Savill P. Exacerbations of COPD associated with significant rise in troponin. Practitioner 2013; 257 (1759): 11
Exacerbations of COPD associated with significant rise in troponin
21 Mar 2013
Article
Patients with acute exacerbation of COPD had four-fold higher levels of cardiac troponin T compared with patients with stable disease, in a small Scandinavian study.
This was a cross-sectional study conducted at a teaching and pulmonary rehabilitation clinic in Norway. Consecutive admissions to the participating units for the years 2010–2011 were included if they met standardised criteria for acute exacerbation of COPD and stable COPD. High sensitivity cardiac troponin T was measured in 50 patients hospitalised for acute exacerbations of COPD and compared with levels in 124 patients with stable COPD. This data was used to generate an acute:stable troponin ratio. Multiple linear regression analyses were performed to adjust for covariables in the two groups.
Mean troponin was 25.8 ng/L (95% CI:21.1-31.7) in the acute group compared with 4.55 ng/L (95% CI:3.72-5.67) in the stable group. After inclusion of relevant covariables the acute:stable ratio was 4.26 (95% CI:3.02-6.00).
Higher troponin levels were also associated with the presence of pathological q-waves (P = 0.012) and electrocardiographic left ventricular hypertrophy (P = 0.039), long-term oxygen treatment (P = 0.002) and decreasing FEV1 (P = 0.014).
There was also a 1.41-fold (95% CI:1.20-1.68) increase in troponin for each quartile increase in leucocyte count in patients with stable COPD but not in those with acute exacerbations.
Troponin is a key component in making the diagnosis of myocardial infarction and is used to risk stratify patients with chest pain. It is accepted that other conditions such as acute pulmonary embolism and septicaemia can elevate troponin and now this study, published in Heart, suggests that acute exacerbations of COPD may also elevate troponin.
The authors suggest that these findings may have several possible explanations, such as acute coronary syndrome, pulmonary embolism or acute heart failure which could mimic acute exacerbations of COPD and cause a rise in troponin.
However, none of the patients included in the study were diagnosed with myocardial infarction, pulmonary embolism or acute congestive heart failure at discharge.
Nevertheless, non-ST elevation myocardial infarction with subendocardial infarction cannot be completely excluded in the absence of echo and MR imaging.
The authors conclude that acute exacerbations of COPD are associated with higher troponin T levels than in stable COPD patients. Furthermore, they found that in stable COPD, troponin appears to be positively associated with indices of COPD severity.
This study has limitations such as its small size and cross-sectional design but should alert us to the association between COPD severity and raised troponin particularly in terms of potential erroneous diagnosis of myocardial infarction.
Dr Peter Savill
• Søyseth V, Bhatnagar R, Holmedahl NH et al. Acute exacerbation of COPD is associated with fourfold elevation of cardiac troponin. Heart 2013;99:122-126 doi:10.1136/heartjnl-2012-302685
