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)

Parathyroid hormone (PTH) influences the calcium metabolism of many different mammalian cell types; indeed, hypertension due to changes in muscle tone is a frequent symptom of hypercalcemic hyperparathyroidism. In a blind study of 81 patients with various forms of heart disease undergoing coronary angiography, the plasma concentrations of the midcarboxyl regional PTH immunoreactivity were determined. PTH concentrations were elevated in 26 of the 56 patients exhibiting organic coronary artery disease (CAD). The plasma PTH levels were highest in those patients with CAD affecting three vessels and in patients with evidence of myocardial infarction. PTH levels were not influenced by previous drug treatments, and did not correlate to stress hormone levels. We propose that increased PTH levels may be a marker for initiation or potentiation of calcium-dependent changes in vascular smooth muscle behavior inducing coronary functional and anatomic lesions typical of CAD.
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PMID:Parathyroid hormone in coronary artery disease--results of a prospective study. 378 41

Impairments in cardiovascular, respiratory and kidney function are considered as risk factors for complications following surgery. As the indication for surgery in asymptomatic primary hyperparathyroidism (HPT) is controversial, 123 patients undergoing surgery for HPT and 104 control subjects scheduled for common surgical procedures were evaluated pre-operatively. Compared with the age- and sex-matched control group, serum calcium (P < 0.001), creatinine (P < 0.01) and glucose (P < 0.02) were all increased in the HPT group, while peak expiratory flow (PEF) was decreased (P < 0.04). Furthermore, the patients with HPT, compared with controls, were more often receiving antihypertensive medication (P < 0.005) and were more likely to have a history of congestive heart disease (P < 0.01), thromboembolic diseases (P = 0.05), stroke (P = 0.06) or diabetes mellitus (P < 0.02). Increased frequencies of ST-segment depression (P < 0.001) and T-wave abnormalities (P = 0.05) at electrocardiography together with an increased prevalence of heart enlargement visible at chest radiography (P < 0.01) were also seen in the HPT group when compared with the controls. All HPT patients and controls survived, but one HPT patient suffered a myocardial infarction in the post-operative period. In conclusion, the present study showed the pre-operative risk factor profile to be altered in HPT subjects with impairments in both cardiovascular and respiratory functions as well as in kidney function and glucose control. These findings should be kept in mind when the indications for surgery in asymptomatic patients with HPT are discussed.
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PMID:Pre-operative evaluation of risk factors for complications in patients with primary hyperparathyroidism. 871 37

Cardiac transplantation has become a successful therapy for end-stage heart disease. However, increased bone loss has been observed in heart transplant recipients, sometimes being responsible for osteoporotic fractures. Glucocorticoids cause dose-related bone loss, particularly in the first 6-12 months of use, but cyclosporine might play a role as well. The evolution of bone mineral density (BMD) and biochemical parameters was prospectively assessed in 24 patients (mean age 52 years) from cardiac transplantation. All patients received cyclosporin A (CsA) and prednisone, the latter at decreasing dosage. The mean current daily dose of CsA was 321 mg and serum levels of CsA were constant. All patients received calcium (500 mg day-1) and vitamin D (1000 U day-1) for prevention of bone loss. BMD (gcm-2) was measured in 17 patients at the lumbar spine, femoral neck and total hip with dual energy X-ray absorptiometry every 6 months. Spinal BMD as well as neck and total hip BMD decreased at 6 and 12 months after transplantation, being statistically significant at the three sites: -5.6 and -3.4% for the lumbar spine, -9.3 and -8.5% for the femoral neck, -4.8% and -6.0% for the total hip respectively. Parathyroid hormone (PTH) and osteocalcin (BGP) increased by 90% and 800% respectively between pretransplantation values and 18 months after transplantation. BGP levels measured every 2 months from transplantation increased continuously from 8.7 micrograms L-1 (mean +/- SEM) before transplantation to 31.3 +/- 10.1 (P < 0.05) at 4 months, to 59.1 +/- 8.8 (P < 0.01) at 6 months and to 72.2 +/- 9.9 (P < 0.01) at 18 months (Kruskal-Wallis analysis: P < 0.0001). PTH showed a biphasic pattern with an initial decrease from 39.3 +/- 4.1 ng L-1 at baseline to 22.0 +/- 2.8 ng L-1 at 2 months, but increasing thereafter to 45.9 +/- 5.7 at 6 months and 74.2 +/- 8.9 at 18 months (Kruskal-Wallis analysis: P < 0.001). These variations represent a glucocorticoid-induced osteoporosis. In summary, cardiac transplant patients lose bone immediately after transplantation at the spine and the hip. Later on, the loss in BMD discontinues at all sites of the skeleton, but predominantly at the spine, and a few patients still lose bone at the hip. This is probably a result of the high bone turnover either due to secondary hyperparathyroidism or induced by cyclosporin A.
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PMID:Cyclosporine induces high bone turnover and may contribute to bone loss after heart transplantation. 886 16

