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Serum cardiac troponin T and plasma brain natriuretic peptide in patients with cardiac decompensation
  1. Y Sato1,
  2. R Taniguchi1,
  3. T Makiyama2,
  4. K Nagai2,
  5. H Okada2,
  6. T Yamada1,
  7. A Matsumori1,
  8. Y Takatsu2
  1. 1Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan
  2. 2Division of Cardiology, Department of Internal Medicine, Hyogo Prefectural Amagasaki Hospital, Hyogo, Japan
  1. Correspondence to:
    Yukihito Sato, MD, Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, 54 Kawaracho Shogoin, Sakyo-ku, Kyoto 606-8397, Japan;
    cardioys{at}kuhp.kyoto-u.ac.jp

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In our earlier study, idiopathic dilated cardiomyopathy patients with persistently high serum troponin T (TnT) concentrations had notably depressed left ventricular ejection fractions, increased left ventricular diastolic dimensions, and adverse long term outcomes.1–,3 Therefore, TnT seems to be a marker of ongoing subclinical myocyte injury, although the mechanism of its release is unknown. Most patients with poor outcomes had persistently high TnT concentrations, even when clinically stabilised by conventional treatment, when they were free of dyspnoea, or radiographic and auscultatory signs of pulmonary congestion. Brain natriuretic peptide (BNP) is an amino acid peptide secreted chiefly by the ventricular myocardium in response to strain. Measurements of plasma concentrations of BNP are being increasingly used as a clinical diagnostic, prognostic, and monitoring tool in patients with congestive heart failure (CHF).4,5 We therefore examined the significance of TnT and BNP concentrations in patients with CHF.

METHODS

The study population comprised 35 consecutive patients who presented to the Hyogo …

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