Determinants of high-sensitivity cardiac troponin T during acute exacerbation of chronic obstructive pulmonary disease: A prospective cohort study

Dept, of Medicine, Akershus University Hospital and Institute of Clinical Medicine, Akershus University Hospital, University of Oslo, Oslo, Norway.
BMC Pulmonary Medicine (Impact Factor: 2.4). 05/2012; 12(1):22. DOI: 10.1186/1471-2466-12-22
Source: PubMed


A high-sensitivity cardiac troponin T (hs-cTnT) concentration above the 99th percentile (i.e. 14 ng/L) is common during Acute Exacerbation of Chronic Obstructive Pulmonary Disease (AECOPD) and associated with increased mortality. The objective of the study was to identify factors associated with hs-cTnT levels during AECOPD.
We included 99 patients with AECOPD on admission. As 41 patients had one or more repeat admissions, there were 202 observations in the final analysis. We recorded clinical and biochemical data, medication, spirometry, chest radiographs, and ECGs. The data were analysed for cross-sectional and longitudinal associations using ordinary least square as well as linear mixed models with the natural logarithm of hs-cTnT as the dependent variable.
Mean age at inclusion was 71.5 years, mean FEV1/FVC was 45%, and median hs-cTnT was 27.0 ng/L. In a multivariable model there was a 24% increase in hs-cTnT per 10 years increase in age (p < 0.0001), a 6% increase per 10 μmol/L increase in creatinine (p = 0.037), and a 2% increase per month after enrollment (p = 0.046). Similarly, the ratios of hs-cTnT between patients with and without tachycardia (heart rate ≥100/min) and with and without history of arterial hypertension were 1.25 (p = 0.042) and 1.44 (p = 0.034), respectively. We found no significant association between arterial hypoxemia and elevated hs-cTnT.
Age, arterial hypertension, tachycardia, and serum creatinine are independently associated with the level of hs-cTnT on admission for AECOPD.

