ACS, is composed of patients with acute myocardial infarction (MI) with ST-segment elevation on their presenting electrocardiogram and those with unstable angina (UA) and non-ST-segment elevation MI. ACS is a medical emergency which, untreated, will progress to myocardial infarction in over 10 per cent of cases. Therapy reduces this rate to less than 5 per cent. However,death within 1 year still occurs in 5-15 per cent.
Unstable Angina (UA) and Non-ST- Elevation (NSTEMI)
UA is defined as angina pectoris or equivalent ischaemic discomfort with at least one of three features: (1) it occurs at rest (or with minimal exertion) usually lasting > 10 min, (2) it is severe and of new onset (i.e., within the prior 4 to 6 weeks), and/or (3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously). The diagnosis of NSTEMIis established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.
Pathophysiology UA/Nstemi can be caused by a reduction in oxygen supply and/or by an increase in myocardial oxygen demand (e.g., by tachycardia or severe anemia) superimposed on a coronary obstruction. Four pathophysiology processes that may contributed to the development of UA have been identified: (1) plaque rupture or erosion with superimposed nonocculsive thrombus, believed to be the most common cause; (2) dynamic obstruction (e.g., coronary spasm,as in prinzmetal’s variant angina; (3) progressive mechanical obstruction (e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention; and (4) secondary UA related to increased myocardial oxygen demand and/or decreased supply (e.g.,anemia). More than one of these processes may be involved in many patients.
Clinical Presentation
History and Physical Examination
The clinical hallmark of UA/NSTEMI is chest pain, typically located in the retrosternal region or sometimes in the epigastrium, that frequently radiates to the neck, left shoulder, and left arm.This discomfort is usually severe enough to be considered painful. Anginal “equivalents” such as dyspnea and epigastric discomfort may also occur. The examination resembles that in patients with stable angina and may be unremarkable.
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| Braunwald Clinical Classification of Unstable Angina or Non- ST Elevation Myocardial Infarction |
ECG in unstable angina shows, ST-segment depression, transient ST-segment elevation, and/or T-wave inversions which occur in 30-50 per cent of patients, depending on the severity of clinical presentation. T-wave changes are sensitive for ischaemia but are less specific, unless they are new, deep symmetrical T-wave inversions (>.3mv).
Patients with ACS who have elevated biomarkers of necrosis, such as CK-MB and troponin are at increased risk for death or recurrent MI. Elevated levels of these markers distinguish patients with NSTEMI from those with UA.Patients require admission for bed rest, oxygen and morphine, plus aspirin and heparin as well as standard medical anti-anginal therapy (i.e. nitrates and beta-blockers). Aspirin decreases the incidence of both death and myocardial infarction. Oral clopidogrel, which inhibits the platelet ADP receptor, should also be given (CURE studly-clopidogrel in unstable angina to prevent recurrent events trial). Heparin, traditionally given intravenously, should be given for at least 3 days. There is increasing evidence that low-molecular-weight heparins (LWMH), such as delteparin or enoxaparin, are at least as effective as standard unfractionated heparin and have the advantage of being able to be given subcutaneously and of not requiring monitoring. Recent trials have shown that infusion of glycoprotein IIb/IIIa receptor inhibitors (e.g. tirofiban, eptifibatide) may have an additional advantage over heparin plus aspirin in reducing the mortality in high-risk patients. These receptors are activated in the final common pathway of platelet aggregation.
In terms of the short-term risk of death or myocardial infarction, it is possible to risk-stratify patients with ACS into high risk, intermediate risk and low risk. Those at high risk should proceed promptly to angiography, with a view to proceeding to revascularization, where appropriate, during that admission. Those at low risk can be discharged and then assessed electively as outpatient. In between, there is much controversy regarding the optimal management of patients at intermediate risk, and in particular those who settle on initial medical therapy. Early intervention does not convincingly appear to influence the medium and long-term outcomes.Irrespective of the immediate success of treatment, early coronary angiography and, depending on the results, referral for revascularisation are usually advised. Thrombolytic therapy has not been shown to be of benefit in patients with ACS. Occasionally, intra-aortic balloon pumping can be helpful in stabilizing the patient, and to enable angiography (± PTCA) to be undertaken.
Patients with ACS who have elevated biomarkers of necrosis, such as CK-MB and troponin are at increased risk for death or recurrent MI. Elevated levels of these markers distinguish patients with NSTEMI from those with UA.Patients require admission for bed rest, oxygen and morphine, plus aspirin and heparin as well as standard medical anti-anginal therapy (i.e. nitrates and beta-blockers). Aspirin decreases the incidence of both death and myocardial infarction. Oral clopidogrel, which inhibits the platelet ADP receptor, should also be given (CURE studly-clopidogrel in unstable angina to prevent recurrent events trial). Heparin, traditionally given intravenously, should be given for at least 3 days. There is increasing evidence that low-molecular-weight heparins (LWMH), such as delteparin or enoxaparin, are at least as effective as standard unfractionated heparin and have the advantage of being able to be given subcutaneously and of not requiring monitoring. Recent trials have shown that infusion of glycoprotein IIb/IIIa receptor inhibitors (e.g. tirofiban, eptifibatide) may have an additional advantage over heparin plus aspirin in reducing the mortality in high-risk patients. These receptors are activated in the final common pathway of platelet aggregation.
In terms of the short-term risk of death or myocardial infarction, it is possible to risk-stratify patients with ACS into high risk, intermediate risk and low risk. Those at high risk should proceed promptly to angiography, with a view to proceeding to revascularization, where appropriate, during that admission. Those at low risk can be discharged and then assessed electively as outpatient. In between, there is much controversy regarding the optimal management of patients at intermediate risk, and in particular those who settle on initial medical therapy. Early intervention does not convincingly appear to influence the medium and long-term outcomes.Irrespective of the immediate success of treatment, early coronary angiography and, depending on the results, referral for revascularisation are usually advised. Thrombolytic therapy has not been shown to be of benefit in patients with ACS. Occasionally, intra-aortic balloon pumping can be helpful in stabilizing the patient, and to enable angiography (± PTCA) to be undertaken.
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