Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D has been proposed as a risk factor of ischaemic heart disease. In 12 patients with acute myocardial infarction the major circulating vitamin D metabolite, 25-hydroxy-cholecalciferol (25-HCC), did not show any fluctuations during the first 4 days after onset of symptoms. The serum 25-HCC level was then measured in 128 patients consecutively admitted because of chest pain, 53 of whom had myocardial infarction and 75 had angina pectoris. The values found did not differ from those measured in 409 normal persons. The seasonal variations of serum 25-HCC were less pronounced in heart patients than in normals, probably due to less sun exposure in the summer months. The levels of serum 25-HCC did not correlate with the concentrations of serum cholesterol, glycerides, calcium or magnesium. Low serum calcium and magnesium were observed in all patients. Serum calcium was further reduced in the course of acute myocardial infarctions while serum parathyroid hormone rose significantly. We conclude that patients with ischaemic heart disease are not ingesting or producing in their skin elevated amount of vitamin D.
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PMID:Vitamin D and ischaemic heart disease. 74 75

In 40 patients with ischaemic heart disease the serum levels of magnesium, parathyroid hormone (PTH), phosphate, calcium, and ionized calcium remained unchanged and within normal limits following treatment for 12 months with alprenolol (n = 20) or placebo (n = 20). No changes occurred during a 2 week withdrawal period. The clinical implication is that the non-cardioselective betablocker alprenolol can be given to patients with ischaemic heart disease without the risk of inducing potentially cardiotoxic disturbances in serum magnesium and serum calcium levels. Whether this applies to cardioselective beta-blockers remains to be established.
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PMID:Serum magnesium, calcium, phosphate and PTH following long-term beta-blockade in ischaemic heart disease. 289 11

Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of intravenous magnesium therapy on serum and urine levels of potassium, calcium, and sodium in patients with ischemic heart disease, with and without acute myocardial infarction. 304 40

The exercise capacity of 20 predialytic uraemic patients (mean age 43 +/- 12 years) was studied prospectively. Nine of these patients were examined twice in a longitudinal study. The maximal working capacity, measured by standardized exercise test on a bicycle ergometer, averaged 74 +/- 19% of the expected normal. Normal exercise ECG were registered in 16 out of 20 patients. Total hemoglobin/kg body weight (THb) was 67 +/- 16% of the expected normal and serum parathyroid hormone concentration (PTH) was 39 +/- 39 micrograms/l (normal range 0.5-1.5). Partial correlation showed a correlation between exercise capacity and PTH (p less than 0.05). In the longitudinal study the decrease in steady state exercise capacity was correlated to the decrease in THb (p less than 0.05), but not to the increase in PTH. In conclusion, patients with predialytic uraemia have a reduced maximal working capacity, due to several possible factors one of which is a reduced THb. Ischaemic heart disease seems to be of minor importance.
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PMID:Factors limiting physical working capacity in predialytic uraemic patients. 367 71

Molecular fragment 1-34 of synthetic bovine parathyroid hormone (bPTH[1-34]) has been found to be a potent coronary vasodilator, a moderate systemic vasodilator, and a positive inotropic agent for the myocardium. On that basis, the hypothesis was tested that "vasoactive" PTH might be effective in the treatment of acute ischemic left ventricular failure (LVF) and the prevention of cardiogenic shock. Dogs whose sympathetic nerve activity was blocked by a combination of reserpine, propranolol, and chlorpromazine were anesthetized and subjected to open-chest occlusion of the left anterior descending coronary artery (LAD) plus sequential ligation of three diagonal branches. In ten untreated animals (control group), acute myocardial ischemia led to LVF and, within 4 hours, to cardiogenic shock (50% or greater reduction in cardiac output; 30% or greater reduction in mean aortic pressure; elevation of left atrial pressure above 20 mm Hg; and significant elevation of arterial blood lactate concentration). At the end of 4 hours, myocardial infarction measured by the incubation of transverse slices of the left ventricle in TTC solution represented 96 +/- 3% of the myocardium "at risk." In ten treated animals (experimental group), PTH(1-34) was administered intravenously, 1 U/kg/min, starting 30 minutes after coronary occlusion. Treatment improved left coronary blood flow from 55 +/- 5 to 120 +/- 11 ml/100 g LV/min, increased cardiac index from 72.5 +/- 7 to 117.5 +/- 12 ml/kg/min, reduced left atrial pressure from 27.5 +/- 2.5 to 15 +/- 2.5 mm Hg (all changes, P less than 0.005), sustained aortic pressure, and prevented the elevation of arterial blood lactate. At the end of 4 hours, myocardial infarction represented 30 +/- 1.2% of the myocardium at risk (difference between the two groups significant, P less than 0.005). Thus, PTH(1-34) exerted a tissue-sparing effect on the myocardium, restored LV function, and prevented the development of shock.
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PMID:Vasoactive parathyroid hormone in the treatment of acute ischemic left ventricular failure and the prevention of cardiogenic shock. 405

