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)

Despite a dramatic decline in mortality over the past three decades, coronary heart disease is the leading cause of death and disability in the U.S. Importantly, recent advances in the field of cardiovascular medicine have not led to significant declines in case fatality rates for women when compared to the dramatic declines realized for men. The current review highlights gender-specific issues in ischemic heart disease presentation, evaluation, and outcomes with a special focus on the results published from the National Institutes of Health-National Heart, Lung, and Blood Institute-sponsored Women's Ischemia Syndrome Evaluation (WISE) study. We will present recent evidence on traditional and novel risk markers (e.g., high sensitivity C-reactive protein) as well as gender-specific differences in symptoms and diagnostic approaches. An overview of currently available diagnostic test evidence (including exercise electrocardiography and stress echocardiography and single-photon emission computed tomographic imaging) in symptomatic women will be presented as well as data using innovative imaging techniques such as magnetic resonance subendocardial perfusion, and spectroscopic imaging will also be discussed.
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PMID:Insights from the NHLBI-Sponsored Women's Ischemia Syndrome Evaluation (WISE) Study: Part I: gender differences in traditional and novel risk factors, symptom evaluation, and gender-optimized diagnostic strategies. 1645 70

The present study provides evidence that inducible nitric-oxide synthase (iNOS)-mediated nitrative stress plays a pivotal role in chronic beta-adrenergic receptor (AR) stimulation-induced cardiac damage. In mice, 14 days of isoproterenol (ISO) stimulation via an osmotic minipump induced an up-regulation of iNOS as evidenced by increases in mRNA, protein expression, and immunochemical staining of myocardial iNOS. Serum level of C-reactive protein, an inflammatory mediator, was also markedly increased. Under chronic ISO stimulation, the up-regulated iNOS produced a significantly increased amount of nitric oxide (NO) and its byproduct, peroxynitrite, in the circulation and heart and subsequently resulted in an accelerated myocardial apoptosis. Forty-minute myocardial ischemia (MI) and 24-h reperfusion (R) further increased NO production and peroxynitrite formation and resulted in an enlarged infarct size in mice receiving chronic ISO stimulation. However, the treatment with a selective iNOS inhibitor [N-(3-(aminomethyl) benzyl)acetamidine] (1400W) or the use of a genetic modified animal (iNOS-knockout mice) markedly reduced iNOS-mediated production of NO and formation of peroxynitrite and consequently significantly decreased myocardial apoptosis and infarct size, showing a crucial link between iNOS-mediated nitrative stress and myocardial injury. In conclusion, chronic beta-AR stimulation up-regulates iNOS expression and increases NO production in the heart, which subsequently markedly enhances formation of reactive nitrogen species/peroxynitrite in the heart, thereby eliciting myocardial apoptosis and potentiating MI/R injury.
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PMID:Chronic beta-adrenergic receptor stimulation induces cardiac apoptosis and aggravates myocardial ischemia/reperfusion injury by provoking inducible nitric-oxide synthase-mediated nitrative stress. 1657 80

Serum levels of inflammatory markers (interleukin-6, monocyte chemoattractant protein-1, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, and C-reactive protein) were measured at baseline in serum samples from 189 patients who were admitted for coronary angiography because of suspected ischemic heart disease. Median duration of follow-up was 28 months. Patients in our sample were enrolled in 4 diagnostic groups: no hemodynamically significant coronary artery disease (CAD) and no coronary vasospasm (control group, n = 32), hemodynamically significant CAD and stable angina pectoris (SAP group, n = 34), coronary vasospastic angina pectoris without hemodynamically significant CAD (vasospasm group, n = 31), and acute coronary syndrome (ACS) and hemodynamically significant CAD (ACS group, n = 92). Overall, the level of serum inflammatory markers was highest in the ACS group and lowest in the control group, with intermediate values observed in the SAP and vasospasm groups, with the exception of soluble intercellular adhesion molecule-1, the level of which was highest in the vasospasm group. Multivariate analysis showed that log (interleukin-6) was independently associated with a diagnosis of coronary vasospastic angina pectoris in patients without hemodynamically significant CAD (odds ratio 8.48, p = 0.027). Patients in the ACS group had a significantly lower survival rate compared with the other 3 groups but without an independent predictor that could be identified in this patient cohort. Recurrent angina pectoris occurred with similar rates in the SAP, vasospasm, and ACS groups. The independent predictor for recurrent angina pectoris was treatment that did not include clopidogrel (odds ratio 3.88, p = 0.007). In conclusion, the results of this study suggest that inflammation can exist in coronary vasospasm without hemodynamically significant CAD.
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PMID:Comparison of serum levels of inflammatory markers in patients with coronary vasospasm without significant fixed coronary artery disease versus patients with stable angina pectoris and acute coronary syndromes with significant fixed coronary artery disease. 1667 78

