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Sir,—We previously reported a group of patients with dilated cardiomyopathy associated with increased concentrations of serum cardiac troponin T (TnT) (measured using a first generation radioimmunoassay kit) and collagen.1These patients had poor short term prognosis. Of 11 patients with positive serum concentrations of TnT or collagen, seven died before April 1998 while all 10 negative patients are currently stable in their clinical course. Five of the positive patients developed acute heart failure several times before death, complaining of dyspnoea and with orthopnoea and pulmonary congestion on chest radiography from compensated chronic heart failure without pulmonary congestion. The causes of decompensation of chronic heart failure to acute heart failure were unclear in most cases—there was no significant infection, no interruption in taking diuretics, and no drinking excess water. Although the mechanisms of decompensation of chronic heart failure to acute heart failure are unknown, five of our patients demonstrated continuously increased serum concentrations of TnT, suggesting ongoing subclinical myocyte degeneration even in the compensated stage of chronic heart failure. We concluded that subclinical myocyte degeneration occurs during compensated chronic heart failure and that this degeneration may lead some patients into acute heart failure.
Since April 1997, we have been using second generation TnT assays, which are different from the first generation assays and have a high specificity. Patients with dilated cardiomyopathy whose prognosis is poor have serum concentrations of TnT about 0.04–0.09 ng/ml as measured by the second generation kit.
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