ACS indicates acute coronary syndromes; BNP, B-type natriuretic peptide; COR, Class of Recommendation; cTnI, cardiac troponin I; cTnT, cardiac troponin T; ECG, electrocardiogram; LOE, Level of Evidence; N/A, not available; NSTE-ACS, non ST-elevation acute coronary syndromes; and NT pro-BNP, N-terminal pro- B-type natriuretic peptide. Figure 2. Global Registry of Acute Coronary Events Risk Calculator for In-Hospital Mortality for Acute Coronary Syndrome. Amsterdam et al 2014 AHA/ACC NSTE-ACS Guideline e357 are less helpful, although by suggesting prior MI, they indi- cate a high likelihood of significant CAD. Isolated Q waves in lead 3 are a normal finding. A completely normal ECG in a patient with chest pain does not exclude ACS, because 1% to 6% of such patients will have a MI, and at least 4% will have Fibrinolytic therapy is contraindicated for patients with ACS without ST-elevation, except for those with electro- cardiographic evidence of true posterior MI (ie, ST-elevation in posterior chest leads [V7 ]). This can be evaluated when acute myocardial infarction (AMI) is suspected but electrocardiographic changes are modest or not present82 84 ; a transthoracic echocardiogram to evaluate for posterior wall motion abnormalities may also be helpful in this setting. Alternative causes of ST-T changes include LV aneurysm, pericarditis, myocarditis, bundle-branch block, LV hypertro- phy, hyperkalemia, Prinzmetal angina, early repolarization, apical LV ballooning syndrome (Takotsubo cardiomyopathy, Section 7.13), andWolff-Parkinson-White conduction. Central nervous system events and therapy with tricyclic antidepres- sants or phenothiazines can cause deep T-wave inversion. 3.3.2.5. Physical Examination The physical examination is helpful in assessing the hemodynamic impact of an ischemic event. Patients with suspected ACS should have vital signs measured (BP in both arms if dissection is sus- pected)andshouldundergoathoroughcardiovascularexamination. 