A study of patients with stable chronic obstructive pulmonary disease (COPD) found acute exacerbations in COPD (AECOPD) and pneumonia were associated with increased levels of high-sensitivity cardiac troponin T (hs-cTnT). Findings of the study, which were recently published in BMJ Open Respiratory Research, suggest that a reduction in systemic inflammation should be an important focus in the management of COPD, said study investigators.

Conducted in Norway over a 5-year period, the study included 320 patients (mean age, 65.1 years; 46% female) with stable COPD who had no evidence of AECOPD in the 6 weeks before enrollment as well as 63 random patients comprising a reference group. Patients were followed for up to 5 years, with hospitalizations tracked and analyzed to compare changes in troponin between stable state and hospitalization for any cause.

A total of 474 hospitalizations were reported during the 5-year follow-up period. Of these, 150 were due to AECOPD and 80 were due to pneumonia. Other diagnoses at hospital admission included other lung diseases (n=43), nonrespiratory infections (n=6), circulatory diseases (n=52), cancer (n=21), digestive diseases (n=26), symptom diagnoses (n=30), and other diagnoses (n=65). In comparison to nonhospitalized patients, researchers found that hospitalized patients were older, had higher baseline hs-cTnT and


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markedly lower spirometry results, and had higher cumulative tobacco consumption, although the prevalence of current smoking did not vary between the 2 groups.  

At baseline, the overall geometric mean of hs-cTnT was 6.9 ng/L; at hospitalization, the overall geometric mean hs-cTnT was 10.6 ng/L. Approximately 75% (n=353) of the hospitalizations had available hs-cTnT measurement data.

Analysis of the association between hs-cTnT and diagnosis at incident hospitalizations adjusted for follow-up time showed that hs-cTnT was significantly higher during

the hospitalization for AECOPD, pneumonia, other lung diseases, nonrespiratory infections, circulatory diseases, and other diagnoses compared with the stable state.

Peripheral leucocytes or C-reactive protein (CRP) was shown to mediate the effect of AECOPD (ratio, 1.16; P =.022), pneumonia (ratio, 1.22; P =.008), and nonrespiratory infections (ratio, 1.26; P =.043) on hs-cTnT.

The researchers emphasized the likelihood that the joint effect of leukocytes and CRP is indirect or mediated by unknown factors. Joint effects of CRP and leucocytes on the indirect effects of pneumonia and AECOPD on hs-cTnT represented 95% (95% CI, 83-100) and 91% (95% CI, 82-100), respectively. For nonrespiratory infections, the corresponding result was 51% (95% CI, 36-74).

The researchers concluded “Cardiac troponin is increased in exacerbation and pneumonia in COPD. This increase is mediated by systemic inflammation that accompanies exacerbation and pneumonia in COPD.”

Investigators also noted that a limitation of the study was its lack of follow-up assessment for nonhospitalized patients, which may limit insight on the natural course of cTnT in patients with COPD.

Disclosure: Multiple authors declared affiliations with the pharmaceutical industry. Please refer to the original article for a full list of disclosures.

Reference

Søyseth V, Kononova N, Neukamm A, et al. Systemic inflammation induced by exacerbation of COPD or pneumonia in patients with COPD induces cardiac troponin elevation. BMJ Open Respir Res. 2021;8(1):e000997. doi:10.1136/bmjresp-2021-000997