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)

The annual statistical survey conducted at the end of 2000 by the Japanese Society for Dialysis Therapy collected responses from 3358 (99.94%) of 3360 institutions. Japan's total dialysis patient population at the end of the year 2000, as identified by this survey, was 206,134, an increase of 8921 (4.5%) over 1999. This translates to 1624.1 patients per million population. The annual crude mortality rate was 9.4% for the period starting at the end of the year 1999 and ending at the end of the year 2000. The mean patient age at the initiation of dialysis treatment was 63.8 (+/- 13.9; +/- SD) years; the mean age of the overall dialysis patient population was 61.2 years (+/- 13.3). Both these mean ages, which had been increasing since 1983, again continued to increase. Among the primary diagnosis, the prevalence of diabetic nephropathy had continued to increase again since 1999, to 36.6%, whereas that of chronic glomerulonephritis had continued to decline, down to 32.5%, during the same one-year period since the 1999 survey. The 2000 years-end survey incorporated the following additional variables for the first time: usage of oral antihypertensives, pre- and post-dialysis systolic and diastolic blood pressures, serum HDL cholesterol level, types and dosage of oral Vitamin D analogs administered, dosage of oral calcium carbonate administered, history of intervention for peripheral vascular disease (bypass surgery, synthetic graft replacement, stenting), history of coronary artery bypass grafting (CABG), history of percutaneous transluminal coronary angioplasty (PTCA), whether stenting had been previously performed for the treatment of ischemic heart disease, number of cigarettes smoked, the type of vascular access used at the initiation of dialysis, and the year and month the vascular access was created. The survey results indicate that 60.9% of the total dialysis patient population was using oral antihypertensives. The patients' mean serum HDL cholesterol level was 47.65 +/- 18.47 mg/dL, showing positive correlation with serum albumin level and reverse correlation with body mass index. 1.6% of all dialysis patients had previously undergone amputation, and 0.7% had a history of bypass surgery for peripheral vascular disorder. 4.5% of hemodialysis patients had a history of cardiac infarction, 1.6% had previously undergone CABG, and 2.8%, PTCA. At the time the survey was conducted, 2.0% of all dialysis patients were undergoing oral Vitamin D analog pulse therapy, and 6% were undergoing intravenous Vitamin D analog pulse therapy. A history of amputation, myocardial infarction, cerebral infarction, and cerebral bleeding were identified as high-risk factors of vital prognosis. Additionally, high mortality risk was associated with the following: glutamic-pyruvic transaminase levels exceeding 20 IU/L; positive HCV antibody status; comorbid conditions such as hepatic cell carcinoma and liver cirrhosis; platelet counts below 100,000/mL or equal to or greater than 200,000/mL; C-reactive protein levels of 0.2 mg/dL and higher, leukocyte counts of less than 3000/mL or equal to or greater than 8000/mL; and body mass index of below 22 kg/m2, as well as total serum cholesterol levels of below 160 mg/dL or equal to or greater than 260 mg/dL.
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PMID:The current state of chronic dialysis treatment in Japan (as of December 31, 2000). 1292 Nov 11

