Cor Vasa 2017, 59(3):e229-e234 | DOI: 10.1016/j.crvasa.2016.12.001

Troponin levels in patients with stable CAD

Josef Daněk^a,*, Tomáš Hnátek^a, Martin Malý^a, Miloš Táborský^b, Jaromír Běláček^c, Jan Škvařil^a, Lenka Pospíšilová^d, Miroslav Černohous^a, Pavel Sedloň^a, Martin Hajšl^a, Miroslav Zavoral^a

^a Kardiologické oddělení, Interní klinika, 1. lékařská fakulta Univerzity Karlovy a Ústřední vojenská nemocnice - Vojenská fakultní nemocnice Praha, Praha, Česká republika

^b I. interní klinika - kardiologická, Lékařská fakulta Univerzity Palackého a Fakultní nemocnice Olomouc, Olomouc, Česká republika

^c Ústav biofyziky a informatiky, 1. lékařská fakulta Univerzity Karlovy, Praha, Česká republika

^d Oddělení klinické biochemie, Ústřední vojenská nemocnice - Vojenská fakultní nemocnice Praha, Praha, Česká republika

Introduction: Cardiac troponins are known as specific markers of myocardial damage. Their elevation in the serum is not always related to acute myocardial ischemia. The increased sensitivity of diagnostic kits has resulted in an increase in the number of positive results in patients without acute coronary syndrome (ACS).
Study objectives: To determine the level of highly sensitive troponin T (hsTnT) in stable patients (without ACS) before selective coronarography (SCG) and to determine the correlation between hsTnT values and the extent of atherosclerotic damage to the coronary arteries.

Methodology: We studied a group of 251 consecutive patients with indications for SCG diagnosis. Indication criteria were stable angina pectoris, shortness of breath, newly diagnosed heart failure, syncope, and ventricular arrhythmia. Exclusion criteria were acute coronary syndrome, including unstable angina pectoris, prior cardiopulmonary resuscitation, cerebrovascular accident (CVA) within the last 6 months, and ongoing sepsis. The hsTnT value was determined before SCG (normal range, 0-0.013 mg/l). Monitored parameters included coronary angiography (70% stenosis of coronary artery diameter was considered significant coronary disease), age, gender, heart rate, and serum creatinine levels. The study included 182 patients with normal renal function and 69 patients with renal insufficiency. The results were processed using STATISTICA (version 12), StatSoft©, Inc. (2013).

Results: The average age of the studied population was 69.6 ± 10.3 years (median, 70 years); 33% of patients were women. The serum level of hsTnT for the entire population was 0.031 ± 0.091 mg/l (0.014). A positive hsTnT was noted in 133 patients. The population study group consisted of 121 patients with normal coronary arteries or with insignificant atherosclerotic disease. Significant damage involving one or more arteries was present in 130 patients. In the subgroup with significant coronary disease, we found a significantly higher hsTnT level than in the group of patients without significant coronary disease: 0.043 ± 0.125 mg/l (0.018) vs. 0.019 ± 0.018 mg/l (0.013) (p = 0.008) (Mann-Whitney test).
Significantly higher troponin levels were found in the group of patients with renal insufficiency than in the subgroup with normal creatinine levels: 0.057 ± 0.150 mg/l (0.023) vs. 0.022 ± 0.053 mg/l (0.012), respectively (p < 0.05) (Mann-Whitney test).

Conclusion: Slightly elevated serum troponin T levels are common in patients with stable coronary artery disease (CAD). We observed a significant correlation between the level of troponin and the presence of atherosclerotic damage to the coronary arteries. A significant correlation between the value of troponin and the extent of atherosclerotic damage (in terms of the number of damaged arteries) could not be demonstrated. On the basis of our findings, the absolute level of troponin T in patients with stable CAD must be interpreted with caution, especially in patients who also have renal insufficiency. Determination of basal troponin T levels in patients with stable CAD is reasonable as they may be used for comparison in case of change in a patient's clinical condition.

Keywords: Selective coronarography; Stable angina pectoris; Troponin

Received: June 25, 2016; Revised: December 8, 2016; Accepted: December 9, 2016; Published: June 1, 2017  Show citation