الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
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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.
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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.