A 74-year-old woman with primary hyperparathyroidism and ischemic heart disease was treated with percutaneous ethanol injection into a single parathyroid adenoma which was confirmed by fine-needle aspiration biopsy. The changes in intact parathyroid hormone (int-PTH), serum calcium, serum phosphate, and alkaline phosphatase after percutaneous ethanol injection therapy (PEIT), and also ultrasonic findings of the injected adenoma were examined before and after PEIT. The values of int-PTH and serum calcium remained high for a few hours after the ethanol injection. About 24 hrs later, however, rapid lowering of the serum concentrations of int-PTH and serum calcium was observed, reaching normal levels about 36 hrs later. Although these parameters recurred once, the patient received another three ethanol injections within three months, which normalized these values. In ultrasonic findings, the parathyroid adenoma was well demarcated and hypoechoic before PEIT. Twenty-four hours after the ethanol injection, the adenoma became hyperechoic with a small hypoechoic lesion as viable tissue. Then the tumor shrank gradually and no apparent side-effects was observed in a total of four PEIT. Since in Japan, PEIT for primary hyperparathyroidism has not been widely performed, we propose that this therapy could be a useful alternative treatment in patients in whom parathyroid surgery would not be indicated such as the elderly, patients with high surgical risks, hypercalcemic crisis and patients who refuse surgery.
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PMID:[Changes in serum intact parathyroid hormone levels and ultrasonic findings after percutaneous ethanol injection therapy in a patient with primary hyperparathyroidism]. 789 65

Elevated serum concentrations of 1-84 parathyroid hormone (PTH) after operation for sporadic parathyroid adenoma have been reported in previous studies, years after operation for primary hyperparathyroidism (pHPT). The cause and significance of this finding have not been elucidated. Primary hyperparathyroidism was diagnosed in 195 patients from January 1987 to December 1998. Operation for pHPT was performed in 124 patients. To evaluate long-term effects of elevated serum 1-84 PTH, biochemical variables and pre- and postoperative diseases were investigated from hospital case records. Of the 124 patients operated on, 103 had a solitary adenoma. Among these patients, 60 had normal serum concentrations of 1-84 PTH and calcium postoperatively, 38 patients had follow-up for more than 12 months (range 12-207 months-group A). Persistent elevated serum concentrations of 1-84 PTH and normocalcemia were found in 23 patients. Fourteen patients had follow-up for more than 12 months (range 15-76 months-group B). Two patients had persistent pHPT, and 18 were normocalcemic, but in this retrospective study data on serum 1-84 PTH were not available. No significant differences were found between groups A and B at the time of diagnosis concerning clinical characteristics. More that 12 months after operation for pHPT, the patients in group B, with persistent elevated serum concentrations of 1-84 PTH, had a significantly (c2 = 11, p = 0.005, and power of test 0.66) higher frequency of cardiovascular diseases from ischemic heart disease and hypertension. Persistent elevated serum concentrations of 1-84 PTH after operation for sporadic parathyroid adenoma may be associated with development of cardiovascular disease. This group of patients therefore needs lifelong control and, possibly, medical intervention.
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PMID:Normocalcemia and persistent elevated serum concentrations of 1-84 parathyroid hormone after operation for sporadic parathyroid adenoma: evidence of increased morbidity from cardiovascular disease. 1205 14

