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A small study to clarify the roles of troponin T (TnT) and brain natriuretic peptide (BNP) in decompensated congestive heart failure (CHF) has suggested that TnT is a marker of myocyte injury and not of CHF.
In patients with decompensated CHF and congested lungs baseline plasma BNP values for were high (mean 927.3 (SD 672.0) pg/ml, range 105–3121 pg/ml). However, serum TnT was either significantly raised (≥0.02 ng/ml)—in 22 (63%) of patients (group 1) or <0.02 ng/ml in 13 patients (37%, group 2). BNP concentration in the two groups was also significantly higher in group 1 than group 2 (1114.3 (708.4) v 610.8 (477.9) pg/ml) and remained so, even once lung congestion had resolved after treatment (510.5 (397.5) v 183.2 (205.8) pg/ml). Patients with high baseline serum TnT concentration continued to have high TnT concentrations despite treatment for CHF. During long term follow up 13 patients in group 1 were readmitted for decompensation, seven of whom died, compared with one readmission in group 2, and no deaths.
Thirty five consecutive patients were studied. None had myocardial infarction or atrial fibrillation in the previous year or echocardiographic changes or raised creatine kinase concentration during the study.
The researchers had already noted that high serum TnT seemed to predict poor long term outcome even when CHF was stabilised. They suspected that this might denote continuing myocyte injury, and in this study chose patients with CHF and lung congestion to determine the role of TnT in relation to BNP—a marker in diagnosing and monitoring CHF.