triiodothyronine--reverse and Angina-Pectoris

In severe illness of any cause, down-regulation of the thyroid hormone system may occur. How this affects patients with acute myocardial infarction (AMI) is largely unknown.. To investigate changes in serum levels of the thyroid hormones during AMI and their association with cardiac function and outcome.. Forty-seven consecutive euthyroid patients with AMI were studied prospectively during the first 5 days and again 6 and 12 weeks later. Time from pain onset was used in all analyses.. The thyroid hormone system was rapidly down-regulated with maximal changes 24 to 36 hours after onset of symptoms. The mean level of the hormone total triiodothyronine (T3) decreased 19% (P =.02), the inactive metabolite reverse T3 (rT3) levels increased 22% (P =.01), and thyrotropin levels declined 51% (P<.001) between the first 6-hour and the 24- to 36-hour period. The prohormone free thyroxine was largely unchanged. Patients with poor heart function or more intense inflammatory reaction showed more pronounced down-regulation of the thyroid system. No correlation was found with cardiac enzymes. Patients with prior angina pectoris had lower T(3) levels in early samples, smaller infarctions, and higher levels of C-reactive protein and the proinflammatory cytokine interleukin 6 on admittance. Peak levels of interleukin 6 correlated negatively with T3 (P =.005) and positively with rT3 (P<.05), suggesting that down-regulation before AMI may be cardioprotective. However, mortality was high among patients with the most pronounced thyroid level depression, indicating that down-regulation after AMI may be maladaptive.. The thyroid hormone system is rapidly down-regulated in AMI. This may be beneficial during acute ischemia. Patients with angina had higher levels of interleukin 6 and C-reactive protein and more depressed thyroid hormone system in early samples. Thyroid level depression in patients with angina may possibly have been present before the infarction process started. This novel finding needs further evaluation in large studies to sort out cause-and-effect relationships.

Topics: Adult; Aged; Aged, 80 and over; Angina Pectoris; Biomarkers; Case-Control Studies; Down-Regulation; Female; Humans; Male; Middle Aged; Myocardial Infarction; Risk Factors; Severity of Illness Index; Thyroid Hormones; Thyrotropin; Thyroxine; Time Factors; Triiodothyronine; Triiodothyronine, Reverse; Ventricular Function

Six patients with hyperthyroxinemia (five men and one woman) were evaluated for possible hyperthyroidism. All were taking large daily doses of propranolol--480 +/- 155 (+/- SE) mg--for treatment of angina pectoris. The patients had no clinical evidence of hyperthyroidism, although three had small goiters. Further evaluation of the patients revealed elevated serum free thyroxine levels and/or free thyroxine index, low-normal serum triiodothyronine levels, and elevated serum reverse triiodothyronine levels in all six. The thyroid-stimulating hormone response to thyrotropin-releasing hormone was normal in two patients, subnormal in three patients, and absent in one patient. One patient was restudied while receiving low-dose propranolol (80 mg a day), with normalization of all thyroid functional parameters. The data suggest that the abnormalities seen in patients taking high doses of propranolol were due to drug-induced blockade of iodothyronine deiodination. Signs and symptoms of hyperthyroidism are lacking in patients taking large doses of propranolol. If such a patient is discovered to have an elevated serum thyroxine level, a more complete evaluation of thyroid function is necessary before the diagnosis of thyrotoxicosis can be made. The thyrotropin-releasing hormone test may be of particular value in this circumstance.

Topics: Aged; Angina Pectoris; Female; Humans; Male; Middle Aged; Propranolol; Thyrotropin-Releasing Hormone; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse