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      Association between increased levels of reverse triiodothyronine and mortality after acute myocardial infarction

      , , , ,

      The American Journal of Medicine

      Elsevier BV

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          Abstract

          The thyroid hormone system may be downregulated temporarily in patients who are severely ill. This "euthyroid sick syndrome" may be an adaptive response to conserve energy. However, thyroid hormone also has beneficial effects on the cardiovascular system, such as improving cardiac function, reducing systemic vascular resistance, and lowering serum cholesterol levels. We investigated whether thyroid hormone levels obtained at the time of myocardial infarction are associated with subsequent mortality. Serum levels of thyroid hormones (triiodothyronine [T3], reverse T3, free thyroxine [T4], and thyroid-stimulating hormone) were measured in 331 consecutive patients with acute myocardial infarction (mean age [+/- SD], 68 +/- 12 years), from samples obtained at the time of admission. Fifty-three patients (16%) died within 1 year. Ten percent (16 of 165) of patients with reverse T3 levels (an inactive metabolite) >0.41 nmol/L (the median value) died within the first week after myocardial infarction, compared with none of the 166 patients with lower levels (P <0.0004). After 1 year, the corresponding figures were 24% (40 of 165) versus 7.8% (13 of 166; P <0.0001). Reverse T3 levels >0.41 nmol/L were associated with an increased risk of 1-year mortality (hazard ratio = 3.0; 95% confidence interval: 1.4 to 6.3; P = 0.005), independent of age, previous myocardial infarction, prior angina, heart failure, serum creatinine level, and peak serum creatine kinase-MB fraction levels. Determination of reverse T3 levels may be a valuable and simple aid to improve identification of patients with myocardial infarction who are at high risk of subsequent mortality.

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          Author and article information

          Journal
          The American Journal of Medicine
          The American Journal of Medicine
          Elsevier BV
          00029343
          December 2001
          December 2001
          : 111
          : 9
          : 699-703
          Article
          10.1016/S0002-9343(01)00980-9
          11747849
          © 2001

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