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Acute coronary syndromes

Fondaparinux, the factor Xa-binding pentasaccharide (Arixtra, MW 1,728 Da), is prepared synthetically, unlike UFH, LMWH and danaparoid, which are obtained from animal sources. Despite only inactivating free factor Xa, clinical trials indicate that fondaparinux is an effective antithrombotic agent, both for venous thromboembolism prophylaxis and treatment, as well as for acute coronary syndrome and ST elevation myocardial infarction [4]. [Pg.110]

The Fifth Organization to Assess Strategies in Acute Ischemic Syndromes Investigators (2006) Comparison of fondaparinux and enoxaparin in acute coronary syndromes. N Engl J Med 354 1464-1476... [Pg.112]

GPIIb/IIIa antagonists have to be administered parenterally. They are currently used prophylactically during intracoronary interventions such as percutaneous transluminal revascularization with balloon angioplasty or intracoronary stenting, as well as to treat acute coronary syndromes like unstable angina and acute myocardial infarction. The main complications... [Pg.170]

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. [Pg.226]

Ray KK, Cannon CP (2005) The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes. J Am Coll Cardiol 46 1425-1430... [Pg.599]

Panagiotakos, D.B. et al., Consumption of fruits and vegetables in relation to the risk of developing acute coronary syndromes the CARDI02000 case-control study, Nutr. J., 2, 2, 2003. [Pg.140]

Infection, acute coronary syndrome, cerebrovascular accidents, trauma, noncompliance with insulin pharmacotherapy, new-onset diabetes mellitus, and medications (e.g., corticosteroids and sympathomimetics)... [Pg.103]

Infection, acute coronary syndrome, cerebrovascular accidents, and trauma... [Pg.105]

Differentiate between the pathophysiology of chronic stable angina and acute coronary syndromes. [Pg.63]

O Ischemic heart disease results from an imbalance between myocardial oxygen demand and oxygen supply that is most often due to coronary atherosclerosis. Common clinical manifestations of ischemic heart disease include chronic stable angina and the acute coronary syndromes of unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. [Pg.63]

The major goals for the treatment of ischemic heart disease are to prevent acute coronary syndromes and death, alleviate acute symptoms of myocardial ischemia, prevent recurrent symptoms of myocardial ischemia, and avoid or minimize adverse treatment effects. [Pg.63]

At this stage, patients may experience symptoms of acute coronary syndrome. If endogenous anticoagulant proteins fail to halt this process, platelet aggregation continues and fibrinogen is converted to fibrin, resulting in an occlusive thrombus (Panel F). [Pg.67]

Define the role of an atherosclerotic plaque, platelets, and coagulation system in an acute coronary syndrome. [Pg.83]

List key electrocardiographic and clinical features identifying a patient with non-ST-segment elevation acute coronary syndrome who is at high risk of myocardial infarction or death. [Pg.83]

Formulate a monitoring plan for a patient with ST-segment elevation acute coronary syndrome receiving fibrinolytics, aspirin, unfractionated heparin, intravenous nitroglycerin, intravenous (3-blockers followed by oral P-blockers, an angiotensin-converting enzyme inhibitor, and a statin. [Pg.83]

O The cause of an acute coronary syndrome is the rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, and aggregation, and the activation of the clotting cascade. Ultimately, a clot forms composed of fibrin and platelets. [Pg.83]

The American Heart Association and the American College of Cardiology recommend strategies, or guidelines, for acute coronary syndrome patient care for ST-segment and non-ST-segment elevation acute coronary syndrome. [Pg.83]

Patients with ischemic chest discomfort and suspected acute coronary syndrome are risk-stratified based upon a 12-lead electrocardiogram, past medical history, and results of the creatine kinase myocardial band and troponin tests. The diagnosis... [Pg.83]

Early reperfusion therapy with either primary percutaneous coronary intervention or administration of a fibrinolytic agent within 3 hours of symptom onset is the recommended therapy for patients presenting with ST-segment elevation acute coronary syndrome. [Pg.83]

Acute coronary syndromes is a term that includes all clinical syndromes compatible with acute myocardial ischemia resulting from an imbalance between myocardial oxygen demand and supply.3 In contrast to stable angina, an ACS results primarily from diminished myocardial blood flow secondary to an occlusive or partially occlusive coronary artery thrombus. Acute coronary syndromes are classified according to electrocardiogram (ECG) changes into STE ACS (STE MI) or NSTE ACS (NSTE MI and unstable angina) (Fig. 5-1). An STE MI, formerly... [Pg.84]

Ischemic chest discomfort symptoms, lasting at least 20 minutes Suspect acute coronary syndrome... [Pg.86]

FIGURE 5-2. Biochemical markers in suspected acute coronary syndromes. (Reprinted from Spinier SA, de Denus S. Acute Coronary Syndromes. In DiPiroJT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy ... [Pg.89]


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