Heart disease is a common cause of morbidity in end-stage renal disease (ESRD) patients. The management of heart disease in these patients requires a multidimensional approach to the management of heart failure, coronary disease, and arrhythmias, and to risk factors such as hypertension, anemia, secondary hyperparathyroidism, and electrolyte/acid-base disturbances. Coronary artery disease management includes use of antianginal drugs and revascularization of coronary arteries with angioplasty +/- stent placement or coronary artery bypass grafting. The long-term outcomes of these procedures need to be assessed and improved. Hypertension occupies a major role in the pathogenesis of heart disease in ESRD, and early and adequate control of hypertension is likely to have a major impact on the progression of cardiac disease. This entails the achievement of optimal volume status, combined with the appropriate use of antihypertensive agents such as calcium channel blockers, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, vasodilators, alpha-blockers, and central sympatholytic drugs. In ESRD patients, specific dialysis-related complications such as intradialytic hypotension and pericardial effusion may have additional effects on cardiac function and require attention. The choice of dialysate composition and membrane may influence clinical outcomes with specific effects on cardiac performance.
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PMID:Cardiac disease in chronic uremia: management. 923 29

We present three cases of patients with prostate carcinoma who underwent total body bone scintigraphy with 99mTc-Hydroxymethylene diphosphonate (99mTc-HMDP), showing myocardial uptake. Complementary diagnostic examinations were performed in these patients: cardiac (electrocardiogram and echocardiography), analysis of plasma electrolytes, including calcium, review of personal background of each patient to rule out associated disease which could have produced this uptake. No evidence of associated disease was found, processes such as heart disease, amyloidosis, hyperparathyroidism, previous chemotherapy or radiotherapy being rule out. Thus, we conclude that the myocardial uptake was secondary to the prostate carcinoma.
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PMID:[Benign myocardial uptake of 99mTc-HMDP in prostate carcinoma: based on three cases]. 1255 32

Vitamin D is taken for granted and is not appreciated for its importance in overall health and well-being. Vitamin D, known as the sunshine vitamin, is appreciated as being important for the prevention of rickets in children. It is now recognized that vitamin D is important for not only the growing skeleton, but for the maintenance of a healthy musculoskeletal system throughout life. Vitamin D deficiency in adults precipitates and exacerbates osteoporosis and causes the painful bone disease osteomalacia. The revelation that vitamin D is biologically inactive and requires sequential hydroxylations in the liver and kidney to form 1,25-dihydroxyvitamin D helps explain why patients with renal failure are often resistant to vitamin D and suffer from secondary hyperparathyroidism and renal osteodystrophy. In addition to its role in maintaining calcium and phosphorus homeostasis, vitamin D is now being recognized as important for maintaining maximum muscle strength and for the prevention of many chronic diseases, including type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common cancers. Vitamin D status is best determined by the measurement of circulating levels of 25-hydroxyvitamin D. Vigilance for maintaining a 25-hydroxyvitamin D level of at least 20 ng/ml and preferably 30-50 ng/ml has important benefits for both healthy children and adults, as well as children and adults suffering from chronic kidney disease.
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PMID:Vitamin D for health and in chronic kidney disease. 1607 48

Vitamin D deficiency is now recognized as an epidemic in the United States. The major source of vitamin D for both children and adults is from sensible sun exposure. In the absence of sun exposure 1000 IU of cholecalciferol is required daily for both children and adults. Vitamin D deficiency causes poor mineralization of the collagen matrix in young children's bones leading to growth retardation and bone deformities known as rickets. In adults, vitamin D deficiency induces secondary hyperparathyroidism, which causes a loss of matrix and minerals, thus increasing the risk of osteoporosis and fractures. In addition, the poor mineralization of newly laid down bone matrix in adult bone results in the painful bone disease of osteomalacia. Vitamin D deficiency causes muscle weakness, increasing the risk of falling and fractures. Vitamin D deficiency also has other serious consequences on overall health and well-being. There is mounting scientific evidence that implicates vitamin D deficiency with an increased risk of type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common deadly cancers. Vigilance of one's vitamin D status by the yearly measurement of 25-hydroxyvitamin D should be part of an annual physical examination.
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PMID:The vitamin D epidemic and its health consequences. 1625 41

