Abstract
A214 Objective: Heart failure is a dynamic process progressing at an individual rate. Some patients remain stable until a donor heart becomes available while others need mechanical circulatory support due to rapid hemodynamic deterioration. Several serum markers were found elevated in chronic heart failure, but it is unknown which marker may predict hemodynamic decompensation. We evaluated whether serum markers are indicative for hemodynamic impairment in heart failure patients. Methods: In 30 patients with heart failure (26 male, 4 female, mean age 47 years) serum cardiac markers (troponin I, CK-MB, myoglobin), vasoactive mediators (big endothelin (big ET), endothelin-1 (ET-1), urotensin II (UT-II)) and proinflammatory markers (procalcitonin (PCT) and ultrasensitive CRP (usCRP)) were measured preoperatively at the time of heart transplantation or assist device implantation. Seventeen patients underwent left ventricular assist device implantation (3 DeBakey, 5 Berlin Heart, 9 Novacor LVADs) because of therapy-resistant heart failure (group I) and 13 patients heart transplantation in clinically stable condition (group II). Results: None of the patients in group II were ventilated or needed inotropic support, whereas all patients in group I needed catecholamine therapy (adrenalin and/or dopamine) and some were mechanically ventilated preoperatively. The CK-MB (1.95±1.1 vs. 1.77±1.4 μg/l) and troponin I (0.28±0.2 vs. 0.79±1.2) concentrations (mean±SED) were not significantly different between groups (group I vs. group II). The serum concentrations of other markers are given in the table.FigureConclusions: Myoglobin, but not CK-MB or troponin I, was significantly increased in decompensated compared to stable heart failure. Elevated vasoactive mediators may predict chronic circulatory compromise in heart failure, whereas increasing of proinflammatory markers suggests an inflammatory involvement in hemodynamic deterioration of stable heart failure.
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