Article

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: 2.76). 05/2012; 12:22. DOI: 10.1186/1471-2466-12-22
Source: PubMed

ABSTRACT 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.

0 Bookmarks
 · 
53 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE: To assess the distribution of high-sensitivity cardiac troponin T (hs-cTnT) concentrations in stable chronic obstructive pulmonary disease (COPD), and whether hs-cTnT is associated with pulmonary function. DESIGN: Prospectively designed, cross-sectional study. SETTING: Outpatient clinic of Norwegian teaching hospital and community-based setting. PARTICIPANTS: Sample of 101 stable COPD patients from the hospital's outpatient clinic and 120 individuals derived from a random general population sample. MAIN OUTCOMES: Ratio of hs-cTnT in stable COPD patients compared with references from the general population. Change in ratio of hs-cTnT per unit increase of relevant covariables. RESULTS: The crude geometric means of circulating hs-cTnT in the cases and the references were 7.75 and 3.01 ng/l, respectively (p <0.001); that is, a relative ratio of 2.57 (95% CI 2.05 to 3.23). After adjustment for relevant confounders, this ratio was moderately attenuated to 1.65 (1.31-2.08). In the total study cohort, as well as among stable COPD patients, we found a significant positive association between hs-cTnT and interleukin-6 concentrations (p <0.001) and the presence of pathologic Q waves (p=0.023). Among stable COPD patients, one quartile increase in forced expiratory volume 1 was associated with a 39% decrease in hs-cTnT and patient category (Global Initiative of Obstructive Lung Disease classification 2011) was positively associated with hs-cTnT (p trend <0.001) after multivariate adjustment. CONCLUSIONS: Stable COPD is independently associated with higher hs-cTnT compared with randomly drawn subjects from the general population. In patients with stable COPD, higher hs-cTnT seems to be associated with immune activation and the severity of the disease.
    Heart (British Cardiac Society) 01/2013; · 5.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a chronic, progressive lung disease resulting from exposure to cigarette smoke, noxious gases, particulate matter, and air pollutants. COPD is exacerbated by acute inflammatory insults such as lung infections (viral and bacterial) and air pollutants which further accelerate the steady decline in lung function. The chronic inflammatory process in the lung contributes to the extrapulmonary manifestations of COPD which are predominantly cardiovascular in nature. Here we review the significant burden of cardiovascular disease in COPD and discuss the clinical and pathological links between acute exacerbations of COPD and cardiovascular disease.
    BioMed research international. 01/2014; 2014:528789.
  • [Show abstract] [Hide abstract]
    ABSTRACT: The classification of myocardial infarction into 5 types was introduced in 2007 as an important component of the universal definition. In contrast to the plaque rupture-related type 1 myocardial infarction, type 2 myocardial infarction is considered to be caused by an imbalance between demand and supply of oxygen in the myocardium. However, no specific criteria for type 2 myocardial infarction have been established. We prospectively studied unselected hospital patients who had cardiac troponin I measured on clinical indication. The diagnosis and classification of myocardial infarction were established, and the frequency and features of type 2 myocardial infarction were investigated by use of novel developed criteria. From January 2010 to January 2011, a total of 7230 consecutive patients who had cardiac troponin I measured were evaluated, and 4499 patients qualified for inclusion. The diagnosis of myocardial infarction was established in 553 patients, of whom 386 (72%) had a type 1 myocardial infarction and 144 (26%) had a type 2 myocardial infarction. Patients in the group with type 2 myocardial infarction were older and more likely to be female, and had more comorbidities. The proportion of patients without significant coronary artery disease was higher in those with type 2 myocardial infarction (45%) than in those with type 1 myocardial infarction (12%) (P < .001). Tachyarrhythmias, anemia, and respiratory failure were the most prevalent mechanisms causing type 2 myocardial infarction. In a cohort of patients with myocardial infarction who were admitted consecutively through 1 year, the category of type 2 myocardial infarction comprised one fourth when diagnosed by the use of newly developed criteria. Approximately half of patients with type 2 myocardial infarction had no significant coronary artery disease.
    The American journal of medicine 07/2013; · 4.47 Impact Factor

Full-text

View
0 Downloads
Available from