Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial infarction results from a platelet-rich occlusive coronary thrombus. Platelet membrane glycoprotein IIb/IIIa plays an important role in platelet adhesion and aggregation. Two polymorphisms of the gene encoding the IIIa subunit. PLA1 and PLA2, have been identified. We investigated the frequency of these polymorphisms in 114 consecutive patients with a history of angina-like chest pain admitted for coronary arteriography. Forty-three of these patients had previously suffered a myocardial infarction. The PLA2 polymorphism was found in 21% of the patients with previous myocardial infarction and in 27% of the patients with angina-like chest pain but no previous myocardial infarction (p = 0.634). There was also no significant association with the extent of coronary disease. There is no evidence, therefore, from this study of an association between the PLA polymorphisms and the occurrence of myocardial infarction.
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PMID:Coronary thrombosis and the platelet glycoprotein IIIA gene PLA2 polymorphism. 971 40

Mechanical revascularization in the acute myocardial infarction by primary angioplasty has several advantages over thrombolytic therapy. The short-term patency rates of the infarct-related artery range from 95 to 99% and a normal flow is achieved in more than 90% of the cases. This prompt and effective reperfusion is probably responsible for the improved prognosis with primary angioplasty. The better outcome after primary angioplasty is observed both in low- and in high-risk patients, in all ages and in patients presenting late (>6 h) after the chest pain. Pooled analysis of randomized studies, show that primary angioplasty as compared to thrombolysis, has a lower incidence of death, stroke and reinfarction. Additional advantages of primary PTCA include the possibility of reperfusion in patients in whom lysis is contraindicated or less effective (e.g. patients in cardiogenic shock, or with prior coronary artery bypass surgery) and the ability to provide prognostic information helpful in the patient triage. Thus, primary PTCA results in better outcome than thrombolysis when performed in centers with success rates comparable to those achieved in the randomized trials. Further studies are still needed to assess its long-term efficacy. Several randomized trials are underway to assess the role of stents and the use of more potent antiplatelet drugs, as the GPIIb/IIIa receptor blockers, in adjunct to balloon angioplasty in the treatment of acute myocardial infarction.
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PMID:Update on mechanical revascularization in acute myocardial infarction: which role and when? 1032 5

A female with mitral valvular disease presented an acute myocardial infarction. She suddenly complained of recurrent chest pain with symptoms of pulmonary edema. The angiogram evidenced multiple coronary thromboemboli. A combined strategy using intracoronary thrombolysis, a platelet glycoprotein IIb/IIIa antagonist (abciximab) and percutaneous transluminal coronary angioplasty to help disrupt the thrombus was performed. Clinical and angiographic signs of coronary reperfusion were rapidly achieved. No bleeding complications appeared.
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PMID:Combined therapeutic strategy for multiple coronary thromboemboli. 1087 35

The treatment of non-Q-wave infarction involves the use of antithrombotic therapy (aspirin and heparin) along with appropriate antianginal medication to reduce myocardial oxygen demands and prevent coronary spasm. In certain high-risk patient subgroups (ie, those with recurrent ischemia, persistent or significant ST segment change, congestive heart failure, or hypotension with chest pain), the use of newer agents such as the platelet glycoprotein IIb/IIIa antagonists is indicated. The role of angiography appears to be changing. In the past, at least in the United States, angiography was performed on nearly all patients with non-Q-wave infarction. Now, risk stratification into high- and low-risk subgroups can be performed based on clinical criteria. In low-risk individuals, we recommend that noninvasive testing be performed before a decision is made about an invasive evaluation. In high-risk patients, it is appropriate to perform angiography and, based on the angiographic findings, to provide appropriate therapy. Although the results of the Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital (VANQWISH) study suggest that if bypass surgery is required, it should not be performed acutely, we do not believe that this is necessarily correct. Therapy must be individualized based on the risk-benefit profile of acute revascularization. Furthermore, the use of percutaneous coronary intervention, particularly with the glycoprotein IIb/IIIa antagonists and stents, is expanding to include multivessel disease, even in the presence of left ventricular dysfunction. Again, we believe therapy must be individualized to include an estimate of short- and long-term risk versus benefit. In the future, however, more data from appropriately designed clinical trials will be required to establish evidence-based therapy.
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PMID:Non-Q-Wave Myocardial Infarction. 1109 7

