11/30/2023 0 Comments Timi risk score early invasive![]() ![]() Risk stratification can be helpful in determining the appropriate testing, pharmacologic interventions, and timing or need for coronary angiography.Acute treatment aims to reduce the symptoms of chest pain and risk of recurrent MI or death.7 Severe elevations of BNP in the setting of ACS in patients without known HF should raise concern for a large infarction and urgent angiography. ![]() Brain natriuretic peptide (BNP) can be a useful biomarker of myocardial stress in patients with ACS, and elevations are associated with worse outcomes.CK-MB may be a useful assay for detecting postinfarct ischemia because a fall and subsequent rise in enzyme levels suggests reinfarction if accompanied by recurrent ischemic symptoms or ECG changes.It lacks specificity because it is present in both skeletal and cardiac muscle cells. Creatine kinase (CK)-MB is no longer a recommended marker for the initial diagnosis of NSTEMI.MI size and prognosis are directly proportional to magnitude of increase in troponin.In patients with troponin below the detectable limit of the assay within 6 hours of the onset of pain, a second sample should be drawn 8–12 hours after symptom onset.Serum troponin levels are usually undetectable in normal individuals, and any elevation is considered abnormal. Troponin T and I assays are highly specific and sensitive markers of myocardial necrosis.Troponin is the recommended biomarker for assessment of myocardial necrosis.Other conditions may be found to be contributing to ischemia (e.g., anemia) or mimicking ischemia (e.g., hyperkalemia-related ECG changes) or may alter management (e.g., severe thrombocytopenia). A complete blood count, basic metabolic panel, fasting glucose, and lipid profile should be obtained in all patients with suspected CAD.Nonspecific ST-segment changes or T-wave inversions (those that do not meet voltage criteria) are nondiagnostic and unhelpful in management of acute ischemia but are associated with a higher risk for future cardiac events.Biphasic or deeply inverted T waves (>5 mm) with QT prolongation in leads V 2 to V 4 in the setting of stuttering chest pain within the past 24 hours suggests a critical lesion in the LAD artery distribution (Wellens syndrome).ST-segment depression in multiple leads plus ST-segment elevation in aVR and/or V 1 suggests ischemia due to multivessel or left main disease.Threshold value for abnormal J-point depression should be 0.5 mm in leads V 2 and V 3 and 1 mm in all other leads.ST-segment depression in two contiguous leads is a sensitive indicator of myocardial ischemia, especially if dynamic and associated with symptoms.Approximately 50% of patients with UA/NSTEMI have significant ECG abnormalities, including transient ST-segment elevations, ST depressions, and T-wave inversions.Posterior leads or urgent echocardiography may more accurately assess the presence of ischemia when the suspicion is high. The posterior circulation (i.e., circumflex coronary artery distribution) is poorly assessed with standard ECG lead placement and should always be considered when evaluating patients with ACS.Comparison to prior ECGs is important when evaluating an ECG for dynamic changes.Serial ECGs should be obtained to assess for dynamic ischemic changes.Isolated Q waves in lead III only are a normal finding.The presence of Q waves, ST-segment changes, or T-wave inversions is suggestive of CAD.A normal tracing does not exclude the presence of disease. Prior to or immediately on arrival to the emergency department, a baseline ECG should be obtained in all patients with suspected ACS.Less common causes include dynamic obstruction of the coronary artery due to vasospasm (Prinzmetal angina, cocaine use), coronary artery dissection (more common in women), coronary vasculitis, and embolus.Ĭlinical Presentation Clinical Presentation.A thin fibrous cap (thin-cap fibroatheroma) is felt to be more vulnerable to rupture and is most frequently represented as only moderate stenosis on angiography. Rupture allows exposure of lipid-rich subendothelial components to circulating platelets and inflammatory cells, serving as a potent substrate for thrombus formation. Plaque rupture may be triggered by local and/or systemic inflammation as well as shear stress.In some cases, markedly increased myocardial oxygen demand may lead to NSTEMI (demand ischemia), as seen in severe anemia, hypertensive crisis, acute decompensated HF, surgery, or any other significant physiologic stressor. In the majority of cases, NSTEMI is due to a sudden decrease in blood supply via partial occlusion of the affected vessel. Myocardial ischemia results from decreased myocardial oxygen supply and/or increased demand. ![]()
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