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)

Functional changes of the vessel wall--specifically dysfunction of endothelial cells--may precede the formation of frank plaques at the initiation of atherosclerosis. Clinically endothelial function and dysfunction can be measured by angiography or ultrasound techniques. Another possibility is the measurement of circulating markers of endothelial dysfunction in human plasma, such as the endogenous NOS inhibitor ADMA (asymmetric dimethylarginine). In our recent studies we were able to show that ADMA accumulates in the presence of metabolic changes such as hyperhomocysteinemia, insulin resistance and type-2 diabetes, and that these elevations of plasma ADMA correlate well with the amount of endothelial dysfunction and with NO bioavailability. Furthermore ADMA was shown to be dynamically regulated and to play an important patho-physiologic role in myocardial ischemia and reperfusion. Thus, measurements of plasma ADMA in patients could help to screen for manifestations of atherosclerosis. Moreover attempts to reduce plasma and tissue ADMA could potentially play an important role in the treatment of endothelial dysfunction, atherosclerosis, but also of ischemia reperfusion injury.
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PMID:[Asymmetric dimethyl arginine (ADMA): a novel cardiovascular risk factor?]. 1734 60

Increased levels of homocysteine (Hcy), recognized as hyperhomocysteinemia (HHcy), were associated with cardiovascular diseases. There was controversy regarding the detrimental versus cardio protective role of inducible nitric oxide synthase (iNOS) in ischemic heart disease. The aim of this study was to test the hypothesis that the Hcy generated nitrotyrosine by inducing the endothelial nitric oxide synthase, causing endothelial-myocyte (E-M) coupling. To differentiate the role of iNOS versus constitutive nitric oxide synthase (eNOS and nNOS) in Hcy-mediated nitrotyrosine generation and matrix remodeling in cardiac dysfunction, left ventricular (LV) tissue was analyzed from cystathionine beta synthase (CBS) heterozygote knockout, iNOS homozygote knockout, CBS-/+/iNOS-/- double knockout, and wild-type (WT) mice. The levels of nitrotyrosine, MMP-2 and -9 (zymographic analysis), and fibrosis (by trichrome stain) were measured. The endothelial-myocyte function was determined in cardiac rings. In CBS-/+ mice, homocysteine was elevated and in iNOS-/- mice, nitric oxide was significantly reduced. The nitrotyrosine and matrix metalloproteinase-9 (MMP-9) levels were elevated in double knockout and CBS-/+ as compared to WT mice. Although MMP-2 levels were similar in CBS-/+, iNOS-/-, and CBS-/+/iNOS-/-, the levels were three- to fourfold higher than WT. The levels of collagen were similar in CBS-/+ and iNOS-/-, but they were threefold higher than WT. Interesting, the levels of collagen increased sixfold in double knockouts, compared to WT, suggesting synergism between high Hcy and lack of iNOS. Left ventricular hypertrophy was exaggerated in the iNOS-/- and double knockout, and mildly increased in the CBS-/+, compared to WT mice. The endothelial-dependent relaxation was attenuated to the same extent in the CBS-/+ and iNOS-/-, compared to WT, but it was robustly blunted in double knockouts. The results concluded that homocysteine generated nitrotyrosine in the vicinity of endothelium, caused MMP activation and endothelium-myocyte uncoupling. The generation of nitrotyrosine was independent of iNOS.
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PMID:Nitrotyrosinylation, remodeling and endothelial-myocyte uncoupling in iNOS, cystathionine beta synthase (CBS) knockouts and iNOS/CBS double knockout mice. 1902 Nov 46

Myocardial ischemia is a condition in which the blood flow to the heart is diminished and thus the supply of oxygen and nutrients to the heart is reduced. The reperfusion to an ischemic myocardium often results in induction of infarction and cardiac dysfunction. The brief episodes of ischemia and reperfusion given before prolonged ischemia and reperfusion denotes ischemic preconditioning, which protects the heart from lethal ischemia-reperfusion injury. However, it is intriguing to note that the cardioprotective effect of preconditioning is suppressed in some pathological conditions such as hypercholesterolemia, hyperglycemia, hypertension, cardiac hypertrophy, aging, obesity and hyperhomocysteinemia. In this review, we have critically discussed the possible mechanisms involved in the modulation of cardioprotective potential of ischemic preconditioning in various pathological conditions.
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PMID:The impairment of preconditioning-mediated cardioprotection in pathological conditions. 1942 81