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 +/-1.34 vs 6.37 +/-1.85 ng/mL, p=0.021 and 8.22 +/-3.13 vs 6.37 +/-1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 +/-5.96 vs 11.40 +/-2.11 micromol/L, p=0.025) and patients with STEMI (15.90 +/-5.02 vs 11.40 +/-2.11 micromol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 +/-1.39 vs 3.45 +/-1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.
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PMID:Increased serum leptin concentrations in patients with chronic stable angina pectoris and ST-elevated myocardial infarction. 1670 86

Cardiovascular diseases are more common in renal transplant recipients than in the general population, and a number of 'traditional' risk factors, such as smoking, diabetes mellitus and dyslipidaemia, are known to be associated with an increased risk. However, concentrating solely on these risk factors can lead to an underestimation of the true risk in this patient population, because other factors such as C-reactive protein and homocysteine levels are also associated with cardiovascular morbidity and mortality. Renal insufficiency also appears to be a key cardiovascular risk factor in the general population, with increasing proteinuria and decreasing glomerular filtration rate related to increased risk. In renal transplant recipients, a high proportion of whom have some renal insufficiency, the role of graft dysfunction in cardiovascular risk is controversial. While some studies have shown no correlation between graft dysfunction and congestive heart failure or ischaemic heart disease, registry data suggest that increased post-transplant serum creatinine levels are strongly associated with cardiovascular risk. This is believed to be the result of cardiovascular disease developing in the pre-transplantation period, as renal transplantation has been shown significantly to improve cardiovascular risk. As such, renal transplant recipients should be routinely screened for cardiovascular disease pre-transplantation, and immunosuppressive therapy should be tailored to minimize further risk. Different immunosuppressive agents, such as corticosteroids and calcineurin inhibitors, are associated with different exposure to cardiovascular risk, and studies involving withdrawal of these agents have generally shown improvement in parameters such as blood pressure and dyslipidaemia. However, these benefits are often associated with an increased incidence of acute rejection, although overall graft loss and mortality rates are not affected. Further studies are required to determine optimal regimens for minimizing cardiovascular risk in renal transplant recipients.
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PMID:Cardiovascular risk factors in renal transplantation--current controversies. 1681 54

Rosuvastatin (10 mg) was given for 3 months to 30 men (mean age 57+/-9 years) with total cholesterol (CH) above 5.2 mmol/l. Questioning, physical examination, registration of ECG, measurement of levels of total, low density lipoprotein (LDL), high density lipoprotein (HDL) CH, and triglycerides (TG), assessment of endothelium-dependent brachial artery dilation were carried out at baseline and in 3 months. It was noted that 3 months therapy with rosuvastatin exerted positive effect on blood lipid spectrum: lowering of concentration of total CH (-31%, baseline 6.52+/-0.92, after therapy 4.47+/-0.96 mmol/l, p<0.0001), TG (-39%, baseline 2.73+/-1.56, after therapy 1.67+/-0.71 mmol/l, p<0.001), LDLCH (-44%, baseline 4.11+/-0.85, after therapy 2.40+/-0.90 mmol/l, p<0.0001), elevation of HDLCH (+6%, baseline 1.15+/-0.27, after therapy 1.22+/-0.34 mmol/l, p=0.08). Target LDL CH level (<2.6 mmol/l) was achieved in 23 patients (77%). Significant lowering of concentration of C-reactive protein (CRP) (-56%) and interleukin 6 (-25%) was also established. Before beginning of therapy mean flow dependent dilation was 6.1+/-1.64%, after therapy -- 10.4+/-5.0% (p<0.05). Treatment of men with ischemic heart disease with rosuvastatin (10 mg for 3 months) led to achievement of target values of LDLCH in 77% of them, to significant lowering of concentrations of CRP and interleukin 6, and to improvement of endothelial function.
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PMID:[Effect of therapy with rosuvastatin on lipid spectrum, factors of inflammation and endothelial function in patients with ischemic heart disease]. 1685 47