The incidence of ischemic heart disease shows a sharp rise after menopause. However, the effects of hormone replacement therapy (HRT) on cardiovascular disease are still controversial. Not only oxidative stress, but also inflammation has been suggested to play an important role in the pathogenesis of cardiovascular events. We compared the effects of HRT on endothelial function, cellular antioxidant system and inflammation between oral and transdermal administration in mild hypercholesterolemic postmenopausal women. Transdermal estradiol replacement was administrated to 12 patients (mean age 53 years) for 12 weeks, and oral conjugated equine estrogen was administrated to 12 patients (mean age 54 years) for 12 weeks. The flow-mediated endothelium-dependent dilation of the brachial artery, serum levels of thioredoxin as a marker of the cytoprotective antioxidant system, and high-sensitivity C-reactive protein (hs-CRP) were measured every 4 weeks. The flow-mediated vasodilation increased with HRT (oral, baseline 4.9 +/- 0.5, 4-week 8.9 +/- 0.7*, 8-week 9.9 +/- 0.6*, 12-week 9.4 +/- 0.7*; transdermal, 4.7 +/- 0.6, 8.3 +/- 0.7*, 9.1 +/- 0.8*, 8.9 +/- 0.9%*, * = p < 0.01 versus baseline). The thioredoxin levels decreased with HRT (oral, 26.1 +/- 7.2, 24.1 +/- 8.2, 22.1 +/- 7.8, 19.1 +/- 7.0*; transdermal, 26.9 +/- 7.4, 23.4 +/- 8.7, 21.1 +/- 7.9, 19.2 +/- 7.2 ng/ml*, * = p < 0.01 versus baseline). There were no differences in the variation of the flow-mediated vasodilation or thioredoxin concentrations between the 2 groups. The hs-CRP levels increased with oral HRT (0.32 +/- 0.12, 0.72 +/- 0.17*, 0.86 +/- 0.23*, 0.88 +/- 0.21 mg/dl*, * = p < 0.01 versus baseline), while transdermal HRT did not elicit any changes (0.35 +/- 0.15, 0.34 +/- 0.17, 0.38 +/- 0.20, 0.36 +/- 0.22 mg/dl). The differences of hs-CRP concentrations between the 2 groups analyzed by 2-way ANOVA were significant (p < 0.01). Oral HRT instigated inflammation, but transdermal did not. Both oral and transdermal HRT, however, improved endothelial function and decreased oxidative stress through affecting the cellular redox state. These differentials in the effects caused by the course of administration may affect the future cardiovascular events.
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PMID:Effects of transdermal and oral estrogen supplementation on endothelial function, inflammation and cellular redox state. 1294 May 91

To investigate whether marked and sustained lipid-lowering in subjects with stable angina pectoris and dyslipidemia reduces exercise-induced myocardial ischemia, 17 subjects were treated with dose-adjusted atorvastatin over 1 year and underwent serial evaluation of exercise electrocardiographic ischemic parameters, serum biomarkers, and brachial artery endothelial function. Endothelial function improved progressively and C-reactive protein, P-selectin, and tissue plasminogen activator inhibitor levels decreased, but there was no decrease in exercise electrocardiographic ischemia.
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PMID:Effect of atorvastatin on exercise-induced myocardial ischemia in patients with stable angina pectoris. 1460 94

Relative deficiency of pentraxin proteins is implicated in the pathogenesis of systemic lupus erythematosus. The C-reactive protein (CRP) response is defective in patients with acute flares of disease, and mice with targeted deletions of the serum amyloid P component gene (Sap) develop a lupus-like illness. In humans, the genes for CRP (CRP) and SAP (APCS) map to 1q23.2 within an interval linked with SLE. We have investigated the candidate genes CRP and APCS in two cohorts totalling 586 UK simplex SLE families. The inheritance of an intronic dinucleotide repeat and seven single nucleotide polymorphisms in the CRP and APCS genes was examined by application of family-based tests of association and linkage. Basal levels of CRP were influenced independently by two polymorphisms at the CRP locus, CRP 2 and CRP 4. Furthermore, the latter polymorphism was linked/associated with SLE and antinuclear autoantibody production. Thus, the polymorphism associated with reduced basal CRP was also associated with the development of SLE. These data support the hypothesis that defective disposal of potentially immunogenic material is a contributory factor in lupus pathogenesis. The identification of polymorphisms that determine basal CRP levels has implications in ischaemic heart disease, where CRP level is an important predictor of risk.
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PMID:Polymorphism at the C-reactive protein locus influences gene expression and predisposes to systemic lupus erythematosus. 1464 6

