Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.1 (ACS)
78,556 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With an understanding of the pathophysiology of ACS and an increasing number of early therapeutic options, there has been a shift in focus from ruling-out MI to identifying and stratifying risk in all patients with potential ACS. The presenting symptoms and ECG still remain the cornerstone of immediate diagnosis and triage. Through the application of new technologies, such as the cardiac troponins, and a reassessment of techniques, such as perfusion imaging and echocardiography, the clinician has an increasing selection of methods to rapidly assess chest pain of potential ischemic etiology. Coinciding with the evaluation of technology has been the development of the concept of the CPU and associated rapid diagnostic protocols. These protocols, whether they utilize the assistance of mathematic predictive instruments or represent simple triage schemes, form the backbone of a system to improve the care of patients with ACS in the current milieu of cost containment.
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PMID:Evaluating the chest pain patient. Scope of the problem. 1038 29

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 accurate assessment and triage of patients with potential ACS is a complex decision-making process based on information that is not entirely reliable. The knowledgeable EP recognizes that assessment of patients with chest pain requires an understanding of the various clinical presentations of ACS and high-risk patient types, as well as careful use of the available modalities to diagnose these syndromes efficiently while incurring minimal risk to the patients safety. The busy EP is faced with sick patients with chest pain daily, so that it behoove anyone in emergency medicine to familiarize themselves with these diagnostic pitfalls.
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PMID:Pitfalls in the emergency department diagnosis of acute myocardial infarction. 1137 83

Traditionally, ST segment depression has been associated with acute coronary syndromes; this electrocardiographic pattern may also be found in patients with nonischemic events, such as left bundle branch block (LBBB), left ventricular hypertrophy (LVH), and those with therapeutic digitalis levels. Using the ECG as an adjunct in distinguishing those patients with acute coronary syndromes from those with more "benign," nonacute causes of STSD will obviously lead to divergent treatment and management plans. The following cases illustrate the use the ECG in patients presenting with chest pain and electrocardiographic ST segment depression attributable to an ACS, LVH, LBBB, or digitalis.
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PMID:Electrocardiographic ST segment depression. 1144 19

It has been shown that the 2-h Stratus II delta creatine kinase-MB (CK-MB) is more sensitive and is equally specific compared to a 2-h Stratus II CK-MB and to a 2-h Stratus II delta cardiac troponin-I (DeltacTnI) for identification of acute myocardial infarction and adverse outcome (AO). Because the newest generation of Stratus (Stratus CS) cTnI assay has an analytical sensitivity of 0.03 ng/mL, compared to 0.35 ng/mL for the first generation assay, we undertook a small pilot study of 120 chest pain patients to compare sensitivities and specificities for 30-day AO of the Stratus CS DeltacTnI immunoassay to the DeltaCK-MB and DeltacTnI, as measured by the Abbott Axsym immunoassay, and to the DeltaCK-MB, as measured by the Stratus CS. A Stratus CS DeltacTnI > or = +0.02 ng/mL in 2 h was more sensitive (61.9%) than an Axsym DeltaCK-MB > or = +1.3 ng/mL (38.1%; p = 0.03), a Stratus CS DeltaCK-MB > or = +0.4 ng/mL (38.1%; p = 0.03), and an Axsym DeltacTnI > or = +0.3 ng/mL (33.3%; p = 0.03) for 30-day AO. There were no differences in specificities. Our data support enhanced identification of ACS with a second generation cTnI assay. Pending larger studies, patients with a rise in DeltacTnI of > or = +0.02 ng/mL in 2 h, as measured by the Stratus CS immunoassay, should receive consideration for aggressive anti-ischemic therapy and further diagnostic testing prior to making an exclusionary diagnosis of non-ischemic chest pain.
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PMID:Improved identification of acute coronary syndromes with second generation cardiac troponin I assay: utility of 2-hour delta cTnI > or = +0.02 ng/mL. 1185 18

CVD are on the first place among death causes in the world. The half of all death at middle age persons is CVD causality, the most often because of ischaemic heart diseases, and there are a few clinic forms: acute coronary syndrome, stabile pectoral angina, variant pectoral angina, syndrome x, and silent myocardial ischemia. Toward definition ACS include clinical manifestation causality of myocardial ischemia due of atherosclerotic plague rupture. ACS include: non-stable pectoral angina non-Q infarction, Q myocardial infarction and sudden cardiac death. Consequence of plague rupture is occlusive thrombus which produces typical ST elevation on ECG after that appearance Q-in ECG with blood markers elevation (Troponin I, T, CK and CK-MB). There are sometimes non-typical ST elevation on ECG with blood markers elevation and chest pain. On that way becomes non-Q infarction. Smaller thrombus make non stable pectoral angina and appearance of ST depression on ECG without blood markers elevation. Sometimes sudden cardiac death is the first sign of coronary disease in the diagnostic management coronary disease due of: clinical symptom of chest pain, ECG (with or without ST elevation) and appearance appsence biochemical blood markers (at myocardial necrosis troponins are present in blood during 14 days, CK-MB is present 3 days). Sometimes echocardiography examination is helpful in estimate of regional kinetic disorders. European society of cardiologists made guidelines for management od ACS without ST elevation and guidelines management of acute myocardial infarction with ST elevation.
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PMID:[New approach in the diagnosis of acute coronary syndrome]. 1520 7

