Determinants of cardiac troponin T elevation in COPD exacerbation - a cross-sectional study
Pål H Brekke1, Torbjørn Omland, Stein Harald Holmedal
1Department of Medicine, Akershus University Hospital, Lørenskog, Norway. pal.brekke@medisin.uio.no
Insights
Elevated cardiac troponin T (cTnT) in COPD exacerbations is linked to higher mortality. Factors like increased neutrophils, creatinine, and heart rate, along with decreased hemoglobin, are associated with cTnT elevation.
Area of Science:
- Cardiology
- Pulmonology
- Biomarkers
Background:
- Elevated cardiac troponin T (cTnT) during COPD exacerbations correlates with increased one-year mortality post-discharge.
- Factors influencing cTnT levels in COPD exacerbations remain largely unknown.
Purpose of the Study:
- To identify clinical and laboratory factors associated with elevated cTnT in patients hospitalized for COPD exacerbation.
Main Methods:
- Retrospective analysis of 441 patients admitted with COPD exacerbation (2000-2003).
- cTnT levels measured, with elevation defined as >= 0.04 microg/l.
- Logistic regression used to calculate odds ratios for cTnT elevation based on clinical and laboratory data.
Main Results:
- 27% of patients (120) exhibited elevated cTnT.
- Independent predictors of elevated cTnT included higher neutrophil count, creatinine, heart rate, and Cardiac Infarction Injury Score (CIIS).
- Lower hemoglobin concentration was also associated with elevated cTnT.
Conclusions:
- Multiple factors, likely reflecting comorbidities in COPD, are associated with cTnT elevation.
- The positive association between neutrophils and cTnT suggests exaggerated inflammation during COPD exacerbations may contribute to myocardial injury.
Background:
Cardiac Troponin T (cTnT) elevation during exacerbations of chronic obstructive pulmonary disease (COPD) is associated with increased mortality the first year after hospital discharge. The factors associated with cTnT elevation in COPD are not known.
Methods:
From our hospital's database, all patients admitted with COPD exacerbation in 2000-03 were identified. 441 had measurement of cTnT performed. Levels of cTnT > or = 0.04 microg/l were considered elevated. Clinical and historical data were retrieved from patient records, hospital and laboratory databases. Odds ratios for cTnT elevation were calculated using logistic regression.
Results:
120 patients (27%) had elevated cTnT levels. The covariates independently associated with elevated cTnT were increasing neutrophil count, creatinine concentration, heart rate and Cardiac Infarction Injury Score (CIIS), and decreasing hemoglobin concentration. The adjusted odds ratios (95% confidence intervals in parentheses) for cTnT elevation were 1.52 (1.20-1.94) for a 5 x 106/ml increase in neutrophils, 1.21 (1.12-1.32) for a 10 micromol/l increase in creatinine, 0.80 (0.69-0.92) for a 1 mg/dl increase in hemoglobin, 1.24 (1.09-1.42) for a 10 beats/minute increase in heart rate and 1.44 (1.15-1.82) for a 10 point increase in CIIS.
Conclusion:
Multiple factors are associated with cTnT elevation, probably reflecting the wide panorama of comorbid conditions typically seen in COPD. The positive association between neutrophils and cTnT elevation is compatible with the concept that an exaggerated inflammatory response in COPD exacerbation may predispose for myocardial injury.
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