elevated such as acute myocardial infarction or unstable angina, myocardial cell damage is defined with further increase of cardiac Troponin-T(>0.1 ng/ml) compare to baseline level. RESULTS: 1) The mean duration of total balloon inflation is 10.7 +/- 2(3-22) minutes and the mean duration of single maximal inflation is 3.9 +/- 0.6(1-8) minutes. There are no significant change in concentration of Troponin-T by inflation time. None of the patients showed electroca rdiographic evidence for myocardial infarction. 2) Troponin-T were increased in 2 patients with unstable angina(0.01 vs 0.11 ng/ml) which were developed major dissection including acute closure during PTCA, and 2 patients with acute myocardial infarction(2.37 vs 3.73 ng/ml) which didn't developed dcomplication. The increase of cardiac Troponin-T were observed in 2 of 10 patients with uncomplicated PTCA(20%). 3)The subacute complications were not developed. CONCLUSION: The cardiac Troponin-T were increased significantly in two AMI patients with uncomplicated PTCA(2/10,20%). The increase of cardiac Troponin-T following PTCA is associated with periprocedural complications but the prognostic significance to detect postprocedural complication did not define in this study because there were no subacute complications after PTCA and may be limited value due to time course of complication(usaully within 1 hour after PTCA) and relatively long analytic time.
