Causes of elevated cardiac troponin I in patients with normal coronary angiogram.
- Author:
Woo Hyung BAE
1
;
Kook Jin CHUN
;
Jun Hyok OH
;
Dong Won LEE
;
Byung Jae AHN
;
Seong Ho KIM
;
Joon Sang LEE
;
Moo Young KIM
;
Hyeon Gook LEE
;
Woo Seog KO
;
Yong Hyun PARK
;
Jun KIM
;
June Hong KIM
;
Taek Jong HONG
;
Yung Woo SHIN
Author Information
1. Department of Internal Medicine, Pusan National University College of Medicine, Busan, Korea. ptca82@hotmail.com
- Publication Type:Original Article
- Keywords:
Coronary angiography;
Myocardial infarction;
Troponin;
Troponin I
- MeSH:
Atrial Fibrillation;
Cerebral Infarction;
Coronary Angiography;
Coronary Artery Disease;
Follow-Up Studies;
Heart Failure;
Hemodynamics;
Humans;
Ischemia;
Myocardial Infarction;
Myocarditis;
Organ Specificity;
Pericarditis;
Retrospective Studies;
Rhabdomyolysis;
Tachycardia;
Tachycardia, Paroxysmal;
Tachycardia, Supraventricular;
Tachycardia, Ventricular;
Troponin I*;
Troponin*
- From:Korean Journal of Medicine
2005;69(5):487-492
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Cardiac troponin I (cTnI) is most recently described and has nearly absolute myocardial tissue specificity, as well as high sensitivity. But an increased value for cTnI that indicates myocardial injury is not always synonym of myocardial infarction or ischemia due to coronary artery disease. METHODS: Retrospective follow-up study for whom underwent coronary angiography for suspected coronary artery disease was done if they had an elevated cTnI value and angiographically normal or minimal disease. RESULTS: 33 patients were qualified. Cut-off value for elevated cTnI was 0.06 ng/mL. Increased cTnI values were attributed to severe congestive heart failure in 7 patients, variant angina in 7 patients, myocarditis in 5 patients, pericarditis in 1 patient, severe myocardial bridge in 1 patient, rhabdomyolysis in 1 patient and cerebral infarction in 1 patient. Tachycardia was precipitating cause in 4 patients (sinus tachycardia, paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation and sustained ventricular tachycardia for each), two of whom had hemodynamic compromise. 2 of 33 patients had no identifiable cause for a rise in cTnI value. There was no acute myocardial infarction at 42+/-34 weeks follow-up. CONCLUSIONS: Although cTnI is a sensitive and specific marker of myocardial injury, an elevation of cTnI value may have a cause other than myocardial infarction or ischemia and may occur without significant angiographic coronary artery disease.