Despite important advances in the management of non-ST segment elevation acute coronary syndromes, adverse outcomes remain common. The recent introduction of low molecular weight heparins and platelet glycoprotein IIb/IIIa receptor inhibitors is an opportunity to make a further impact on the mortality and morbidity of this common condition. Optimal use of these agents will likely result from the recognition of patients at a higher risk of an adverse outcome who are most likely to benefit. At the same time, identification of lower risk patients will avoid the use of unnecessary and potentially harmful medications. Guidelines for the application of these new agents were developed at three meetings of a multidisciplinary group of health professionals. Evidence for risk stratification of patients with non-ST segment acute coronary syndromes and the results of clinical trials for the individual antithrombotic and antiplatelet agents were reviewed. A practical algorithm for patient management is presented, which uses observations available to the physician in the first few hours after the onset of chest pain.
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PMID:Guidelines for the early management of acute coronary syndromes: focus on antithrombotic and antiplatelet therapy. 1110 39

Acute coronary syndrome (ACS) refers to the spectrum of cardiac disease, from unstable angina to ST-segment-elevation myocardial infarction. In the emergency medical services (EMS) setting, ACS may be more broadly thought to include patients with chest pain or other symptoms believed to have a cardiac origin who have evidence of ischemia or acute myocardial infarction on a 12-lead electrocardiogram, or symptomatic patients with a previous cardiac event or known cardiac disease. Pharmacologic management of these patients is based on the use of three primary classes of drugs: those that affect clotting, those that establish and maintain hemodynamic control, and those that relieve pain. Many of these agents have been evaluated in large clinical trials for in-hospital use, and a number of ongoing studies are assessing their efficacy in the prehospital setting. The appropriateness of prehospital use of specific agents within each class depends on proper patient selection, the necessity of immediate intervention, ease of use in the field, expertise of EMS personnel, and cost-effectiveness of therapy. This consensus group reviewed agents from all three classes (including aspirin, GPIIb/IIIa inhibitors, unfractionated and low-molecular-weight heparins, fibrinolytics, beta-adrenergic blockers, calcium antagonists, nitrates, and morphine) for their overall indication, applicability to the prehospital setting, and current prehospital use.
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PMID:Acute coronary syndrome: pharmacotherapy. 1119 71

It is nearly impossible to follow and integrate all the new information in each subspeciality of cardiology. In the last months, important data has been published which may change clinical practice. In this domain, over half the cases of suspected coronary chest pain would only require a very short stay in a chest pain unit. The history, an accurate evaluation of symptoms, the application of Bayesian analysis, ECG interpretation and serum troponine measurement, associated with a degree of clinical experience, will allow orientation of the patient to a coronary care unit or hospital discharge (with possible out-patient referral). Patients with true unstable angina will no longer be treated by continuous intravenous injection of non-fractionated heparin because, in theory and in practice, this has been replaced with subcutaneous LMW heparin.... On the other hand, the electric syringe will continue to be required for the integration of the anti-GPIIB-IIIA for the treatment of unstable angina after the recommendations published concomitantly in the United States and Europe. This type of patient, especially with a "positive" troponine, will probably not be kept waiting long before referral to the catheter laboratory for coronary angiography and revascularisation. The long-term results of the FRISC II trial are confirmed by an even earlier invasive approach (Tactics-Timi 18) using anti-GPIIb-IIIa. In the first hours, and independently of other older prognostic factors, it will be possible to "predict or compare" the risk of coronary recurrence based on the results of certain biological "markers". In many centres, cases with ST elevation on the ECG could well be included in a phase III "medical protocol", associating a half-dose thrombolytic and an anti-GPIIb-IIIa. Finally, patients who will have been admitted to the chest pain unit with a suspected pulmonary embolism, for example because they had not been treated prophylactically with aspirin before hip surgery, will probably have the choice, after d-dimer measurement, between pulmonary scintigraphy and helicoidal CT scan. If the diagnosis of pulmonary embolism is confirmed, a single subcutaneous injection of LMW heparin could replace the conventional continuous intravenous injection of heparin. The earliest possible oral anticancer ... pardon me I anticoagulant treatment should be prescribed and explained.
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PMID:[The best in 2000 on thrombosis]. 1126 Aug 41

