Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 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

Forty-nine diabetics with primary thyroid failure, as indicated by an elevated TSH concentration (TSH 38.0 +/- 5.4 mU/L, T4 63.0 +/- 4.0 nmol/L), without overt clinical evidence of hypothyroidism, had a higher (p less than 0.025) mean plasma cholesterol concentration (6.8 +/- 0.2 nmol/L vs 6.0 +/- 0.2 nmol/L) than 49 euthyroid diabetics (TSH 3.16 +/- 0.2 mU/L, T4 99.1 +/- 2.81 nmol/L) of equivalent age, sex, weight, diabetic treatment and duration of diabetes. No significant difference in triglyceride concentration was observed between the two groups of diabetics. Thyroxine replacement therapy in 18 diabetics with subnormal T4 concentrations was associated with a reduction (p less 0.01) in mean plasma cholesterol concentration to 5.8 +/- 0.3 nmol/L, but no significant change in triglyceride concentration. Clinically unrecognised thyroid failure may contribute to the high mortality from ischaemic heart disease observed in diabetics by virtue of accompanying, reversible hypercholesterolemia.
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PMID:Hypercholesterolemia in diabetics with clinically unrecognised primary thyroid failure. 729 21

The increased risk for ischemic heart disease (IHD) associated with subclinical hypothyroidism (SH) has been partly attributed to dyslipidemia. There is limited information on the effect of SH on lipoprotein (a) [Lp(a)], which is considered a significant predictor of IHD. Serum Lp(a) levels are predominantly regulated by apolipoprotein [apo(a)] gene polymorphisms. The aim of our study was to evaluate the Lp(a) levels and apo(a) phenotypes in patients with SH compared to healthy controls as well as the influence of levothyroxine substitution therapy on Lp(a) values in relation to the apo(a) isoform size. Lp(a) levels were measured in 69 patients with SH before and after restoration of a euthyroid state and in 83 age- and gender-matched healthy controls. Apo(a) isoform size was determined by sodium dodecyl sulfate (SDS) agarose gel electrophoresis followed by immunoblotting and development via chemiluminescence. Patients with SH exhibited increased Lp(a) levels compared to controls (median value 10.6 mg/dL vs. 6.0 mg/dL, p = 0.003]), but this was not because of differences in the frequencies of apo(a) phenotypes. There was no association between thyrotropin (TSH) and Lp(a) levels in patients with SH. In subjects with either low (LMW; 25 patients and 28 controls) or high (HMW; 44 patients and 55 controls) molecular weight apo(a) isoforms, Lp(a) concentrations were higher in patients than in the control group (median values 26.9 mg/dL vs. 21.8 mg/dL, p = 0.02 for LMW, and 6.0 mg/dL versus 3.3 mg/dL, p < 0.001 for HMW). Levothyroxine treatment resulted in an overall reduction of Lp(a) levels (10.6 mg/dL baseline vs. 8.9 mg/dL posttreatment, p = 0.008]). This effect was mainly evident in patients with LMW apo(a) isoforms associated with high baseline Lp(a) concentrations (median values 26.9 mg/dL vs. 23.2 mg/dL pretreatment and posttreatment, respectively; p = 0.03). In conclusion, even though a causal effect of thyroid dysfunction on Lp(a) was not clearly demonstrated in patients with SH, levothyroxine treatment is beneficial, especially in patients with increased baseline Lp(a) levels and LMW apo(a) isoforms.
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PMID:Lipoprotein (a) levels and apolipoprotein (a) isoform size in patients with subclinical hypothyroidism: effect of treatment with levothyroxine. 1281 13