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)

Anticardiolipin and anti-beta2 glycoprotein I antibodies are associated with an increased tendency to thrombosis by various mechanisms. This study aimed to evaluate the association between micro and macrovascular complications of diabetes and anticardiolipin and anti-beta2 glycoprotein I antibodies. Forty-six patients with type 2 diabetes mellitus (T2DM) were studied. Twenty-one patients had coronary artery disease as a macrovascular complication. Twenty-five age and sex matched healthy subjects formed a control group. Anticardiolipin IgM, IgG, anti-beta2 glycoprotein IgM and IgG antibody levels were studied in both patient and control groups. Diabetic patients with ischaemic heart disease had significantly higher titres of anticardiolipin IgG antibody than patients without ischaemic heart disease (P < 0.001). However, none of these patients had an anticardiolipin IgG antibody level higher than 20 GPL, which is accepted as a clinically significant value, so this association may not be clinically important. There was no association with the microvascular complications. There was also no significant association between anti-beta2 glycoprotein I antibodies in type 2 diabetic patients and micro and macrovascular complications. Anticardiolipin and anti-beta2 glycoprotein I antibodies do not have a major role in the pathogenesis of diabetic complications in type 2 diabetic patients. Prospective studies of large populations are needed to explore this association further.
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PMID:Anticardiolipin and anti-beta2 glycoprotein I antibody concentrations in patients with type 2 diabetes mellitus. 1593 58

Platelet activation and the formation of platelet microaggregates in coronary vessels play pivotal roles in myocardial ischemia and reperfusion injury. The Fc receptor gamma-chain (FcR gamma) is coexpressed with glycoprotein (GP) VI, forming a platelet collagen receptor, and the activation of platelets by collagen is closely coupled with tyrosine phosphorylation of the FcRgamma. To examine the functional significance of platelet FcR gamma/GPVI complex in the early phase of myocardial ischemia and reperfusion injury in mice, we performed coronary occlusion and reperfusion experiments using wild type mice and FcRgamma-deficient (FcRgamma(-/-)) mice that lack GPVI. The infarct size was significantly smaller in FcRgamma(-/-) mice subjected to occlusion and reperfusion of the coronary artery than in control FcR gamma(+/+) mice. Twenty-four hours after the reperfusion, electron microscopy of the injured tissue showed substantially more platelet aggregation and occlusive platelet microthrombi in the capillaries of the damaged areas of the wild type mice than in those of the FcR gamma(-/-) mice. Platelet Syk was scarcely activated in the FcR gamma(-/-) mice after myocardial ischemia and reperfusion, but significantly activated in the FcR gamma(+/+) mice. CD11b expression on neutrophils was elevated after myocardial ischemia and reperfusion in both mouse groups, whereas myeloperoxidase activity in the injured areas was significantly lower in the FcRgamma(-/-) mice than in the FcRgamma(+/+) mice. These results suggest that the collagen-induced activation of platelets through the FcR gamma plays a pivotal role in the extension of myocardial ischemia-reperfusion injury. FcRgamma and GPVI may be important therapeutic targets for myocardial ischemia-reperfusion injury.
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PMID:Platelets activated by collagen through the immunoreceptor tyrosine-based activation motif in the Fc receptor gamma-chain play a pivotal role in the development of myocardial ischemia-reperfusion injury. 1624 61

Ischemic heart disease in the young woman is rare, and even more so in the pregnant woman, but it is reasonable to expect an increase with the increasing average age of children bearing. The etiology of acute coronary syndrome during pregnancy can be divided into two main groups: atherosclerotic mechanisms, more common in older mothers, and non-atherosclerotic mechanisms like dissection, coronary spasm and thrombosis. Management of these patients remains difficult; the treatment should follow the usual principles of care for acute coronary syndrome but taking in account that many standard treatments, such the angiotensin converting enzyme inhibitors, are contraindicated. There is also little experience with many of the newer treatments such as clopidogrel and IIb/IIIa glycoprotein inhibitors or percutaneous coronary intervention. We describe a case of a 38-week pregnant woman who suffered an acute myocardial infarction without ST segment elevation and review the literature.
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PMID:[Acute coronary syndrome without ST elevation during pregnancy. A case report]. 1675 81