Hyperhomocysteinemia (HHcy) is considered an independent risk factor for cardiovascular disease, including ischemic heart disease, stroke, and peripheral vascular disease. Mutations in the enzymes and/or nutritional deficiencies in B vitamins required for homocysteine metabolism can induce HHcy. Studies using genetic- or diet-induced animal models of HHcy have demonstrated a causal relationship between HHcy and accelerated atherosclerosis. Oxidative stress and activation of proinflammatory factors have been proposed to explain the atherogenic effects of HHcy. Recently, HHcy-induced endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) have been found to play a role in HHcy-induced atherogenesis. This review will focus on the cellular mechanisms of HHcy in atherosclerosis from both in vivo and in vitro studies. The contributions of ER stress and the UPR in atherogenesis will be emphasized. Results from recent clinical trials assessing the cardiovascular risk of lowering total plasma homocysteine levels and new findings examining the atherogenic role of HHcy in wild-type C57BL/6J mice will also be discussed. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.
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PMID:Contributions of hyperhomocysteinemia to atherosclerosis: Causal relationship and potential mechanisms. 1944 39

Hyperhomocysteinemia and other major cardiovascular risk factors are associated with increased vascular oxidative stress. To access the effects preoperative plasma homocysteine levels and other atherosclerotic risk factors on myocardial ischemia-reperfusion injury after conventional coronary artery bypass, 213 patients with normal renal function were enrolled prospectively. Cardiac troponin T was measured postoperatively to determine myocardial injury. There was a significant relationship between hyperhomocysteinemia and postoperative peak troponin T. This was more marked in patients without major atherosclerotic risk factors than in those who had at least one risk factor. Moreover, among current cigarette smokers, those with the highest preoperative plasma homocysteine levels had the lowest postoperative troponin T levels. From multivariate linear regression analysis, the predictors of high postoperative troponin T were hyperhomocysteinemia, hypertension, and aortic crossclamp time, but the presence of major atherosclerotic risk factors paradoxically modified the effects of hyperhomocysteinemia on postoperative myocardial ischemia-reperfusion injury.
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PMID:Hyperhomocysteinemia-induced myocardial injury after coronary artery bypass. 1991 90

Current epidemiological data support the association between psoriasis and cardiovascular (CV) risk, in apparent correlation with psoriasis severity. Although less unanimously, evidence of an increased prevalence of CV diseases among psoriasis patients has been reported, including ischemic heart disease, cerebrovascular, peripheral vascular and heart structural disorders. In particular, various studies showed a correlation between psoriasis and major CV events (i.e., myocardial infarction, stroke), while others investigated subclinical changes of blood vessels, such as intima-media thickness increase, arterial stiffness and coronary artery calcification. A series of different mechanisms, like traditional CV risk or iatrogenic risk factors, inflammation, hemostasis dysregulation, hyperhomocysteinemia, and shared genetic susceptibility, are thought to underlie this epidemiological association. Among these elements, inflammation and its related cytokine milieu, including Th1-mediated response and Th17/Treg imbalance, C reactive protein and the newly implicated osteopontin are considered to play a primary role, even if yet to be fully understood.
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PMID:Psoriasis and cardiovascular disease. 2041 21

