Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pre-menopausal patient with a six-year history of symptoms of the metastatic carcinoid syndrome leading to progressively worsening carcinoid heart disease is described. The failure of anti-oestrogenic therapy (sequential bilateral oophorectomy and Tamoxifen therapy) to halt progression of disease was documented. Death resulted from right ventricular failure associated with pulmonary and tricuspid valvular disease.
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PMID:Malignant carcinoid syndrome. Failure of anti-oestrogenic therapy. 233 98

Female reproductive hormones cause breast cancer. Long-term use of postmenopausal hormones increases the risk of breast cancer. The apparent survival advantage seen in women diagnosed with breast cancer while taking postmenopausal hormones may be due to the hormone-responsive nature of their tumors, diagnosis at an earlier stage, or other biases. Thus, the data indicating a survival advantage do not specify what the policies were on the use of hormones after diagnosis. Substantial evidence from studies of obesity confirms the association of higher estrogen levels with poorer prognosis. Tamoxifen (Nolvadex), acting as an antiestrogen in breast tissue, increases the likelihood of survival, as does oophorectomy in premenopausal women. Given these data, women diagnosed with breast cancer should use hormones sparingly. Alternatives to hormone therapy should be used for long-term prevention of heart disease and osteoporosis.
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PMID:Estrogen replacement therapy for breast cancer patients. 959 75

-Tamoxifen reduces the incidence of breast cancer in women at risk for that disease. Because heart disease is the leading cause of death in women and because tamoxifen is also associated with venous thrombosis, an improved understanding of the association of tamoxifen with cardiovascular disease risk factors is required. In 111 healthy women at a single center, who were participating in a randomized double-blind breast cancer prevention trial, the 6-month effects of oral tamoxifen (20 mg/d) compared with placebo on factors related to inflammation, hemostasis, and lipids were studied. Tamoxifen was associated with reductions of 26% in median C-reactive protein, 22% in median fibrinogen, and 9% in cholesterol (all P:<0.01 compared with placebo). There were no differences in treatment effects on factor VII coagulant activity, fragment 1-2, and triglycerides. In secondary analyses, the effect of tamoxifen on C-reactive protein was larger in postmenopausal women and in women with higher waist-to-hip ratios. The effect on fibrinogen was larger in women with higher baseline cholesterol. Tamoxifen demonstrated effects on inflammatory markers that were consistent with reduced cardiovascular risk. These findings are in contrast to recent reports of increased C-reactive protein associated with postmenopausal estrogen. The potential for beneficial cardiovascular effects of tamoxifen in healthy women is suggested.
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PMID:Tamoxifen and cardiac risk factors in healthy women: Suggestion of an anti-inflammatory effect. 1115 62

Tamoxifen is the most commonly used antiestrogen for the treatment of breast cancer. Several clinical trials demonstrate that tamoxifen reduces the risk of heart disease and osteoporosis. However, the mechanism by which tamoxifen causes cardioprotection is unclear. Because increased levels of tumor necrosis factor alpha (TNFalpha) in tissue and/or plasma have been observed in virtually all forms of cardiac injury, we investigated whether tamoxifen prevents cardiac injury in a murine model of acute TNFalpha challenge. Five- to six-week-old female mice were injected (ip) with tamoxifen at 0.25 mg/kg daily for 3 or 7 days before receiving an injection of TNFalpha. Ultrastructural examination of cardiac tissues revealed remarkable protection against TNFalpha-induced mitochondrial damage in tamoxifen pretreated mice. Tamoxifen treatment significantly improved the mitochondrial respiratory function and enhanced superoxide-scavenging activity of mitochondria. These findings reveal a novel mitochondria-mediated mechanism by which tamoxifen exerts its cardiac protection effect against acute TNFalpha-induced heart injury.
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PMID:Tamoxifen protects against acute tumor necrosis factor alpha-induced cardiac injury via improving mitochondrial functions. 1654 92

Recent findings suggest that inhibition of AMP-deaminase (AMPD) could be effective therapeutic strategy in heart disease associated with cardiac ischemia. To establish experimental model to study protective mechanisms of AMPD inhibition we developed conditional, cardiac specific knock-outs in Cre recombinase system. AMPD3 floxed mice were crossed with Mer-Cre-Mer mice. Tamoxifen was injected to induce Cre recombinase. After two weeks, hearts, skeletal muscle, liver, kidney, and blood were collected and activities of AMPD and related enzymes were analyzed using HPLC-based procedure. We demonstrate loss of more than 90% of cardiac AMPD activity in the heart of AMPD3-/-mice while other enzymes of nucleotide metabolism such as adenosine deaminase, purine nucleoside phosphorylase were not affected. Surprisingly, activity of AMPD was also reduced in the erythrocytes and in the kidney by 20%-30%. No change of AMPD activity was observed in the skeletal muscle and the liver.
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PMID:Effect of AMP-deaminase 3 knock-out in mice on enzyme activity in heart and other organs. 2494 Jun 86