E Missov1, C Calzolari, B Pau. 1. Department of Cardiology and INSERM U-390, University Hospital of Montpellier, France. missov@u390.montp.inserm.fr
Abstract
BACKGROUND: Spontaneous progression of severe congestive heart failure is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The cardiac muscle isoform of troponin I is uniquely expressed in the adult human myocardium, and an increase in its circulating levels is highly indicative of myocardial injury. Accordingly, we addressed the usefulness of cardiac troponin I as a sensitive and specific molecular marker of congestive heart failure in patients with severely reduced left ventricular performance. METHODS AND RESULTS: A new generation single-step immunoenzymoluminometric assay with high analytical sensitivity was used to assess cardiac troponin I in patients with severe congestive heart failure, healthy blood donors, and hospitalized control subjects without known cardiac disease. The cardiac troponin I concentration (mean+/-SEM) was 72.1+/-15.8 pg/mL in heart failure patients and 20.4+/-3.2 and 36.5+/-5.5 pg/mL in healthy and hospitalized control subjects, respectively (P<.01 versus heart failure patients). When both control groups were considered, the mean cardiac troponin I level was 25.4+/-2.9 pg/mL (P<.01 versus heart failure patients). Creatine kinase MB mass and myoglobin concentrations remained within the normal range in all groups. CONCLUSIONS: These data (1) provide the first evidence for ongoing myofibrillar degradation and increased cardiac troponin I levels in patients with advanced heart failure and (2) show potential usefulness of cardiac troponin I as a specific and sensitive new serum marker molecule in severe congestive heart failure.
BACKGROUND: Spontaneous progression of severe congestive heart failure is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The cardiac muscle isoform of troponin I is uniquely expressed in the adult human myocardium, and an increase in its circulating levels is highly indicative of myocardial injury. Accordingly, we addressed the usefulness of cardiac troponin I as a sensitive and specific molecular marker of congestive heart failure in patients with severely reduced left ventricular performance. METHODS AND RESULTS: A new generation single-step immunoenzymoluminometric assay with high analytical sensitivity was used to assess cardiac troponin I in patients with severe congestive heart failure, healthy blood donors, and hospitalized control subjects without known cardiac disease. The cardiac troponin I concentration (mean+/-SEM) was 72.1+/-15.8 pg/mL in heart failurepatients and 20.4+/-3.2 and 36.5+/-5.5 pg/mL in healthy and hospitalized control subjects, respectively (P<.01 versus heart failurepatients). When both control groups were considered, the mean cardiac troponin I level was 25.4+/-2.9 pg/mL (P<.01 versus heart failurepatients). Creatine kinase MB mass and myoglobin concentrations remained within the normal range in all groups. CONCLUSIONS: These data (1) provide the first evidence for ongoing myofibrillar degradation and increased cardiac troponin I levels in patients with advanced heart failure and (2) show potential usefulness of cardiac troponin I as a specific and sensitive new serum marker molecule in severe congestive heart failure.
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