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

https://doi.org/10.1016/S0002-9343(01)00980-9Get rights and content

Abstract

Purpose

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.

Patients and methods

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.

Results

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.

Conclusion

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.

Section snippets

Methods

On arrival in the coronary care unit at Huddinge University Hospital, Karolinska Institute, Stockholm, Sweden, a sample of venous blood was drawn from 385 consecutive patients with myocardial infarction. All samples were obtained before reperfusion therapy, if any. Diagnosis of myocardial infarction was established by an elevation of serum creatine kinase level and its subunit MB, in addition to characteristic chest pain or typical electrocardiographic changes. Blood samples were centrifuged

Results

Twenty-nine patients (9%) died within the first month and 53 patients (16%) within the first year. Patients who died during the first year were older (mean age, 75 ± 10 years vs. 68 ± 12 years), had larger infarctions (estimated by peak levels of creatine kinase-MB fraction), and were more likely to have had renal dysfunction and a history of prior heart failure or angina (Table 1).

Among all 331 patients, the mean serum concentration levels were as follows: T3, 1.8 ± 0.4 nmol/L; reverse T3,

Discussion

Normal thyroid homeostasis is altered in patients with myocardial infarction; the point of equilibrium appears to be changed and the thyroid hormone axis appears to be downregulated, such that serum levels of T3, the active hormone, were somewhat reduced in our patients, whereas levels of the inactivated metabolite reverse T3 and the weakly active precursor hormone free T4 were increased. Normally, this would result in a feedback increase in TSH levels to restore T3 levels; however, TSH levels

Acknowledgements

We are grateful to Susanne Bergman, Diana Karlsson, Hildegard Magnusson, and Gun Wesley for their skillful assistance, to Hanna Svensson for statistical assistance, to Niklas Hammar, PhD, for statistical advice, and to Nancy Pedersen, PhD, and Sarah Wamala, PhD, for their helpful comments.

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Supported by grants from the Ansgarius Foundation, Belvén Foundation, Karolinska Institutet, and Swedish Medical Research Council (Project 19X-11629).

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