The incidence of coronary artery disease (CAD) has dramatically increased in India during the recent years. There are two facets of CAD: stable CAD and unstable CAD which includes patients with acute coronary syndrome (unstable angina, non-ST elevation myocardial infarction, ST elevation myocardial infarction). The treatment of stable CAD (stable angina) includes anti-anginal medication, medication to modify atherosclerosis and aggressive treatment of causative risk factors. Those patients with stable CAD who have symptoms refractory to medical treatment usually require coronary angiography to be followed by either percutaneous or surgical revascularization. Percutaneous coronary revascularization using drug eluting stents has been a major revolution during the last five years for symptomatic relief of angina in symptomatic CAD and can be applied to large subsets of patients. Off-pump surgical revascularization using arterial grafts is a major advance and bypass surgery continues to remain treatment of choice in diabetics with multi-vessel CAD, left main CAD and in patients with multivessel disease and impaired ventricles. Acute coronary syndromes are usually caused by plaque rupture with resultant thrombus and present as unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI). It is now increasingly realized that these patients (particularly the one with high risk) are best managed in advanced cardiac care centres with facilities for cardiac catheterization laboratory, percutaneous coronary interventions and coronary bypass surgery. In both, NSTEMI and STEMI aggressive medical management involving nitrates, ACE inhibitors, beta-blockers, dual anti-platelet agents, heparin and statins are recommended. High risk patients with NSTE-ACS require use of glycoprotein IIa / IIIb inhibitors along with early invasive approach involving coronary angiography, angioplasty using drug eluting stent and in some patients bypass surgery. Early reperfusion is key to management of patients presenting with STEMI. If facilities are available, primary percutaneous coronary intervention (angioplasty with stenting) is treatment of choice for patients with STEMI. In our country, thrombolysis still remains the most frequently utilized reperfusion therapy and all efforts should be devoted to provide this therapy at the earliest. All high risk patients with STEMI (including cardiogenic shock) are best treated in higher centres and these patients should be promptly transported to such centres. Early coronary angiography is recommended for majority of patients following thrombolysis for risk stratification and further treatment. In acute coronary syndromes there is drift towards early invasive treatment and this is reflected in marked increase in cardiac care (catheterization laboratories and cardiac surgery centers) facilities throughout India. All patients with CAD require life-long supervised treatment which includes medication, control of risk factors and lifestyle modification. Avoidance of smoking, heart healthy diet, proper exercise, ideal weight management are important for all the patients. Statins, ACE inhibitors, beta-blockers, antiplatelet agents have a great role to play in treatment and prevention and these drugs should be utilized under medical supervision. It is important that the medical profession play an important role in critically evaluating the use of diagnostic procedures and therapies as they are introduced and tested in the detection and management of cardiac disorders. The American College of Cardiology (ACC), American Heart Association (AHA), European Society of Cardiology (ESC), Society for Cardiovascular Angiography and Interventions (SCAI) and several other societies engage in production of guidelines in the area of cardiovascular diseases from time to time. These guidelines attempt to define practices that meet the needs of most patients in most circumstances. The aim of the guidelines is to improve the patient care. The ultimate judgement regarding the care of the particular patient is to be made by the clinician / healthcare provider keeping in mind all the circumstances. The incidence and prevalence of coronary artery disease (CAD) has increased tremendously in India during the last two decades and this change is largely attributable to lifestyle changes. There has also been a rapid progress in the treatment of CAD with proliferation of specialized cardiac care units, intensive care units, cardiac catheterization laboratories and facilities for bypass surgery. It is estimated that there are over 400 catheterization laboratories currently in India and nearly half of them are located in six major cities. The increase in disease and availability of facilities has resulted in a dramatic change and the focus is shifting from only medical treatment to invasive treatment. This document is an expert consensus document which has been prepared by going through the available guidelines and other relevant literature on the subject. The experts have performed a formal review of the literature and have weighed the strength of evidence for or against a particular therapy as it can be applied in Indian scenario. The consensus document deals with the management of ischemic heart disease (IHD) under following sections: 1) Stable Angina 2) Non ST Elevation Acute Coronary Syndrome (NSTE-ACS) 3) ST Elevation Acute Coronary Syndrome (STE-ACS) or Acute Myocardial Infarction (AMI).
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PMID:API expert consensus document on management of ischemic heart disease. 1721 32