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    • "Moreover, heart disease often remains undiagnosed in these patients [7-10]. This may in part be because the symptoms and signs of MI and heart failure may mimic an acute exacerbation of COPD (AECOPD), but also because the classic symptom and sign of MI, i.e. chest pain and ECG changes, are poorly associated with myocardial injury during AECOPD [11-13]. Using a highly sensitive assay, we have previously shown that nearly three quarters of patients admitted with AECOPD have cardiac troponin T (cTnT) above the 99th percentile (14 ng/L), and that even modest elevation is associated with increased mortality [14,15]. "
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    ABSTRACT: Background Cardiovascular disease is prevalent and frequently unrecognized in patients with chronic obstructive pulmonary disease (COPD). NT-proBNP is an established risk factor in patients with heart failure. NT-proBNP may also be released from the right ventricle. Thus serum NT-proBNP may be elevated during acute exacerbations of COPD (AECOPD). The prognostic value of NT-proBNP in patients hospitalized with AECOPD is sparsely studied. Our objective was to test the hypothesis that NT-proBNP independently predicts long term mortality following AECOPD. Methods A prospective cohort study of 99 patients with 217 admissions with AECOPD. Clinical, electrocardiographic, radiological and biochemical data were collected at index and repeat admissions and analyzed in an extended survival analysis with time-dependent covariables. Results Median follow-up time was 1.9 years, and 57 patients died during follow-up. NT-proBNP tertile limits were 264.4 and 909 pg/mL, and NT-proBNP in tertiles 1 through 3 was associated with mortality rates of 8.6, 35 and 62 per 100 patient-years, respectively (age-adjusted log-rank p<0.0001). After adjustment for age, gender, peripheral edema, cephalization and cTnT in a multivariable survival model, the corresponding hazard ratios for dying were 2.4 (0.95-6.0) and 3.2 (1.3-8.1) (with 95% confidence intervals in parentheses, p-value for trend 0.013). Conclusions NT-proBNP is a strong and independent determinant of mortality after AECOPD.
    Respiratory research 10/2012; 13(1):97. DOI:10.1186/1465-9921-13-97 · 3.09 Impact Factor
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    ABSTRACT: Objective To investigate if acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is associated with myocardial injury, expressed as elevated high sensitive cardiac troponin T (hs-cTnT), and to identify determinants of hs-cTnT in chronic obstructive pulmonary disease (COPD) patients. Design In a cross-sectional study, hs-cTnT in patients hospitalised for AECOPD was compared with hs-cTnT in COPD patients in their stable state. Setting The study was conducted at a teaching and a pulmonary rehabilitation clinic. Participants Consecutive admissions to participating units for the years 2010–2011 meeting objective, standardised criteria for AECOPD and stable COPD. Main outcomes Ratio of hs-cTnT in hospitalised AECOPD patients compared with stable COPD patients. Change in the ratio of hs-cTnT per unit increase of relevant covariables. Results The geometric mean of hs-cTnT in the index group was 25.8 ng/l (95% CI 21.1 to 31.7) compared with 4.55 ng/l (95% CI 3.72 to 5.67) in the reference group. After inclusion of relevant covariables, multiple linear regression analyses showed that the ratio between hs-cTnT in AECOPD patients and the references was 4.26 (95% CI 3.02 to 6.00) and that hs-cTnT increased 1.41-fold (95% CI 1.20 to 1.68), for each quartile increase in leucocyte count in stable COPD but not in AECOPD. Higher hs-cTnT 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 forced expiratory volume in 1 s (p=0.014). A significant univariable association between cTnT and arterial hypoxaemia was also found but this association was attenuated almost to a zero effect after inclusion of relevant covariates. Conclusions AECOPD is associated with higher hs-cTnT as compared with stable COPD. In stable COPD, hs-cTnT appears to be positively associated with indices of COPD severity, whereas we were unable to identify significant determinants of hs-cTnT in AECOPD.
    Heart (British Cardiac Society) 09/2012; 99(2). DOI:10.1136/heartjnl-2012-302685 · 5.60 Impact Factor
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    ABSTRACT: Congestive heart failure is underdiagnosed in patients with chronic obstructive pulmonary disease (COPD). Pulmonary congestion on chest radiograph at admission for acute exacerbation of COPD (AECOPD) is associated with an increased risk of mortality. A standardized evaluation of chest radiographs may enhance prognostic accuracy. We aimed to evaluate whether a standardized, liberal assessment of pulmonary congestion is superior to the routine assessment in identifying patients at increased risk of long-term mortality, and to investigate the association of heart failure with N-terminal prohormone of brain natriuretic peptide (NT-proBNP) concentrations. This was a prospective cohort study of 99 patients admitted for AECOPD. Chest radiographs obtained on admission were routinely evaluated and then later evaluated by blinded investigators using a standardized protocol looking for Kerley B lines, enlarged vessels in the lung apex, perihilar cuffing, peribronchial haze, and interstitial or alveolar edema, defining the presence of pulmonary congestion. Adjusted associations with long-term mortality and NT-proBNP concentration were calculated. The standardized assessment was positive for pulmonary congestion in 32 of the 195 radiographs (16%) ruled negative in the routine assessment. The standardized assessment was superior in predicting death during a median follow up of 1.9 years (P=0.022), and in multivariable analysis, only the standardized assessment showed a significant association with mortality (hazard ratio 2.4, 95% confidence interval [CI] 1.2-4.7) (P=0.016) and NT-proBNP (relative concentration 1.8, CI 1.2-2.6) (P=0.003). By applying a standardized approach when evaluating pulmonary congestion on chest radiographs during AECOPD, a group of patients with increased risk of dying, possibly due to heart failure, is identified.
    International Journal of COPD 12/2013; 8:621-9. DOI:10.2147/COPD.S52854 · 3.14 Impact Factor
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