Otto Mayer1, Jitka Seidlerová2, Jan Bruthans3, Jiří Vaněk4, Lenka Černá5, Peter Wohlfahrt6, Jan Filipovský2, Renata Cífková6, Jindra Windrichová7, Ondřej Topolčan7. 1. 2nd Department of Internal Medicine, Medical Faculty of Charles University and University Hospital, Pilsen, Czech Republic; Biomedical Center, Medical Faculty of Charles University, Pilsen, Czech Republic. Electronic address: mayero@fnplzen.cz. 2. 2nd Department of Internal Medicine, Medical Faculty of Charles University and University Hospital, Pilsen, Czech Republic; Biomedical Center, Medical Faculty of Charles University, Pilsen, Czech Republic. 3. 2nd Department of Internal Medicine, Medical Faculty of Charles University and University Hospital, Pilsen, Czech Republic; Centre for Cardiovascular Prevention of the First Faculty of Medicine, Charles University and Thomayer Hospital, Prague, Czech Republic. 4. 2nd Department of Internal Medicine, Medical Faculty of Charles University and University Hospital, Pilsen, Czech Republic. 5. Department of Neurology, University Hospital, Pilsen, Czech Republic. 6. Centre for Cardiovascular Prevention of the First Faculty of Medicine, Charles University and Thomayer Hospital, Prague, Czech Republic; International Clinical Research Centre, St. Anne's University Hospital Brno, Czech Republic. 7. Department of Immunodiagnostics, University Hospital, Pilsen, Czech Republic.
Abstract
OBJECTIVES: Due to improved analytical performance of the newest generation of troponin assays, several patients have mild elevations of this parameter. Nevertheless, they do not show any signs of acute coronary syndrome. We speculated whether non-acute cardiac troponin I (cTnI) concentrations may improve prediction of residual mortality risk in clinically stable outpatients with chronic vascular disease. DESIGN AND METHODS: We followed 830 patients (mean age 65.2years) after myocardial infarction, coronary revascularization or first ischemic stroke (pooled Czech samples of EUROASPIRE III and EUROASPIRE-stroke surveys, interviewed in 2006/2007) in a prospective cohort study. In addition to standard protocol, troponin I and brain natriuretic peptide (BNP) was estimated from frozen samples. Vital status and declared cause of death from death certificates was registered to ascertain a 5-year all-cause and cardiovascular mortality. RESULTS: During a median follow up of 2050days (5.6years) 168 patients died. In the multivariate Cox proportional hazard model, cTnI≥0.03ng/mL independently predicted an all-cause 5-year mortality with HRR 1.76 (95% CI: 1.09-2.83). In the Cox model, the better predictor of mortality was BNP >150ng/L [HRR 3.47 (95% CI: 2.23-5.41)]. However, the combination of BNP with cTnI did not substantially improve its sensitivity or predictive power. CONCLUSION: We cannot confirm the utility of asymptomatic mild cTnI elevation as a tool to detect residual risk of stable patients with vascular disease. On the other hand, BNP seems to be more appropriate for this purpose.
OBJECTIVES: Due to improved analytical performance of the newest generation of troponin assays, several patients have mild elevations of this parameter. Nevertheless, they do not show any signs of acute coronary syndrome. We speculated whether non-acute cardiac troponin I (cTnI) concentrations may improve prediction of residual mortality risk in clinically stable outpatients with chronic vascular disease. DESIGN AND METHODS: We followed 830 patients (mean age 65.2years) after myocardial infarction, coronary revascularization or first ischemic stroke (pooled Czech samples of EUROASPIRE III and EUROASPIRE-stroke surveys, interviewed in 2006/2007) in a prospective cohort study. In addition to standard protocol, troponin I and brain natriuretic peptide (BNP) was estimated from frozen samples. Vital status and declared cause of death from death certificates was registered to ascertain a 5-year all-cause and cardiovascular mortality. RESULTS: During a median follow up of 2050days (5.6years) 168 patients died. In the multivariate Cox proportional hazard model, cTnI≥0.03ng/mL independently predicted an all-cause 5-year mortality with HRR 1.76 (95% CI: 1.09-2.83). In the Cox model, the better predictor of mortality was BNP >150ng/L [HRR 3.47 (95% CI: 2.23-5.41)]. However, the combination of BNP with cTnI did not substantially improve its sensitivity or predictive power. CONCLUSION: We cannot confirm the utility of asymptomatic mild cTnI elevation as a tool to detect residual risk of stable patients with vascular disease. On the other hand, BNP seems to be more appropriate for this purpose.