Systolic and diastolic left ventricular dysfunction is common and important predictor of risk of death in end-stage renal failure. Systolic dysfunction is defined echocardiographically by a shortening fraction < 25% or an ejection fraction < 40%. Systolic dysfunction has a poor prognosis, strongly associated with myocardial ischemia and left ventricular hypertrophy (LVH). Diastolic dysfunction combines relaxation problems with compliance abnormalities and usually is associated with LVH. It is not clinically possible to distinguish systolic from diastolic LV dysfunction. This underlines the importance of echocardiographic diagnosis. In the present study we have analysed echocardiographically the left ventricular systolic and diastolic function and some possible risk factors contributing to its dysfunction development in patients with chronic renal failure (crf) treated by hemodialysis (HD). From a cohort of 85 patients with crf we selected for analysis 59 clinically stable patients. Echocardiography (ECHO), ECG, body mass index (BMI), serum creatinine, urea, total protein, albumin, hemoglobin, hematocrit, electrolytes, endothelin (ET-1) and parathyroid hormone (PTH) concentrations were evaluated in all patients after HD session. In all HD patients systolic and diastolic LV dysfunction was observed as well as LVH: concentric LVH was detected by ECHO in 46 patients and in 13 patients excentric LVH was observed. Mean serum concentrations of urea, creatinine, endothelin (ET-1), PTH and phosphate were increased while serum concentration of hemoglobin, total protein, albumin, sodium, potassium, calcium were in the normal range. Positive correlation was found between PTH serum concentration and LVM r = 0.704 (p < 0.001), between PTH serum concentration and IVS r = 0.267 (p < 0.04), between PTH serum concentration and PW r = -0.238 (p < 0.04), between ET-1 and RWT r = 0.447 (p < 0.04) and negative correlation between BMI and LVMI r = -0.451 (p < 0.05). Our observations suggests that uremic cardiomyopathy is heterogenous (systolic and diastolic dysfunction) and multifactoral. The correlations between serum PTH concentration and LVH and between BMI and LVH confirmed that both hyperparathyroidism and malnutrition are important factors influencing the development of LVH which plays an important role in the systolic and diastolic cardiac failure in HD patients.
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PMID:[Left ventricular systolic and diastolic dysfunction in patients with chronic renal failure treated with hemodialysis]. 1293 88

Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants-atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis-arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. In end-stage renal disease, a "perfect storm" of vascular calcification often occurs, with hyperglycemia, hyperphosphatemia, hypercholesterolemia, hypertension, parathyroid hormone resistance, and iatrogenic calcitriol excess contributing to severe calcific vasculopathy. This brief review recounts emerging themes in the pathobiology of vascular calcification and highlights some fundamental deficiencies in our understanding of vascular endocrinology and metabolism that are immediately relevant to human health and health care.
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PMID:Osteogenic regulation of vascular calcification: an early perspective. 1510 15

The reduction of cardiovascular disease risk in kidney failure involves treatment of modifiable risk factors and provision of proven interventions to patients with established disease. Volume status management is key to blood pressure control. Statins are the agents of choice for the treatment of dyslipidemia. Target hemoglobin levels should be achieved using intravenous iron and erythropoietic agents. Combinations of calcium and noncalcium-containing phosphorus binders and vitamin D and its analogues should be used to attain target parathyroid hormone, phosphorus, and calcium phosphorus product levels. beta Blockers and aspirin are recommended in patients with ischemic heart disease and angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers), and beta blockers are recommended in patients with heart failure with reduced ejection fraction. In patients who require revascularization, studies suggest a survival benefit of coronary artery bypass graft surgery over percutaneous transluminal coronary angioplasty and coronary artery stenting.
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PMID:Treating the Patient with Kidney Failure to Reduce Cardiovascular Disease Risk. 1521 21


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