[Troponin release following exercise test in patients with stable angina pectoris - risk factors and prognostic
Piotr Kokowicz1, Sebastian Stec, Katarzyna Flasińska
1Postgraduates Medical School, Warsaw, Poland. kokowicz@kkcmkp.pl
Insights
Troponin I (cTnI) release after exercise testing (ExT) in stable coronary artery disease (CAD) patients is linked to lower ejection fraction and high blood pressure. This cTnI increase does not predict future cardiac events or mortality.
Area of Science:
- Cardiology
- Clinical Diagnostics
- Exercise Physiology
Background:
- Cardiac troponin (cTn) elevation indicates myocardial injury from various causes.
- Exercise testing (ExT) aids in predicting myocardial ischemia risk, particularly in multivessel coronary artery disease (CAD), but has limitations in sensitivity and specificity.
Purpose of the Study:
- To investigate the causes of troponin I (cTnI) release following ExT.
- To assess the clinical and prognostic significance of cTnI release in stable CAD patients undergoing elective coronary angiography (ANG).
Main Methods:
- 118 stable CAD patients without systolic heart failure underwent baseline NT-proBNP, hsCRP, cTnI, and CK-MB measurements.
- Maximal ExT was performed, followed by cTnI and CK-MB measurements at 12 and 24 hours.
- Coronary angiography, echocardiography, and a mean 35.5-month follow-up were conducted.
Main Results:
- cTnI elevation (≥0.14 ng/mL) occurred in 9% of patients 24 hours post-ExT.
- Predictors of cTnI release included ejection fraction ≤50%, low physical activity, and peak systolic blood pressure >160 mm Hg.
- Post-ExT cTnI increase did not correlate with multivessel CAD or adverse clinical events.
Conclusions:
- cTnI release post-ExT in stable CAD is associated with reduced ejection fraction, low physical activity, and high peak systolic blood pressure.
- Elevated cTnI after ExT in this cohort showed no correlation with coronary artery disease extent.
- Post-ExT cTnI elevation had no prognostic value for future adverse cardiovascular events or mortality.
Background:
Increase of troponin (cTn) is a marker of myocardial injury caused by different mechanisms. Exercise testing (ExT) is a useful clinical tool in predicting the risk of myocardial ischemia, especially in patients with multivessel coronary artery disease (CAD), who are more often endangered by medical complications. The test is however limited by its low sensitivity and specificity.
Aim:
To evaluate the reasons for troponin I (cTnI) release after ExT, and to determine its clinical and prognostic implications in patients with stable CAD, referred for elective coronary angiography (ANG).
Methods:
118 patients without signs of systolic heart failure, referred for planned coronary ANG were included in the analysis. After baseline measurements of NT-proBNP, hsCRP, cTnI, CK-MB levels, maximal ExT was performed, followed by the consecutive measurements of cTnI and CK-MB 12 and 24 hours after examination. All patients underwent coronary ANG and ECHO within 7 days of taking blood samples. All patients were followed up on average for 35.5 months.
Results:
The cTnI elevation > or = 0.14 ng/mL (> or = 99th percentile value of the reference group) after 24 hours of the ExT was observed in 11 (9%) patients. Predictors of cTnI release in patients after ExT were as follows: ejection fraction < or = 50%, lack or insufficient physical activity, max systolic blood pressure > 160 mm Hg at peak of ExT (OR 6.6, 95% CI 1.2-35.4, p = 0.027; OR 5.5, 95% CI 1.1-28.8, p = 0.04; OR 6.3, 95% CI 1.3-31.6, p = 0.025, respectively). Increase of cTnI after ExT did not correlate with multivessel CAD nor with future adverse clinical events.
Conclusions:
The cTnI release post ExT is more frequently observed in patients with stable CAD with ejection fraction < or = 50%, low physical activity, and max systolic blood pressure > 160 mm Hg at peak ExT. Post ExT cTnI increase in patients with stable CAD did not correlate with the number of atherosclerotic coronary vessels, and had no prognostic implications. Increase of cTnI after ExT did not have any predictive value in respect to acute coronary syndrome and/or death during long-term follow up.
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