Coronary thrombosis is a pivotal event in the pathogenesis of acute coronary syndromes and ischemic complications resulting from coronary intervention. Activation of the platelet glycoprotein (GP) IIb/IIIa receptor is the final common pathway leading to platelet aggregation, coronary thrombus formation, and myocardial ischemia. Inhibitors of platelet GP IIb/IIIa are potent agents to prevent progression to myocardial infarction and death. We prospectively surveyed the indications, frequency, and complications associated with the use of GP IIb/IIIa inhibitors in percutaneous coronary intervention in a tertiary center setting. A total of 170 patients underwent screening over a period of 6 weeks. One hundred four (61%) had coronary intervention, out of which eight (8%) had failed intervention. Glycoprotein IIb/IIIa inhibitors were used in 57 (55%) patients; 47 (45%) did not have any agent periprocedure. Eptifibatide was the most commonly used agent in 35 (33%), followed by abciximab in 19 (18%) and tirofiban in 3 (3%). Out of 57 patients in whom GP IIb/IIIa agents were used, 22 (38%) had visible intracoronary thrombus, 22 (38%) had diffuse disease, 8 (14%) had complex intervention, and 5 (9%) had diabetes. The overall incidence of complications was not increased by the use of GP IIb/IIIa inhibitors; serious complications were rare with the use of GP IIb/IIIa agents; no stroke, thrombocytopenia, gastrointestinal bleed, or death was recorded. The overall use in emergency settings was not associated with increased complications. Bradycardia and vomiting were more common with abciximab group, whereas puncture site pain was commoner in eptifibatide group.
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PMID:An audit of the use and complications of glycoprotein IIb/IIIa inhibitors in percutaneous coronary intervention against national UK standards. 1717 71

The platelet collagen receptor glycoprotein (GP) VI is critical for the formation of arterial thrombosis. GPVI platelet surface expression was examined in patients with stable angina and in patients with acute coronary syndrome (ACS). Surface expression of platelet activation markers such as P-selectin, GPIbalpha, and platelet GPVI was determined by flow cytometry. Patients with ACS showed a significantly enhanced GPVI expression compared with patients with stable angina and healthy controls. The expression of GPVI correlated well with CD62P. Elevated platelet GPVI expression was associated with ACS independent of markers of myocardial necrosis such as troponin and creatine kinase. In ACS, platelet surface GPVI expression was already elevated several hours before troponin and creatine kinase indicated myocardial injury. We conclude that the determination of the platelet-specific thrombotic marker GPVI may help to identify patients at risk before myocardial ischemia is evident.
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PMID:Platelet glycoprotein VI: a novel marker for acute coronary syndrome. 1734 Apr 67

Erythropoietin (EPO) is a glycoprotein hormone implicated in the regulation of red blood cell production. Anemia is common in chronic heart failure (CHF) patients and associated with an inappropriately low EPO-production, suggesting a role for its recombinant human form (rhEPO) in treatment. Although safety concerns have been raised regarding treatment with rhEPO in patients with chronic kidney disease, treatment with rhEPO in patients with CHF has so far been safe and well tolerated. The effect of rhEPO on outcome in anemic CHF patients is under investigation in a phase III clinical trial. In addition to its erythropoietic effects, EPO has been detected in the cardiovascular system, fueling intense research into possible non-hematopoietic effects. EPO has been shown to exert protective effects on the heart during acute myocardial ischemia and improve cardiac function in experimental CHF. Acute protection is mediated through reduction of apoptotic cell death. Improvement of cardiac function in CHF is related to myocardial neovascularization. EPO exhibits a vast array of beneficial effects in cardiovascular disease. In addition to the correction of anemia in CHF, rhEPO might benefit patients with cardiovascular disease.
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PMID:Therapeutic potential of erythropoietin in cardiovascular disease: erythropoiesis and beyond. 1788 87