Cardiovascular disease (CVD) rates in dialysis patients are very high. One of the many associated risk factors is chronic inflammation. The relationship of baseline markers of chronic inflammation with the presence of CVD was assessed in a large cohort of stable dialysis patients. Median time (IQR) on dialysis treatment was 20(9-52) months. Forty-one patients had CVD (as defined by the history / clinical presence of ischemic heart disease, peripheral vascular disease, or cerebrovascular disease). Patients with CVD were significantly older than patients without (67 + /- 11 vs. 54 + /- 10 yrs, p < 0.03). Time from dialysis, urea reduction ratio (hemodialysis only) and smoking history were similar between the two groups. Patients with CVD had significantly higher levels of sialic acid (SA) (91.2 +/- 24.2 vs. 82.0 + /- 18.2 mg/dL, p = 0.03). Body weight, plasma fibrinogen, C-reactive protein (CRP), homocysteine, creatinine, total-, LDL (low density lipoprotein)-, or HDL (high density lipoprotein)-cholesterol, systolic, diastolic and pulse pressures did not differ between the CVD and CVD(-) groups. Patients on chronic ambulatory peritoneal dialysis (CAPD) had more elevated lipid fractions, inflammatory markers, and SA levels than did patients on hemodialysis (HD). The presence of diabetes, the use of lipid-lowering therapy, and smoking history was not associated with any difference in SA levels. In contrast to C-reactive protein (CRP) concentrations, SA levels were unaffected by the hemodialysis session. SA was strongly correlated with CRP (r = 0.59, p < 0.0001), but not with patient age, any measure of blood pressure (BP), urea reduction ratio, plasma creatinine, lipid fractions or homocysteine. Levels of the chronic inflammation marker sialic acid correlate strongly with CRP and are increased in patients with cardiovascular disease, but show no relationship to hemodialysis session. Thus sialic acid may be a superior marker to CRP for assessment of chronic inflammation in patients undergoing dialysis.
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PMID:Raised plasma total sialic acid levels are markers of cardiovascular disease in renal dialysis patients. 1469 56

Cardiovascular diseases (CVD) remain the major cause of death in postmenopausal women. Before menopause, women are relatively protected from ischemic heart disease and thromboembolism by their circulating estrogens, but this protection is lost after menopause. Following menopause, adverse lipid changes occur and the levels of several coagulation factor increase. One of the major predisposing factors for CVD is the metabolic syndrome, including myriad risk biomarkers: abdominal girth, blood pressure, fasting glucose, triglycerides, lipids. In many ways, the metabolic syndrome is a precursor to the development of abnormalities of insulin action and diabetes. In parallel, there are effects upon blood coagulation and fibrinolysis. Common preventive therapies require rigorous evaluation. Hormone replacement therapy (HRT) has not produced the expected reduction in CVD and the ideal HRT is probably unobtainable. For long-term HRT users, the risk of thromboembolism needs to be weighed against probable benefits. With respect to the effects of HRT, oral estrogen is associated with elevation in C-reactive protein and varied effects on IL-6, but transdermal estradiol has no significant effect on these parameters. Despite the varied effects of HRT on inflammatory biomarkers, there is no definitive evidence that change in these markers results in modification of cardiovascular risk.
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PMID:[The metabolic syndrome in postmenopausal women. Clinical implications]. 1472 60

Platelet-leukocyte conjugates are increased in patients with coronary artery disease but the relationship between conjugate formation and myocardial ischemic outcome is unknown. We prospectively evaluated the relationship between conjugate formation and the development of recurrent myocardial ischemia in patients with acute coronary syndromes (ACS). Platelet-leukocyte conjugate formation (induced by thrombin receptor activating peptide (TRAP)) and platelet aggregation (induced by ADP and arachidonic acid) were assessed in 30 patients with unstable angina or non-ST elevation myocardial infarction. All patients were treated with beta-blockers, aspirin, heparin, and GPIIb-IIIa antagonists and were followed for in-hospital recurrent myocardial ischemia. Troponin I and C-reactive protein (CRP) were also measured. Seven patients (23%) experienced recurrent ischemia. Platelet-neutrophil conjugates were greater in ischemic patients (59 +/- 9 and 36 +/- 4%, P = 0.007, for + ischemia and -ischemia, respectively). Platelet aggregation did not differ between ischemic and nonischemic patients, and there was no significant relationship between aspirin resistance and ischemic outcome. Troponin I was greater in patients who developed recurrent ischemia (3.04 +/- 1.73 vs. 0.70 +/- 0.21 ng/ml, P = 0.03, for +ischemia and -ischemia, respectively) but CRP was not. TRAP-induced platelet-neutrophil conjugate formation was an independent predictor of ischemic outcome (OR 1.07, 95% CI 1.00-1.15, for each 1% increase in conjugate formation). Receiver operator characteristic analysis showed platelet-neutrophil conjugates to have good ability to discriminate between ischemic and nonischemic patients (AUC of 0.84, P < 0.05). TRAP induced platelet-neutrophil conjugate formation is related to in vivo ischemic risk in ACS patients.
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PMID:Prospective evaluation of the relationship between platelet-leukocyte conjugate formation and recurrent myocardial ischemia in patients with acute coronary syndromes. 1498 71