Patients admitted with suspicion of an acute coronary syndrome (ACS) still constitute a diagnostic, prognostic and therapeutic challenge for the treating physician. The final diagnosis ranges from a noncardiac diagnosis to a full-blown myocardial infarction (MI). Biochemical markers of myocardial damage are essential for diagnosis and, especially troponin T and troponin I, have been shown to be valuable for early risk stratification and for selection of treatment in ACS. Patients identified to be at low risk of future cardiac events might be discharged early, and unnecessary investigations and treatments avoided. On the contrary, a more intense treatment can be started in patients identified to be at high risk. Unstable angina patients with, compared to without, elevation of troponin, have a more activated coagulation system and more frequently complex lesions and visible thrombus in their coronary arteries. Accordingly, antithrombotic and antiplatelet therapies, i.e. l.m.w heparin and GP IIb/IIIa receptor antagonists, have been proved to have beneficial effects in troponin positive patients, but little or no beneficial effects in troponin negative patients. Also, the beneficial effects of an invasive compared to a noninvasive approach seem to be much more pronounced in troponin positive patients. In patients with ST-elevation MI, an elevated troponin T level at admission are associated with an increased mortality. However, the therapeutic implications of this finding remain speculative. Patients admitted with chest pain and left bundle branch block (LBBB) and who develop an MI have a poor prognosis. Current guidelines in acute myocardial infarction state that these patients should receive thrombolysis. Despite that, only a minority of these patients do receive thrombolysis, most probably because of the great diagnostic uncertainty. Rapid testing with a cardiac marker, e.g. myoglobin, would most probably increase the proportion of patients with chest pain and LBBB who receive appropriate reperfusion treatment.
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PMID:Markers of myocardial damage in acute coronary syndromes--therapeutic implications. 1155 49

This guideline describes the recognition and management of unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI). These are two of the three components of the acute coronary syndrome (ACS). These forms of ACS most often arise from erosion or rupture of coronary atherosclerotic plaque and subsequent thrombus formation causing incomplete coronary occlusion. The term ACS, as used in this guideline, refers to these two components only. The third component, not discussed here, is ST-segment elevation myocardial infarction (STEMI), which is most frequently associated with complete coronary occlusion. ACS is a clinical emergency requiring urgent assessment. It is characterised by chest pain, ST-segment changes in the electrocardiogram (ECG) and a rise in the serum markers of myocardial injury/infarction. ACS encompasses a variety of clinical presentations. Risk stratification is essential to enable triage of patients to the optimal level of care and specific therapy. Careful clinical assessment is the cornerstone of this risk stratification. The pharmaceutical treatment of ACS is directed primarily at the dissolution of the developing intracoronary thrombus by antiplatelet (aspirin and clopidogrel) and anticoagulant therapy (heparin), and secondarily to the relief of symptoms by anti-anginal and analgesic medications. Low-molecular-weight heparin (LMWH) is at least as effective and safe as standard intravenous unfractionated heparin (UH). Coronary angiography is advised for all high-risk patients and those in whom reversible ischaemia or left ventricular dysfunction is discovered. The need for coronary revascularisation is dictated by the findings at angiography. In high-risk patients, appropriate, early revascularisation is recommended in preference to standard medical therapy and 'ischaemia-driven' revascularisation. The glycoprotein IIb/IIIa (GPIIb/IIIa) inhibitors should be used in association with percutaneous coronary intervention (PCI) in high-risk patients. All patients with ACS should receive secondary preventive treatment. It is imperative that they stop smoking. Dietary modification, physical rehabilitation, long-term low-dose aspirin use, b-blockade for those diagnosed with myocardial infarction, tight control of blood pressure, cholesterol lowering with a statin, and treatment with an angiotensin-converting enzyme (ACE) inhibitor should be prescribed.
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PMID:Management of acute coronary syndromes clinical guideline. 1243 90

The high mortality rate of acute myocardial infarction underline the importance of this entity in the differential diagnosis of acute chest pain. Medical history, clinical presentation, ECG, biochemical markers of myocardial injury and imaging techniques are used to establish a correct diagnosis. Myocardial infarction can be divided into ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction. In the case of ST-segment elevation myocardial infarction thrombolytic therapy or percutaneous transluminal coronary angioplasty should be instituted as soon as possible. In patients without persistent ST-segment elevation biochemical markers of myocardial damage, especially troponin T and troponin I, are of major importance for risk stratification. Patients with elevated troponin levels should be treated with GPIIb/IIIa antagonists and early intervention.
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PMID:[Rapid assessment of thoracic pain. Is it a myocardial infarct?]. 1204 44


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