Despite improvements in the safety and efficacy of percutaneous transluminal coronary angioplasty (PTCA), ischaemic procedural complications continue to occur in up to 10 to 20% of patients. As the pivotal role of platelets in the formation of arterial thrombosis following coronary intervention was elucidated, it became apparent that an inhibitor of platelet aggregation might reduce the rate of acute ischaemic complications and restenosis following PTCA. Attention has focused on the platelet glycoprotein (GP) IIb/IIIa integrin, a receptor that mediates the final common pathway of platelet aggregation. A murine monoclonal antibody that binds to and blocks the IIb/IIIa receptor inhibits the binding of fibrinogen to platelets and thus inhibits platelet aggregation. To minimise the potential for human anti-murine antibody responses, this antibody was modified to a chimaeric antibody fragment, abciximab (c7E3 Fab), composed of an antigen-binding fragment with human constant regions and mouse variable regions. Abciximab was recently approved by the US Food and Drug Administration for clinical use. The efficacy and safety of abciximab have been demonstrated in 3 recently completed phase III clinical trials which enrolled a total of 6156 patients undergoing coronary angioplasty. The study results have unequivocally demonstrated that platelet GP IIb/IIIa receptor inhibition with abciximab during coronary intervention markedly reduces the incidence of postprocedural ischaemic events. In the EPIC trial, a dose-related effect of abciximab in the prevention of ischaemic complications was observed, with a significant 35% reduction in the incidence of the composite end-point among the patients receiving the abciximab bolus and 12-hour infusion compared with the double-placebo group. In the EPILOG trial, patients treated with abciximab bolus and 12-hour infusion with low-dose heparin had a significant 56% reduction in the incidence of the composite end-point at 30 days. In the CAPTURE study, the primary end-point was reduced at 30 days by 29% with abciximab therapy. The treatment effect observed at 30 days for reduction in acute ischaemic complication was maintained throughout the 6-month follow-up period. Although abciximab therapy may carry an increased risk of bleeding complications, such excess haemorrhagic risk can be eliminated by strategies such as reduction of adjunctive heparin dosage, early sheath removal, and conservative management of the vascular access site. The role of platelet glycoprotein IIb/IIIa receptor inhibition in the acute coronary syndromes of unstable angina and acute myocardial infarction treated by percutaneous intervention or with thrombolytic therapy is an exciting new frontier in ischaemic heart disease and is currently under investigation. The complementarity of these agents with new devices for coronary revascularisation, such as stents, is also the subject of important new trials. Finally, future studies will also focus on the role of long term GP IIb/IIIa inhibition with the new generation of orally active agents.
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PMID:Clinical experience with abciximab during coronary revascularisation: an overview. 1802 May 84

Platelets are now regarded as playing a dominant role in cardiovascular medicine since our recent understanding of acute coronary syndrome as an atherothrombotic process. This development has led to the widespread use of antiplatelet agents, such as aspirin, thienopyridines and glycoprotein-IIb/IIIa receptor blockers, for the prevention of ischemic heart disease. Nevertheless, recent evidence suggests that not all patients receive appropriate antiplatelet therapy because there may be resistance or a variable response to the drug used or because of an increased risk of hemorrhage. Moreover, the reported lack of efficacy of the combination of clopidogrel and aspirin when used for primary prevention has raised concerns about the general concept that greater inhibition implies greater efficacy. At present, research efforts are focused on improving current antiplatelet treatment with the aim of increasing efficacy and safety. Alternative ADP-receptor antagonists (e.g., prasugrel, cangrelor and AZD6140) and thrombin-receptor antagonists (e.g., E5555 and SCH 530348) are being developed. They may provide faster, more potent and more stable platelet inhibition. In addition, new insights into platelet structure and into the mechanisms underlying thrombus formation could lead to the discovery of new therapeutic targets. This article reviews what is known about the pathophysiological role of platelets in the atherothrombotic process, considers the current state of the art in antiplatelet therapy, and provides a commentary on new therapeutic approaches.
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PMID:Coronary atherothrombotic disease: progress in antiplatelet therapy. 1846 54

The aim of this review is to summarize present evidence of a causal association of lipoprotein(a) with risk of ischemic heart disease (IHD). Evidence for causality includes reproducible associations of a proposed risk factor with risk of disease in epidemiological studies, evidence from in vitro and animal studies in support of pathophysiological effects of the risk factor, and preferably evidence from randomized clinical trials documenting reduced morbidity in response to interventions targeting the risk factor. Elevated and in particular extreme lipoprotein(a) levels have in prospective studies repeatedly been associated with increased risk of IHD, although results from early studies are inconsistent. Data from in vitro and animal studies implicate lipoprotein(a), consisting of a low density lipoprotein particle covalently bound to the plasminogen-like glycoprotein apolipoprotein(a), in both atherosclerosis and thrombosis, including accumulation of lipoprotein(a) in atherosclerotic plaques and attenuation of t-PA mediated plasminogen activation. No randomized clinical trial of the effect of lowering lipoprotein(a) levels on IHD prevention has ever been conducted. Lacking evidence from randomized clinical trials, genetic studies, such as Mendelian randomization studies, can also support claims of causality. Levels of lipoprotein(a) are primarily determined by variation in the LPA gene coding for the apolipoprotein(a) moiety of lipoprotein(a), and genetic epidemiologic studies have documented association of LPA copy number variants, influencing levels of lipoprotein(a), with risk of IHD. In conclusion, results from epidemiologic, in vitro, animal, and genetic epidemiologic studies support a causal association of lipoprotein(a) with risk of IHD, while results from randomized clinical trials are presently lacking.
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PMID:Lipoprotein(a) and ischemic heart disease--a causal association? A review. 2010 78


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