ABSTRACT
CONTEXT: Troponin (hs-TnT) levels predict mortality after acute exacerbation of COPD (AECOPD). Whether this is independent of heart failure (HF) is not established. MATERIAL AND METHODS: Prospectively included AECOPD patients adjudicated for acute HF categorized into three groups: (A) AECOPD, but acute HF the primary cause for hospitalization; (B) AECOPD the primary cause, but co-existing myocardial dysfunction and (C) AECOPD without myocardial dysfunction. RESULTS: About 103 AECOPD patients; 18% A, 27% B and 54% C. Hs-TnT level differed between the groups: (ng/l, median) A: 41, B: 25 and C: 15, p = 0.03 for A versus B and p = 0.005 for B versus C. During a median 826 days, 47% died. In Cox analysis, hs-TnT levels remained associated with mortality (hazard ratio per 10 ng/l 1.3, p < 0.0001). CONCLUSION: hs-TnT levels are influenced by myocardial dysfunction/HF in AECOPD, but provide independent prognostic information. The prognostic merit of hs-TnT cannot be attributed to HF alone.
Subject(s)
Biomarkers/blood , Heart Failure/blood , Pulmonary Disease, Chronic Obstructive/blood , Troponin T/blood , Aged , Aged, 80 and over , Comorbidity , Female , Heart Failure/diagnosis , Heart Failure/epidemiology , Heart Function Tests/statistics & numerical data , Hospitalization/statistics & numerical data , Humans , Least-Squares Analysis , Linear Models , Male , Middle Aged , Myocardial Infarction/blood , Myocardial Infarction/diagnosis , Myocardial Infarction/epidemiology , Norway/epidemiology , Prognosis , Proportional Hazards Models , Prospective Studies , Pulmonary Disease, Chronic Obstructive/diagnosis , Pulmonary Disease, Chronic Obstructive/epidemiologyABSTRACT
OBJECTIVES: Reduced arterial vasodilatatory capacity is a marker of coronary heart disease. The aim was to investigate if the difference between the vasodilatory response before and after exercise, as assessed by non-invasive methodology, is related to endothelial and inflammatory biomarkers. DESIGN: Post-ischemic hyperemia after 5 min of arterial occlusion was examined before and after a bicycle test with strain-gauge plethysmography (measuring peak reactive hyperemia in the forearm) and peripheral arterial tonometry (PAT hyperemia ratio: measuring pulse waves in the index finger relative to the contra-lateral index finger) in 30 healthy males. A low PAT hyperemia ratio or a low peak reactive hyperemia reflects endothelial dysfunction. Inflammatory and endothelial biomarkers were assessed. RESULTS: A low peak reactive hyperemia and a low PAT hyperemia ratio before the bicycle test was associated with a high percentage increase in peak reactive hyperemia after exercise (r = - 0.68, p < 0.001; r = - 0.35, p = 0.06, respectively). Asymmetric dimethylarginine and interleukin-10 were associated with the percentage increase in peak reactive hyperemia in multiple linear regression analyses (ß: 165 (confidence interval [CI], 34-296), p = 0.02; ß: 19 (CI, - 0.5-39), p = 0.06, respectively). CONCLUSIONS: The difference in the vasodilatory response before and after exercise, as assessed by non-invasive methodology, is related to endothelial and inflammatory biomarkers in healthy males.