Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment for patients with ischemic heart disease and hypothyroidism contains many difficulties, such as a dilemma that thyroid hormone to hypothyroid patients may worsen angina. The purpose of this study is to propose an appropriate control of thyroid function in these patients before coronary artery bypass grafting (CABG), and to clarify the change of thyroid function during postoperative period. Because of progressive angina pectoris, five hypothyroidism patients underwent CABG. Preoperatively, minimal dose of L-Thyroxine (0-75 micrograms, daily) was administered orally to keep thyroid function at slightly low level before CABG. Ten consecutive CABG patients with normal thyroid function were selected as control group. Between both groups, there was no significant difference in age, coronary artery disease, and the number of bypass grafts. Serum T4, free-T4, T3, free-T3, and TSH were measured at 1st, 2nd, 3rd, and 7th P.O.D. In control group, pituitary-thyroid function was suppressed transiently. In hypothyroid group, T4 revealed no change and was kept at slightly low level during observed period. There was no significant difference in postoperative hemodynamics between both groups. Postoperatively all of hypothyroid patients got free from angina and received an adequate thyroid hormone replacement therapy without complications. It is concluded that CABG for patients with angina and hypothyroidism can be performed safely by keeping preoperative thyroid function at slightly low level.
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PMID:[Surgical treatment of ischemic heart disease combined with hypothyroidism]. 221 71

Hypothyroidism results in decreased platelet aggregation and has unique effects on the development of atherosclerosis and angina pectoris. Because prostacyclin and thromboxane A2 profoundly influence platelet function and vascular tone and are thought to be important in the development of atherosclerosis and angina pectoris, we studied the effects of hypothyroidism in rats on the in vitro elaboration of prostacyclin passively by aortic tissue and of thromboxane A2 by thrombin-stimulated whole blood. Hypothyroidism induced by iodine 131 (given at age 7 weeks) persistently caused a mild decrease in platelet count (P less than 0.01) and 30% decrease in immunoreactive thromboxane B2 (the hydrolysis product of thromboxane A2) generation per platelet (P less than 0.01) compared with age-matched euthyroid rats. Between 20 and 23 weeks of age immunoreactive 6-ketoprostaglandin F1 alpha (the hydrolysis product of prostacyclin) generation decreased by 30% in euthyroid rats. In hypothyroid rats less than 23 weeks of age, 6-ketoprostaglandin F1 alpha production was the same as that of age-matched euthyroid rats. With further aging, 6-ketoprostaglandin F1 alpha production did not decrease as it did in euthyroid rats. Hypothyroid rats more than 20 weeks old had, therefore, significantly greater 6-ketoprostaglandin F1 alpha production than age-matched euthyroid rats (P less than 0.005). L-Thyroxine given daily for 28 days to 23-week-old hypothyroid rats caused a rapid increase in platelet count and a delayed normalization of the thromboxane synthetic abnormality. 6-Ketoprostaglandin F1 alpha production transiently increased in response to L-thyroxine, but decreased to the euthyroid level after 28 days of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothyroidism and short-term aging on whole blood thromboxane and arterial prostacyclin synthesis. 366 59