The current criteria for diagnosing ACS are chest pain and presence of a new infiltrate on the chest radiograph (CXR). This study was designed to evaluate the role of ventilation and perfusion (V/Q) scan to assist in the early diagnosis of ACS. An abnormal V/Q scan was associated with a diagnosis of ACS that reached a statistical significance (P < 0.038). The sensitivity and specificity were found to be 60% and 100%, respectively. We conclude that V/Q scan may play a role in the early diagnosis of ACS.
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PMID:Potential role of the ventilation and perfusion (V/Q) lung scan in the diagnosis of acute chest syndrome in adults with sickle cell disease. 1555 Dec 81

In patients with stable CAD, PCI can be considered a valuable initial mode of revascularization in all patients with objective large ischaemia in the presence of almost every lesion subset, with only one exception: chronic total occlusions that cannot be crossed. In early studies, there was a small survival advantage with CABG surgery compared with PCI without stenting. The addition of stents and newer adjunctive medications improved the outcome for PCI. The decision to recommend PCI or CABG surgery will be guided by technical improvements in cardiology or surgery, local expertise, and patients' preference. However, until proved otherwise, PCI should be used only with reservation in diabetics with multi-vessel disease and in patients with unprotected left main stenosis. The use of drug-eluting stents might change this situation. Patients presenting with NSTE-ACS (UA or NSTEMI) have to be stratified first for their risk of acute thrombotic complications. A clear benefit from early angiography (<48 h) and, when needed, PCI or CABG surgery has been reported only in the high-risk groups. Deferral of intervention does not improve outcome. Routine stenting is recommended on the basis of the predictability of the result and its immediate safety. In patients with STEMI, primary PCI should be the treatment of choice in patients presenting in a hospital with PCI facility and an experienced team. Patients with contra-indications to thrombolysis should be immediately transferred for primary PCI, because this might be their only chance for quickly opening the coronary artery. In cardiogenic shock, emergency PCI for complete revascularization may be life-saving and should be considered at an early stage. Compared with thrombolysis, randomized trials that transferred the patients for primary PCI to a 'heart attack centre' observed a better clinical outcome, despite transport times leading to a significantly longer delay between randomization and start of the treatment. The superiority of primary PCI over thrombolysis seems to be especially clinically relevant for the time interval between 3 and 12 h after onset of chest pain or other symptoms on the basis of its superior preservation of myocardium. Furthermore, with increasing time to presentation, major-adverse-cardiac-event rates increase after thrombolysis, but appear to remain relatively stable after primary PCI. Within the first 3 h after onset of chest pain or other symptoms, both reperfusion strategies seem equally effective in reducing infarct size and mortality. Therefore, thrombolysis is still a viable alternative to primary PCI, if it can be delivered within 3 h after onset of chest pain or other symptoms. Primary PCI compared with thrombolysis significantly reduced stroke. Overall, we prefer primary PCI over thrombolysis in the first 3 h of chest pain to prevent stroke, and in patients presenting 3-12 h after the onset of chest pain, to salvage myocardium and also to prevent stroke. At the moment, there is no evidence to recommend facilitated PCI. Rescue PCI is recommended, if thrombolysis failed within 45-60 min after starting the administration. After successful thrombolysis, the use of routine coronary angiography within 24 h and PCI, if applicable, is recommended even in asymptomatic patients without demonstrable ischaemia to improve patients' outcome. If a PCI centre is not available within 24 h, patients who have received successful thrombolysis with evidence of spontaneous or inducible ischaemia before discharge should be referred to coronary angiography and revascularized accordingly--independent of 'maximal' medical therapy.
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PMID:Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. 1676 Feb 7

To achieve rapid assessment of chest pain in emergency/cardiology departments, a short turnaround time for cardiac marker testing is necessary. Nevertheless, Total Quality Management principles must be incorporated into the management of point-of-care testing (POCT); in this setting we implemented the Stratus CS assay as POCT for cardiac markers in our emergency/cardiology department. The analytical performance of the troponin I method was evaluated; information connectivity between the Stratus CS data management system and the laboratory information system was implemented and practical training of testing personnel was carried out at the POCT site. A total of 41 non-ST-segment elevation patients admitted to the hospital were followed to evaluate the appropriateness of hospital admission, formulated on the basis of the cardiac troponin-I level measured at the POCT site by clinical staff. Our preliminary clinical data suggest that the high sensitivity of the Stratus CS troponin method could play an important role in the early identification of patients with acute myocardial infarction in a low to intermediate-risk population for acute coronary syndrome. Our POCT model suggests that the central laboratory could ensure that the POCT program remains in compliance with quality requirements. Nevertheless, our comparison studies suggest that the implementation of POCT requires a high level of integration between cardiologists and pathologists to guarantee appropriate interpretation of the monitoring results for suspected ACS patients.
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PMID:Integration between point-of-care cardiac markers in an emergency/cardiology department and the central laboratory: methodological and preliminary clinical evaluation. 1584 18

Accurate and rapid diagnostic tests can help identify high-risk patients with ACS among those presenting to the emergency department with chest pain. Such tests can also differentiate low-risk patients with chest pain who are suitable for early emergency department discharge. In this article, Drs Amsterdam and Deedwania elucidate the varieties of ACS, their pathophysiology, and the methods used for diagnosis. The authors also explore the potential of point-of-care testing for cardiac injury markers in the timely and accurate identification of ACS.
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PMID:Bedside evaluation of cardiac markers. Point-of-care testing can differentiate acute coronary syndromes. 1620 4


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