Left ventricular hypertrophy (LVH) is a cardiovascular complication highly prevalent in patients with chronic kidney disease (CKD) and end-stage renal disease. LVH in CKD patients has generally a negative prognostic value, because it represents an independent risk factor for the development of arrhythmias, sudden death, heart failure and ischemic heart disease. LVH in CKD patients is secondary to both pressure and volume overload. Pressure overload is secondary to preexisting hypertension, but also to a loss of elasticity of the vessels and to vascular calcifications, leading to augmented pulse pressure. Anemia and the retention of sodium and water secondary to decreased renal function are responsible for volume overload, determining a hyperdynamic state. In particular, the correction of anemia with erythropoietin in CKD patients is advantageous, since it determines LVH reduction. Other risk factors for LVH in CKD patients are documented: some are specific to CKD, as mineral metabolism disorders (hypocalcemia, hyperphosphatemia, low serum vitamin D levels and secondary hyperparathyroidism), others are non-traditional, such as increased asymmetric dimethylarginine, oxidative stress, hyperhomocysteinemia and endothelial dysfunction that, in turn, accelerates the process of atherogenesis, triggers the inflammation and pro-thrombotic state of the glomerular and the vascular endothelium and aggravates the process of both CKD and LVH.
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PMID:Hypertension, left ventricular hypertrophy and chronic kidney disease. 2111 11

Chronic kidney disease is a pathology progressively increasing in the world. Patients with renal disease have an about 20 times greater chance of dying for cardiovascular disease than to reach the stage of dialysis and, compared to general population, they have a three times greater risk of developing acute myocardial infarction. Based on these considerations, we analyzed the most important metabolic changes that occur in renal failure, predisposing to ischemic heart disease. Changes in lipids and calcium-phosphorus metabolism, inflammation and oxidative stress, hyperhomocysteinemia, renin-angiotensin-aldosterone axis, anemia, left ventricular hypertrophy and albuminuria have been considered.
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PMID:[From kidney disease to ischemic heart disease]. 2157 94

Cardiovascular diseases are the leading cause of death in patients on haemodialysis. Cardiovascular mortality rate in these patients is approximately 9% per year, with the highest prevalence of left ventricular hypertrophy, ischemic heart disease and congestive heart failure being the most frequent cardiovascular complications. Risk factors for cardiac failure include hypertension, disturbed lipid metabolism, oxidative stress, microinflammation, hypoalbuminemia, anaemia, hyperhomocysteinemia, and increased concentration of asymmetric dimethylarginine, increased shunt blood flow and secondary hyperparathyroidism. Diagnostic strategy for early detection of patients with increased risk for the development of asymptomatic disturbances of systolic and diastolic left ventricular function should include echocardiografic examination, tests for determining coronary vascular disease, as well as tests of myocardial function (BNP, Nt-proBNP). Early detection of patients with a high risk of congestive heart failure enables timely implementation of adequate therapeutic strategy to provide high survival rate of HD patients.
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PMID:[Heart failure in haemodialysis patients: evaluation and treatment]. 2162 74

Hyperhomocysteinemia is a known risk factor for the development of deep vein thrombosis (DVT). Various studies have been conducted in the western countries to know the prevalence of hyperhomocysteinemia in patients with DVT and in general population. There is no documented literature of the prevalence of hyperhomocysteinemia in Indian population. Thus the aim of this study was to determine the prevalence of hyperhomocysteinemia in cases of DVT in our population. To evaluate the prevalence of hyperhomocysteinemia, a prospective cross sectional study done on a total of 70 patients admitted in KLES Dr Prabhakar Kore hospital, Belgaum, India. DVT was confirmed by Doppler examination. Serum homocysteine was measured and the data analysed. Statistical significance was calculated using chi square test. A total of 70 patients were studied of which 53 were males and 17 were females. The prevalence of hyperhomocysteinemia among the cases of DVT was 31.428%.The prevalence among males was 35.85% and among females was 17.64%.There was statistically significant association between hyperhomocysteinemia and presence of ischaemic heart disease with a p value of 0.005 on chi square analysis. The prevalence of hyperhomocysteinemia in cases of deep vein thrombosis in our population was 31.428%. There was a statistically significant association between hyperhomocysteinemia and ischaemic heart disease.
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PMID:A cross-sectional study to detect the prevalence of hyperhomocysteinemia in cases of deep vein thrombosis. 2193 96


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