This study examined the relation between high-sensitivity C-reactive protein (CRP), exercise-induced myocardial ischemia, and exercise tolerance in 288 stable patients who underwent maximal treadmill stress testing. CRP was correlated with peak exercise workload, which was consistent with the long-term predictive value of peak workload and CRP for outcome events. There was no correlation of high-sensitivity CRP with stress-induced ischemia, which is consistent with a lack of correlation between CRP and the degree of chronic luminal coronary arterial narrowing.
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PMID:Relation between C-reactive protein, treadmill exercise testing, and inducible myocardial ischemia. 1499 91

We observed the association between a persistent elevation of C-reactive protein (CRP) level and the presence of ischemic heart disease in 73 peritoneal dialysis (PD) patients. Twenty-six patients showed an elevation of CRP for more than 6 months. Seventeen (65%) of the 26 patients had positive thallium single photon computed tomography (SPECT). Three of 9 patients who had a persistent elevation of CRP and negative thallium SPECT had a history of cerebral infarction or peripheral vascular disease. Therefore, 77% (20/26) of an elevated CRP level that lasted longer than 6 months can be explained by the presence of atherosclerotic vascular disease. There are as yet no valid recommendations on how chronic inflammation should be handled. We found that aspirin 200 mg daily for 8 weeks induce no significant changes of the CRP levels in PD patients (0.22 vs. 0.18 mg/dL, p > 0.05). However, 62 HD patients were randomly assigned to treatment group (simvastatin 20 mg/day) and control group. After 8 weeks medication, hs-CRP levels significantly reduced from a median of 0.23 mg/dL to 0.12 mg/dL.
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PMID:C-reactive protein as a cardiovascular risk factor and its therapeutic implications in end-stage renal disease patients. 1501 90

For the first time the involvement of C-Reactive protein (CRP) in early (acute) and delayed ischemic (IPC) and pharmacological (chemical) preconditioning (CPC) in an in vivo model of rat myocardial infarction was presented. Acute IPC was produced by three 5 minute occlusion (ischemia) periods interspersed with 5 minute reperfusion, followed by 30 minute occlusion of the left coronary artery and 2 hour reperfusion injury. Acute CPC was produced by a k-opioid receptor agonist U50488H (5 mg/kg) applied i.v. 15 minutes before 30 minute ischemia/ 2 hour reperfusion. Delayed preconditioning was produced by 30 minute ischemia/ 2 hour reperfusion, induced 24 hour after either ischemic or pharmacological preconditioning. The myocardial ischemia/reperfusion injury was evaluated on the basis of total and cardiac creatine kinase isoenzyme activity, functional recovery of the heart (ECG), infarct size (% IS/RA) and mortality at the end of the experiments. The results obtained showed that: k-opioid receptor agonist U50488H mimics both the acute and delayed IPC in the above experimental protocol; Both acute IPC and most probably CPC act by opening of K(ATP) channels (the effects were blocked by nonspecific ATP-sensitive K channel blocker glybenclamide), and via activation of protein kinase C (a selective protein kinase C inhibitor chelerythrine blocked the efects); C-reactive protein (CRP) was significantly elevated by 54% in non-preconditioned acute ischemia/reperfusion injury. The elevation was more pronounced (82% increase) 24 hour after non-preconditioned ischemia/reperfusion injury. It reflected very well the increase in cardiac isoenzymes, infarct size and mortality of the rats, and can be used as a marker of the severity of myocardial injury in this model; The increase of CRP was prevented by both IPC and CPC in early, and especially in late preconditioning. This confirms the involvement of CRP as a marker in cardiac ischemic/reperfusion injury. It was concluded that in addition to the established involvement of adenosine, bradykinin, opioid and other receptors, a suppression of myocardial CRP/complement production might be involved in the biological mechanism of preconditioning. This could be a promising perspective in clinical interventions against ischemia/reperfusion injuries of the heart.
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PMID:The role of C-reactive protein in ischemia/reperfusion injury and preconditioning in a rat model of myocardial infarction. 1519 50


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