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المستخلص WHO estimated that in 2002, 12.6% of deaths worldwide were from ischemic heart disease. Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries. Acute coronary syndromes (ACS) are conditions characterized by the sudden onset of coronary insufficiency as a result of thrombotic occlusion of one or more coronary arteries. Three such conditions are identified: STsegment elevation myocardial infarction (STEMI), non ST-segment elevation myocardial infarction (non-STEMI), and unstable angina. The first condition (STEMI) is the result of complete and sustained thrombotic coronary occlusion, while the last two conditions (non-STEMI and UA) are result of either partial thrombotic coronary occlusion or transient complete occlusion with spontaneous revascularization. The immediate diagnosis of a patient with an acute coronary syndrome is determined by the characteristics of the presenting electrocardiogram and, in particular, the presence or absence of ST segment elevation. In combination with the clinical presentation, mainly chest pain and presence or absence of cardiac enzymes in the assay The anatomy of the Heart and the coronaries plays a corner stone in identifying the lesion and further steps of treatment Virtually all regional acute myocardial infarcts are caused by thrombosis developing on a culprit coronary atherosclerotic plaque. The very rare exceptions to this are spontaneous coronary artery dissection, coronary arteritis, coronary emboli, coronary spasm, and compression by myocardial bridges. Thrombosis is also the major initiating factor in unstable angina, particularly when rest pain is recent and increasing in severity. Multiple risk factors play important role in the process of the Acute coronary syndromes include smoking, hypertension, diabetes mellitus, dyslipidemia, metabolic syndrome, obesity and homocysteinemia UA and NSTEMI are considered to be closely related conditions whose pathogenesis and clinical presentations are similar but of differing severity; that is, they differ primarily in whether the ischemia is severe enough to cause Summary. - 121 - sufficient myocardial damage to release detectable quantities of a marker of myocardial injury, most commonly Troponin I (TnI), Troponin T (TnT), or CK-MB. Once it has been established that no biochemical marker of myocardial necrosis has been released the patient with ACS may be considered to have experienced UA, whereas the diagnosis of NSTEMI is established if a marker has been released. Diagnosis depend on the history, anginal symptoms regarding the criteria of pain (location, severity, duration, nature, radiation, precipitating factors and relation to nitrate) while differential diagnosis of other cardiac and non-cardiac pain are in consideration. ECG, biochemical cardiac markers (Creatin Kinase, Cardiac Troponins and Myoglobin) are the main key of diagnosing ACS. A high quality portable chest X-ray, transthoracic and/or transesophageal echocardiography, and a contrast chest CT scan can be useful for differentiating acute MI from aortic dissection in patients for whom this distinction is clinically unclear. SPECT radionuclide imaging at rest is not routinely indicated to establish the diagnosis of MI in patients with STEMI, although it can provide valuable, accurate diagnostic and prognostic information in patients who present to the ED with symptoms suggestive of acute cardiac ischemia and a normal or non diagnostic ECG. Patients with ECG ST-segment deviations, or positive cardiac markers who are stable hemodynamically should be admitted to an inpatient unit with continuous rhythm monitoring and careful observation for recurrent ischemia (a step-down unit) and managed according to the acute ischemia pathway. Curative measures to be given to the patient are oxygen, Anti –ischemic drugs (Nitrates , Morphine, beta Blockers and Calcium Channel Blockers), Anti- platelets (Aspirin, Clopidogrel, ticlopidine and platelet GP IIb/IIIa receptor antagonists) and Anti- Coagulants (Heparin, Low-Molecular-Weight Heparin and Hirudin). Management of STEMI depends mainly on Reperfusion either pharmacological or surgical. For Fibrinolytic therapy (The earlier therapy begins, the better the outcome) with the greatest benefit decidedly occurring whentherapy is given within the first 3 hours. List of the contraindication, precaution and complication of Fibrinolytic therapy are listed. Also Percutaneous coronary intervention is a very effective method for reestablishing coronary perfusion and is suitable for at least 90% of patients. Considerable data support the use of PCI for patients with STEMI. Studies demonstrate that PCI-treated patients experience lower short-term mortality rates (5.0% versus 7.0%), less nonfatal reinfarction (3.0% versus 7.0), and less hemorrhagic stroke (0.05% versus 1.0) than those treated by fibrinolysis but with an increased risk for major bleeding (7.0% versus 5.0%). Medical contact–to-balloon or door-to balloon times less than 90 minutes are strict performance criteria must be mandated for primary PCI programs. Coronary artery bypass graft surgery should be considered when recurrent ischemia occurs in patients with STEMI whose coronary artery anatomy is not suitable for PCI. Complications of acute coronary syndromes include Hemodynamic Disturbances (hypotension, low - Output state, pulmonary congestion and Cardiogenic shock), Mechanical disturbance (Mitral Valve Regurgitation, Ventricular Septal Rupture, Left Ventricular Free-Wall Rupture and Left Ventricular Aneurysm), different types of arrhythmia and ischemic strock can be seen as complications. Late management of ACS include Antiplatelet therapy, Beta Blockers, Angiotensin-converting enzyme inhibitors, Nitroglycerin, Calcium channel blockers, Warfarin, Lipid management and Blood pressure control. |