Recent years have brought many new advances concerning etiology and pathology of atherosclerosis and cardiovascular risk. However, there are still researches taking place to improve currently used Scales of Cardiovascular Risk, which introduce novel biomarkers of inflammatory process, hemostasis or oxidative stress in order to identify individuals who are the most endangered group of cardiovascular event. This study's aim was to review existing cardiovascular risk factors and risk assessment scales and to confront their clinical usefulness with novel biomarkers emerging in this field with special respect to high sensivity C-reactive protein (hsCRP). Existing cardiovascular risk assessment scales seem not to be endangered in their prognostic role mainly due to crucial role of individual medical history in diagnosis ischaemic heart disease and evaluating the cardiovascular risk. For the time being, despite many novelties appearing in cardiovascular risk evaluation, only hsCRP has unarguably proven prognostic ability in terms of coronary events and may have addictive informative power towards existing cardiovascular risk scales. The level of hsCRP < 1 mg/l should be interpreted as low cardiovascular risk (CVR), 1-3 mg/I as moderate CVR and > 3 mg/I as high CVR. Unfortunately, hsCRP is unpopular and not widely used in standard biochemical tests in Polish hospitals in patients with ischaemic heart disease.
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PMID:[High sensivity C-reactive protein as a complement to classical methods in the evaluation of coronary event's risk]. 1688 74

The commonly used laboratory markers of coronary involvement in subjects with acute coronary syndrome (ACS) are not yet myocardial ischemia-specific and show a late irreversible involvement of the myocardium. A laboratory test has been searched for in order to distinguish persons with myocardial ischemia and typical CAD symptoms to CAD-free individuals. Reg-Ialpha is the product of Reg-I gene which plays a significant role in myocardial regeneration. 38 individuals with suspicion of acute coronary syndrome were tested on admission, after 2 and 6 hours. In all of them cardiac troponin I, myoglobin, C-reactive protein (CRP) and Reg-I alpha were analysed. Our findings did not support the hypothesis that measurement of Reg-Ia maybe the useful marker of myocardial stress.
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PMID:Reg-Ialpha in the diagnosis of acute coronary syndrome--a pilot study. 1693 8

Amyloid containing senile plaques (SP) and neurofibrillary tangles (NFT) are histologic hallmarks of Alzheimer's disease (AD). Interestingly the SP and NFT found in non-demented, age-matched individuals with ischemic heart disease and/or hypertension are morphologically and topographically identical to those in AD. Cholesterol plays a significant role in production and accumulation of amyloid beta (Abeta) and progression of AD. Cholesterol is also a major contributor in atherosclerotic changes and cardiovascular disease. Numerous studies acknowledged benefits of cholesterol-lowering statins in slowing down the progression of AD, improving cognitive status and significantly reducing risk of cardiovascular events. Accumulating evidence suggests that there is a chronic inflammatory reaction in the areas of the brain affected by AD and C-reactive protein (CRP) is identified as a key molecule of acute phase of inflammation. CRP is also a very sensitive marker for cardiovascular events and excellent prognostic tool in post-heart attack and post-coronary artery bypass surgery recovery. Here we report that cholesterol lowering with atorvastatin produces no significant change in CRP levels in treating AD patients who participated in ADCLT (AD cholesterol lowering trial).
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PMID:Change in circulating C-reactive protein is not associated with atorvastatin treatment in Alzheimer's disease. 1694 13

Main aim of the clinical study FARVATER was comparison of effects of 10 and 20 mg/day of atorvastatin on levels of lipids, high-sensitivity C-reactive protein (CRP), fibrinogen (F), and structural-functional state of vascular wall in patients with documented and primary hyperlipidemia (HLP). Fifty patients (mean age 60.8 years) with documented ischemic heart disease and HLP were randomized to continuous administration of 10 and 20 mg/day atorvastatin for 24 weeks. Initial levels of total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDLCH), high density lipoprotein cholesterol (HDL CH), CRP and F were 6.22, 1.86, 4.15, 1.24 mmol/l, 1.46 and 2.93 g/l, respectively. After 6 weeks lowering of TCH, TG and LDLCH was significant both in 10 (24.5, 18.4, and 34.9%, respectively) and 20 mg (29.1, 28.2, and 40.9%, respectively) groups. After 24 weeks TG levels decreased by 22 and 15% in 10 and 20 mg subgroups, respectively. Changes of HDLCH (+11 and +12% in patients treated with 10 and 20 mg, respectively) were not significant. There were no significant changes of CRP and F levels. Seven side effects (4%) were registered during 24 weeks; 2 were related to study drug (allergy and symptomless elevation of creatine kinase).
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PMID:[Randomized FARVATER Study. Part 1. Effect of 10 and 20 mg/day atorvastatin on levels of lipids, C-reactive protein, and fibrinogen in patients with ischemic heart disease and hyperlipidemia]. 1704 15


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