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High Likelihood (any of the following)
Intermediate Likelihood (absence of high-likelihood features and presence of any of the following)
Low Likelihood (absence of high- or intermediate-likelihood features but may have the following)
History
Chest or left arm pain or discomfort as chief symptom reproducing prior documented angina
Known history of CAD, including myocardial infarction
Chest or left arm pain or discomfort as chief symptom Age <70 yr Male sex Diabetes mellitus
Probable ischemic symptoms in absence of any of the
intermediate-likelihood characteristics
Recent cocaine use
Examination Transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema, or rales
Extracardiac vascular disease
Chest discomfort reproduced by palpation
Electrocardiogram New, or presumably new, transient ST segment deviation (>0.05 mV) or T wave inversion (>0.2 mV) with symptoms Fixed Q waves Abnormal ST segments or T waves not documented to be new
T wave flattening or inversion in leads with dominant R waves Normal electrocardiogram
Cardiac markers Elevated cardiac troponin I, troponin T, or creatine kinase myocardial band
Normal Normal
Modified from Braunwald E, Mark DB, Jones RH et al: Unstable angina: diagnosis and management, Rockville, Md, 1994, Agency for Health Care Policy and Research and the National Heart, Lung, and Blood Institute, U.S. Public Health Service, U.S. Department of Health and Human Services; AHCPR Publication No. 94-0602.
CAD, coronary artery disease.
II. DIAGNOSIS
All patients being evaluated for ACS should be placed on a cardiac monitor, and a 12-lead electrocardiogram should be obtained within 10 minutes of presentation and repeated if the chest discomfort changes. A careful physical examination (including assessment of blood pressure in both arms) should be performed and a chest film obtained. A blood sample should be sent for analysis of the comprehensive metabolic panel, troponin level, fractionated creatine kinase (CK) concentration, complete blood cell count, and prothrombin and activated partial thromboplastin times. Risk stratification of the patient should then be used.
A. ELECTROCARDIOGRAM
1. A 12-lead electrocardiogram should be obtained immediately for every patient with signs or symptoms suggestive of ACS and compared with a previous electrocardiogram if available.
2. The electrocardiogram differentiates ST segment elevation ACS from non–ST segment elevation ACS. This distinction is vital because treatment differs greatly between the two syndromes.
3. The current ECG criteria for the diagnosis of ST elevation ACS require more than 1 mm ST elevation in two or more anatomically contiguous limb leads, more than 2 mm ST elevation in two or more anatomically contiguous precordial leads, or a new or presumed new left bundle branch block.
4. Serial ECG analysis is essential because a suspected non–ST segment elevation ACS may evolve into an ST segment elevation ACS.
5. A right-sided electrocardiogram should be obtained in all patients with ST segment elevations in the inferior leads to determine whether right ventricular MI is present. ST segment elevation in V4 of the right-sided leads suggests a right ventricular infarction.
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6. When the electrocardiogram meets ST segment elevation ACS criteria, the patient becomes eligible for acute reperfusion therapy. The current recommendations are to administer thrombolytic therapy within 30 minutes or perform percutaneous coronary intervention (PCI) within 90 minutes of diagnosis.
7. Patients with non–ST segment elevation ACS may initially have a normal electrocardiogram or nonspecific ST-T wave changes. Thus a normal electrocardiogram does not exclude this diagnosis. ST segment depressions of more than 1 mm in two or more contiguous limb leads (or more than 2 mm in two or more contiguous precordial leads) may be present and predict adverse cardiac events.
B. CARDIAC BIOMARKERS
1. In patients with a non–ST segment elevation ACS, serum biomarkers (e.g., cardiac enzymes) indicative of myocardial necrosis are helpful in stratifying risk and differentiating ischemia from infarction. It takes several hours from the time myocardial injury occurs until biomarkers are detectable in the serum, so the patient with a non–ST segment elevation ACS may have normal values initially at presentation. Therefore blood samples should be obtained at the time of presentation and again 6 to 12 hours later.
2. Traditional biomarkers included CK, troponin I or T, and myoglobin. Based on current guidelines, the cardiac-specific troponins such as troponin T and troponin I are the preferred markers. Troponin T is detectable in the serum within 4 hours after myocardial injury, with elevated serum levels for 7 to 10 days. Troponin I is typically detectable within 6 hours of myocardial injury, and the serum levels remain elevated for 7 to 10 days. Troponin I is less likely to be associated with false elevations than troponin T in patients with renal insufficiency.
3. CK exists in three isoforms (MM, MB, BB), of which CK-MB is cardiac-specific. CK-MB serum levels typically increase 3 to 6 hours after myocardial injury, peak at 12 to 24 hours, and return to normal within 3 days. CK-MB is less cardiospecific than troponin, and serum levels may be elevated in the patient with trauma, surgery, rhabdomyolysis, sepsis, hypothyroidism, or renal dysfunction.
4. Myoglobin is a highly sensitive and early marker of myocardial damage. Serum myoglobin levels begin to increase within 2 hours of myocardial injury and peak at 24 hours. However, serum myoglobin has very low specificity because myoglobin increases with skeletal muscle injury, trauma, intramuscular injections, alcohol abuse, renal dysfunction, and hypothermia or hyperthermia. Therefore a negative myoglobin within 8 hours of the onset of chest pain may be useful to help rule out myocardial ischemia.
III. MANAGEMENT: NON–ST SEGMENT ELEVATION ACS A. RISK STRATIFICATION
Risk stratification is integral in the management of a non–ST segment elevation ACS because not all patients with ACS are equally likely to have adverse cardiac events (i.e., death, MI, or urgent revascularization). Patients are classified as being at high, intermediate, or low risk of having an adverse cardiac event, and therapy is tailored to the patient's risk profile. The following clinical tools help risk stratify patients:
1. Electrocardiogram and cardiac biomarkers. ST segment depression and elevated cardiac biomarkers are associated with a higher risk of adverse outcomes. Patients with only one of the two are at intermediate risk, and those with neither are at low risk.
2. A list of historical and physical findings the American Heart Association has adopted in assisting with risk stratification is provided in Table 8-2 .
3. Thrombolysis in Myocardial Infarction (TIMI) risk score assessment. The TIMI risk factor score predicts the probability of adverse cardiac outcomes in patients with non–ST segment elevation ACS based on data available at the bedside.[2] Seven variables are assessed ( Box 8-1 ), with the likelihood of an adverse cardiac event predicted by the number of variables present. Patients with a score of less than 3 are at low risk, those with a score of 3 or 4 are at intermediate risk, and those with a score of 5 or higher are at high risk for having a cardiac event over the next 30 days.
BOX 8-1
THROMBOLYSIS IN MYOCARDIAL INFARCTION RISK FACTOR SCORE