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The diagnosis of ACS requires two of the following: ischemic symptoms, diagnostic electrocardiogram (ECG) changes, or elevated serum marker of cardiac injury.
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By themselves, signs and symptoms are not sufficient to diagnose or rule out ACS, but they start the investigatory cascade. Having known risk factors for coronary artery disease (CAD) (Table 20-1) or prior ACS increases the likelihood of ACS. Up to one-third of people with CAD progress to ACS with chest pain. While chest pain is the predominant symptom of ACS, it is not always present. Symptoms include the following:
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Chest pain
Classic: substernal pain that occurs with exertion and alleviates with rest (In a person with a history of CAD, this called “typical” or “stable” angina)
Dull, heavy pressure in or on the chest
Sensation of a heavy object on the chest
Initiated by stress, exercise, large meals, sex, or any activity that increases the body’s demand on the heart for blood
Lasting >20 minutes
Radiating to the back, neck, jaw, left arm or shoulder
Accompanied by feeling clammy or sweaty
Associated with sensation of dry mouth (women)
Not affected by inspiration
Not reproducible with chest palpation
Right-sided chest pain, occasionally
Pain high in the abdomen or chest, nausea, extreme fatigue after exercise, back pain, and edema can occur in anyone, but are more common in women
Extreme fatigue or edema after exercise
Shortness of breath
This can be the only sign in the elderly
More common in African-American than white patients
More common in women than men
Levine’s sign—chest discomfort described as a clenched fist over the sternum (the patient will clench his/her fist and rest it on or hover it over his/her sternum)
Angor anami—great fear of impending doom/death
Nausea, lightheadedness, or dizziness
Less commonly
Mild, burning chest discomfort
Sharp chest pain
Pain that radiates to the right arm or back
A sudden urge to defecate in conjunction with chest pain
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Chest pain that is present for days, is pleuritic, is positional, or radiates to the lower extremities or above the mandible is less likely to be cardiac in origin.
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Examination findings that increase the probability that symptoms are from ACS include hypotension, diaphoresis, and systolic heart failure indicated by a new S3 gallop, new or worsening mitral valve regurgitation, pulmonary edema, and jugular venous distention.
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Chest pain reproducible with palpation is significantly less likely to be ACS.
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C. Diagnostic Testing
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Anyone suspected of having ACS should be evaluated with a 12-lead electrocardiogram (ECG) and serum cardiac biomarkers (eg, troponin, CPK-MB).
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Notable ECG findings are as follows:
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ST-T segment (>1–mm elevation or depression) and T-wave (inversion) changes suggest ischemia.
Q wave suggests accomplished infarction.
ST elevation is absent in unstable angina and NSTEMI.
New bundle branch block or sustained ventricular tachycardia indicates a higher risk of progression to infarction.
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Accurate ECG interpretation is essential for diagnosis, risk stratification, and guiding the treatment plan. Many findings are non-specific, and the pre-existing presence of bundle branch block (BBB), interventricular conduction delay (IVCD), or Wolff-Parkinson-White syndrome reduce the diagnostic reliability of an ECG in patients with chest pain. If there is a recent ECG for comparison the presence of a new BBB or IVCD raises the suspicion of ACS.
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A normal ECG does not exclude ACS. Up to 25–50% of people with angina or silent ischemia have a normal ECG; 10% of ACS is subsequently diagnosed with an MI after an initial normal ECG.
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Cardiac biomarkers are blood tests that indicate myocardial damage. Troponins T and I are preferred because of their high sensitivity and specificity for myocardial injury. Troponin I is most preferred because troponin T is more likely to be elevated by renal disease, polymyositis, or dermatomyositis. Newer highly sensitive troponin I assays have a 97–99%, negative predictive value of depending on the chosen cutoff value, as early as 3 hours after the onset of symptoms. However, the specificity is lower, resulting in a tradeoff–fewer false negatives afford earlier diagnosis at the cost of more false positives. The potential impact of this will be discussed in the treatment section of this chapter. Troponin remains elevated for 7–10 days, and can therefore help identify prior recent infarctions.
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When initial ECG and cardiac markers are normal, they should be repeated within 6–12 hours of symptom onset. If they are normal a second time, exercise or pharmacological cardiac stress testing should be done to evaluate for inducible ischemia. Exercise stress testing (EST) is preferred, but stress testing with chemicals (dobutamine, dipyridamole, or adenosine) can be used to simulate the cardiac effects of exercise in those unable to exercise enough to produce a test adequate for interpretation.
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Exercise stress testing is the main test for evaluating those with suspected angina or heart disease (Table 20-2). Interpretation of the test is based on the occurrence of signs of stress-induced impairment of myocardial contraction, including ECG changes (Table 20-3) and/or symptoms and signs of angina. The false-positive rate is 10%.
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Adding radionuclide myocardial perfusion imaging (Table 20-4) to EST can improve sensitivity, specificity, and accuracy, especially in patients with a nondiagnostic exercise test or limited exercise ability. Acute rest myocardial perfusion imaging is very similar, but is performed during or shortly after resolution of angina symptoms that were not induced by a stress test. Radionucleatide EST can be advantageous in women because EST is less accurate in women compared to men.
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Chest radiography (CXR) is used to assess for non-ACS causes of chest pain (eg, aortic dissection, pneumothorax, pulmonary embolus, pneumonia, rib fracture).
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Echocardiography can be used to determine left ventricle ejection fraction, assess cardiac valve function, and detect regional wall motion abnormalities that correspond to areas of myocardial damage. Its high sensitivity and low specificity make it most useful to exclude ACS if the study is normal. It can also be used as an adjunct to stress testing. Since stress-induced impairment of myocardial contraction precedes ECG changes and angina, stress echocardiography, done and interpreted by experienced clinicians, can be superior to EST.
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Cardiac magnetic resonance imaging does not yet have a clinical role because its sensitivity and specificity for detecting significant CAD plaque do not eclipse angiography, the gold standard.
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Electron-beam computed tomography (EBCT) currently lacks utility since a positive test does not correlate well to an ACS episode. The future role of EBCT may change as more studies are done with higher resolution CT machines.
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Coronary angiography is the gold standard. Main indications are in Table 20-5. Risks include death (1 in 1400), stroke (1 in 1000), coronary artery dissection (1 in 1000), arterial access complications (1 in 500), and minor risks such as arrhythmia; 10–30% of angiography studies are normal.
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