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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this article we have outlined the current rationale and role of invasive management in ACS. For the majority of patients with ACS, who are either at high risk or unstable, invasive management is a critical element in breaking the sequence of recurrent ischemia leading to early cardiac events (Fig. 11). Secular trends in the care of cardiovascular patients predict even more sophisticated, invasive methods of treating coronary occlusion in the future. A futurist's view on this subject may envision the following type of scenario. A patient with prior CAD experiences persistent chest pain and notifies the emergency medical system. The paramedics arrive, and perform a rapid fingerstick cardiac biomarker panel and ECG. The results are interpreted by an emergency physician via a telecommunication system, and the patient is determined to be at high risk. He or she is triaged to a center capable of angioplasty and bypass surgery. On the way to the hospital, the patient is treated with aspirin, IV heparin, and an IV glycoprotein IIb/IIIa inhibitor. The patient undergoes triage angiography within 1 hour of hospital arrival, culprit lesion(s) are identified, and a revascularization plan is made--setting a critical pathway that is definitive. This vision is not far off on the horizon. We anticipate additional clinical trial results will help form the decision points in this optimal treatment scenario, which for a large proportion of patients will involve invasive management.
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PMID:Early use of coronary angiography and intervention. 1038 33

The emergency department (ED) evaluation of patients with potential acute coronary syndromes (ACS) has traditionally included initial cardiac marker testing for suspected acute myocardial infarction (AMI). While ED management decisions for patients with ACS have largely been based on history, physical examination, and a presenting 12-lead electrocardiogram (ECG), there is ample evidence that markers impact treatment decisions and provide risk stratification. Newer, more sensitive markers of myocardial necrosis have blurred the distinction between patients with and without classically defined AMI, and have focused attention on the continuum of ACS from angina to transmural Q-wave MI. Newer antiplatelet agents, the glycoprotein IIb/IIIa receptor blockers, are likely to receive increased ED utilization. This use will be partially driven by ED cardiac marker determination. Bedside, point-of-care testing is reliable technology that may shorten time to diagnosis and treatment of ACS in the emergency setting. The ED-based chest pain center (CPC) has become a popular tool to evaluate patients at low- to moderate-risk for ACS and a non-diagnostic ECG. Such centers use serial cardiac marker testing as a mainstay for evaluation and risk stratification. Cost issues have driven many diagnostic patient evaluations from the inpatient setting to such ED observation units. As this becomes more common for low- to moderate-risk patients with chest pain, serial assessment of cardiac markers, and their interpretation by emergency physicians, will become essential.
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PMID:The role of cardiac markers in the emergency department. 1045 Dec 45

Management of acute coronary syndromes has been the focus of increased interest in recent years. This has come about with the recognition that the majority of patients who present to the hospital with chest pain have unstable angina or non-Q-wave myocardial infarction (MI). Further, sensitive biochemical markers of myocardial necrosis, such as troponin and creatine kinase, have improved early diagnosis. Markers of inflammation such as C-reactive protein (CRP), although not in wide clinical practice, may provide an early and important marker of prognosis. The current approach to management of acute coronary syndromes is careful risk stratification so as to select appropriate medical therapies and to guide the clinician to appropriate interventions such as angiography or percutaneous coronary intervention (PCI). Established therapies such as aspirin, heparin, intravenous nitrates, and, in selected patients, beta blockers or calcium antagonists, are being used concomitantly with, or are being supplanted by, newer therapies such as low-molecular-weight heparins and glycoprotein IIb/IIIa inhibitors. The role of hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) in patients with acute coronary syndromes is being investigated and shows promise.
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PMID:Medical therapy of unstable angina and non-Q-wave myocardial infarction. 1108 46

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

The development of potent inhibitors of platelet aggregation has led to significant decreases in morbidity and mortality rates among patients undergoing percutaneous coronary intervention. Clinical trials have demonstrated that agents that block glycoprotein IIb/IIIa receptor-mediated platelet aggregation have an outcome benefit when used acutely in patients with chest pain and ST depression or elevated cardiac enzymes, leading to the integration of these agents into emergency medicine clinical practice. This article provides an overview of the pathophysiology of acute coronary syndrome and the pharmacology of platelet inhibition and reviews the evidence from the clinical trials pertaining to the use of these agents in the emergency department.
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PMID:Advances in the pharmacology of acute coronary syndrome. Platelet inhibition. 1113 Sep 35

We hypothesized that certain clinical and angiographic characteristics on presentation predict suboptimal infarct artery flow after percutaneous intervention during acute myocardial infarction (AMI). The goal of angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) during AMI is the prompt restoration of normal flow to achieve myocardial reperfusion. However, inadequate epicardial coronary flow is observed in 10% to 20% of patients. From 2 large randomized trials-Global Use of Strategies To open Occluded arteries in Acute Coronary Syndromes-IIb, and Randomized Placebo-Controlled Trial of Platelet glycoprotein IIb/IIIa Blockade With Primary Angioplasty for Acute Myocardial Infarction-patients undergoing primary PTCA during AMI were included in the analysis. A multivariate logistic model was used to identify factors associated with final Thrombolysis In Myocardial Infarction (TIMI) flow grade < or =2. The 891 patients were aged (mean +/- SD) 61 +/- 12 years, 75% were men, and 39% had an anterior wall AMI. Patients underwent PTCA within 4.8 +/- 3.2 hours from the onset of chest pain. The incidence of final TIMI 3 flow was 81%. TIMI flow grade < or =2 was independently associated with increasing age (odds ratio [OR] 1.39 for every 10 years, 95% confidence interval [CI] 1.19 to 1.62), increasing heart rate (OR 1.16 for every 10 beats, 95% CI 1.05 to 1.28), and presence of visible thrombus on baseline angiogram (OR 1.89, 95% CI 1.18 to 3.05). Conversely, baseline TIMI 2 or 3 flow grade (OR 0.46, 95% CI 0.28 to 0.75) and left circumflex intervention (OR 0.42, 95% CI 0.23 to 0.79) correlated with normal postprocedural coronary flow. Mortality was significantly higher in patients with TIMI < or =2 than TIMI 3 flow grade (10.2% vs 1.5%, p <0.001, respectively). Thus, angiographic evidence of thrombus and 2 pivotal clinical characteristics, advanced age and elevated heart rate, predict lack of adequate coronary reperfusion. Conversely, the presence of normal or near-normal coronary flow before intervention correlates with a good angiographic result. Mortality risk is increased in patients with postprocedural suboptimal angiographic coronary flow.
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PMID:Predictors and prognosis of suboptimal coronary blood flow after primary coronary angioplasty in patients with acute myocardial infarction. 1144 7