Most public health statements regarding exposure to solar ultraviolet radiation (UVR) recommend avoiding it, especially at midday, and using sunscreen. Excess UVR is a primary risk factor for skin cancers, premature photoageing and the development of cataracts. In addition, some people are especially sensitive to UVR, sometimes due to concomitant illness or drug therapy. However, if applied uncritically, these guidelines may actually cause more harm than good. Humans derive most of their serum 25-hydroxycholecalciferol (25(OH)D3) from solar UVB radiation (280-315 nm). Serum 25(OH)D3 metabolite levels are often inadequate for optimal health in many populations, especially those with darker skin pigmentation, those living at high latitudes, those living largely indoors and in urban areas, and during winter in all but the sunniest climates. In the absence of adequate solar UVB exposure or artificial UVB, vitamin D can be obtained from dietary sources or supplements. There is compelling evidence that low vitamin D levels lead to increased risk of developing rickets, osteoporosis and osteomaloma, 16 cancers (including cancers of breast, ovary, prostate and non-Hodgkin's lymphoma), and other chronic diseases such as psoriasis, diabetes mellitus, hypertension, heart disease, myopathy, multiple sclerosis, schizophrenia, hyperparathyroidism and susceptibility to tuberculosis. The health benefits of UVB seem to outweigh the adverse effects. The risks can be minimized by avoiding sunburn, excess UVR exposure and by attention to dietary factors, such as antioxidants and limiting energy and fat consumption. It is anticipated that increasing attention will be paid to the benefits of UVB radiation and vitamin D and that health guidelines will be revised in the near future.
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PMID:Sunshine is good medicine. The health benefits of ultraviolet-B induced vitamin D production. 1716 34

The progressive loss of kidney function in patients with chronic kidney disease (CKD) is associated with a number of complications, including cardiovascular diseases, anemia, hyperparathyroidism, inflammation, metabolic acidosis, malnutrition and protein-energy wasting. The excess cardiovascular risk related to CKD is due in part to a higher prevalence of traditional atherosclerotic risk factors, in part to non-traditional, emerging risk factors peculiar to CKD. While even minor renal dysfunction is an independent predictor of adverse cardiovascular prognosis, nutritional changes are more often observed in an advanced setting. In addition, factors related to renal-replacement treatment may be implicated in the pathogenesis of heart disease and protein-energy wasting in dialysis-treated patients. Progressive alterations in kidney metabolism may cause progressive effects on cardiovascular status and nutrition. Altered kidney amino acid/protein metabolism and or excretion may be a key factor in the homeostasis of several vasoactive compounds and hormones in patients with more advanced disease. In this discussion recent research regarding the kidney handling of amino acids and protein turnover and their potential link with cardiovascular disease, progressive kidney dysfunction and nutritional status are reviewed.
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PMID:Amino acid and protein metabolism in the human kidney and in patients with chronic kidney disease. 2020 54

Chronic kidney disease has been increasingly recognized as a risk factor for incident heart failure. Despite advances in chronic heart failure treatment, the prognosis remains poor. The annual mortality from all cardiovascular causes in the end stage renal disease population is significantly higher than the general population, accounting for more than half of all deaths in this group. The mechanisms underlying the enhanced susceptibility to myocardial ischemia in chronic kidney disease are not well defined. Traditional cardiovascular risk factors, although common in chronic kidney disease, do not exert the same impact as in the general population. The presence of "renal-specific" non-traditional risk factors including endothelial dysfunction, inflammation, oxidative stress, anaemia, proteinuria and changes in vitamin D metabolism (encompassing the complex interactions of calcium and phosphate metabolism, hyperparathyroidism and vascular calcification) play an important role in cardiovascular disease progression. An increased understanding of the array of metabolic changes/adaptations occurring in uraemic heart disease have allowed one to consider optimal management strategies and to develop new strategies for future management of uraemic heart disease.
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PMID:Risk factors and metabolic mechanisms in the pathogenesis of uraemic cardiac disease. 2119 37


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