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

Since the Spanish Society of Cardiology Clinical Practice Guidelines on Unstable Angina/Non-Q-Wave Myocardial Infarction were released in 1999, the conclusions of several studies that have been published make it advisable to update current clinical recommendations. The main findings are related to the developing role of Chest Pain Units in the management and early risk stratification of acute coronary syndromes in the emergency department; new information concerning the efficacy of glycoprotein IIb/IIIa inhibitors, clopidogrel and low-molecular-weight heparins in the pharmacological treatment of acute coronary syndromes without ST-segment elevation; and the role of early invasive strategy in improving the prognosis of these patients. The published evidence is reviewed and the corresponding clinical recommendations for the management of acute coronary syndromes without persistent ST-segment elevation are updated.
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PMID:[2002 Update of the Guidelines of the Spanish Society of Cardiology for Unstable Angina/Without ST-Segment Elevation Myocardial Infarction]. 1242 82

Despite utilizing optimal anticoagulant therapy during percutaneous coronary intervention (PCI), the incidence of periprocedural myocardial infarction (PPMI) remains 5 7% and evaluation of preprocedural clinical/angiographic characteristics has failed to reliably predict the likelihood of a PPMI. We hypothesized that immediate post-PCI assessment could identify a group of patients at very low risk for PPMI. A consecutive series of 258 PCI patients was stratified into 3 groups based on immediate post-PCI assessment. Group I (PPMI not expected) included those with an acceptable angiographic result of treated vessel (residual stenosis < 50%), TIMI 3 flow and absence of any intraprocedural complications. Group II (PPMI not unexpected) included those with an acceptable angiographic result, TIMI 3 flow but with any/all of the following: saphenous vein graft (SVG) PCI, transient closure of culprit vessel or major sidebranch, intracoronary thrombus, prolonged chest pain, electrocardiographic (ECG) changes, hypotension, resolved slow flow/no reflow, bailout glycoprotein IIb/IIIa inhibitor use, loss of a minor sidebranch or any angiographic residual stenosis > 50% with TIMI 3 flow. Group III (PPMI expected) included those with any angiographic result of native coronary artery or SVG with < TIMI 3 flow, unresolved chest pain, hypotension or ECG changes at the end of the PCI, loss of a major sidebranch or vessel, or persistent no-reflow. Group stratification was analyzed in relation to the incidence of PPMI (CK-MB > 3 times the upper limit of normal; 18 24 hours post-PCI). Rate of PPMI: Group I (1/141; 0.7%), Group II (7/71; 9.9%), Group III (5/11; 45.5%) (p < 0.001). The 3 groups did not differ in age, clinical presentation or stent use (p = NS). Sixty out of 105 patients (57.1%) with unstable angina, seventy-seven out of 146 patients (52.7%) with B2/C lesions, and 105/180 patients (58.3%) with unstable angina or B2/C lesions were stratified to Group I. This study demonstrates that immediate post-PCI evaluation of the clinical/angiographic characteristics can predict the likelihood of PPMI and a group of patients at a very low risk for a PPMI can be identified, in whom implications exist for limited hospitalization and post-procedural antithrombotic therapy.
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PMID:Patients at low risk for periprocedural myocardial infarction can be identified by assessment immediately following percutaneous coronary intervention. 1277 74

Acute ischemic chest pain at rest consistent with unstable angina or non-ST-elevation myocardial infarction is a common problem that may cause death or recurrent myocardial infarction within 30 days unless identified and risk stratified acutely. The latter may be done within 15 minutes by the history, physical exam, and electrocardiogram, and is aided by the measurement of troponin T/I. According to the Agency for Health Care Policy and Research guidelines, low-risk patients can be discharged home and rechecked within 72 hours. Intermediate-risk patients with no ST-segment changes with continuous monitoring and no elevation of troponin should undergo exercise stress testing by electrocardiogram (or nuclear or echocardiographic evaluation if electrocardiogram is non-analyzable). Patients with a negative stress test are low risk (no death or myocardial infarction at 30 days or 6 months) and can be discharged home. Patients with a positive test or who are at high risk according to the Agency for Health Care Policy and Research guidelines should undergo acute invasive testing for possible revascularization. Aspirin and low molecular weight heparin or unfractionated heparin, along with anti-ischemia therapy, is indicated in intermediate- or high-risk patients. The addition of clopidogrel is indicated in these patients, except in those who are potential candidates for coronary artery bypass graft. Platelet glycoprotein IIb/IIIa inhibitors are indicated in high-risk patients likely to undergo percutaneous coronary intervention, should be started early if recurrent ischemia occurs, but are not indicated in lower-risk patients who do not require percutaneous coronary intervention. Intensive secondary prevention should be started before dismissal.
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PMID:Acute coronary syndromes: pathogenesis, acute diagnosis with risk stratification, and treatment. 1553 72


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