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Harrison’s Manual of Medicine



Unstable Angina
Coronary Vasospasm
Silent Ischemia
Angina pectoris, the most common clinical manifestation of CAD, results from an imbalance between myocardial O2 supply and demand, most commonly resulting from atherosclerotic coronary artery obstruction. Other major conditions that upset this balance and result in angina include aortic valve disease (Chap. 118), hypertrophic cardiomyopathy (Chap. 119), and coronary artery spasm (see below).
SYMPTOMS   Angina is typically associated with extension or emotional upset; relieved quickly by rest or nitroglycerin (Chap. 2). Major risk factors are cigarette smoking, hypertension, hypercholesterolemia (
LDL fraction; ¯HDL), diabetes, and family history of CAD below age 55.
PHYSICAL EXAMINATION   Often normal; arterial bruits or retinal vascular abnormalities suggest generalized atherosclerosis; S4 is common. During acute anginal episode, other signs may appear: loud S3 or S4, diaphoresis, rales, and a transient murmur of mitral regurgitation due to papillary muscle ischemia.
LABORATORY   ECG   May be normal between anginal episodes or show old infarction (Chap. 113). During angina, ST- and T-wave abnormalities typically appear (ST-segment depression reflects subendocardial ischemia; ST- segment elevation may reflect acute infarction or transient coronary artery spasm). Ventricular arrhythmias frequently accompany acute ischemia.
Stress Testing   Enhances diagnosis of CAD (Fig. 122-1). Exercise is performed on treadmill or bicycle until target heart rate is achieved or pt becomes symptomatic (chest pain, light-headedness, hypotension, marked dyspnea, ventricular tachycardia) or develops diagnostic ST-segment changes. useful information includes duration of exercise achieved; peak heart rate and bp; depth, morphology, and persistence of ST-segment depression; and whether and at which level of exercise pain, hypotension, or ventricular arrhythmias develop. Thallium 201 (or 99m-technetium sestamibi) imaging increases sensitivity and specificity and is particularly useful if baseline ECG abnormalities prevent interpretation of test (e.g., LBBB). Note: Exercise testing should not be performed in pts with acute MI, unstable angina, or severe aortic stenosis. If the pt is unable to exercise, intravenous dipyridamole (or adenosine) testing can be performed in conjunction with thallium or sestamibi imaging or a dobutamine echocardiographic study can be obtained (Table 122-1).

FIGURE 122-1. Role of exercise testing in management of CAD, RVG, radionuclide ventriculogram; EF, left ventricular ejection fraction. [Modified from LS Lilly, in Textbook of Primary Care Medicine, J Nobel (ed.) St. Louis Mosby, 1996, p. 224.]

Table 122-1 Stress Testing Recommendations

Some pts do not experience chest pain during ischemic episodes with exertion (“silent ischemia”) but are identifed by transient ST-T-wave abnormalities during stress testing or Holter monitoring (see below).
Coronary Arteriography   The definitive test for assessing severity of CAD; major indications are (1) angina refractory to medical therapy, (2) markedly positive exercise test (³2-mm ST-segment depression or hypotension with exercise) suggestive of left main or three-vessel disease, (3) recurrent angina or positive exercise test after MI, (4) to assess for coronary artery spasm, and (5) to evaluate pts with perplexing chest pain in whom nonivasive tests are not diagnostic.


Identify and treat risk factors: mandatory cessation of smoking; treatment of diabetes, hypertension, and lipid disorders (Chap. 178).

Correct exacerbating factors contributing to angina: marked obesity, CHF, anemia, hyperthyroidism.

Reassurance and pt education.
Drug Therapy
Sublingual nitroglycerin (TNG 0.3–0.6 mg); may be repeated at 5-min intervals; warn pts of possible headache or light-headedness; teach prophylactic use of TNG prior to activity that regularly evokes angina. If chest pain persists for more than 10 min despite 2–3 TNG, pt should report promptly to nearest medical facility for evaluation of possible unstable angina or acute MI.
Long-Term Angina Suppresion
Three classes of drugs are used, frequently in combination:
Long-Acting Nitrates May be administered by many routes (Table 122-2); start at the lowest dose and frequency to limit tolerance and side effects of headache, light-headedness, tachycardia.

Table 122-2 Examples of Commonly Used Nitrates

Beta Blockers (See Table 124-1) All have antianginal properties; b1- selective agents are less likely to exacerbate airway or peripheral vascular disease. Dosage should be titrated to resting heart rate of 50–60 beats/min. Contraindications to beta blockers include CHF, AV block, bronchospasm, “brittle” diabetes. Side effects include fatigue, bronchospasm, depressed LV function, impotence, depression, and masking of hypoglycemia in diabetics.
Calcium Antagonists (See Table 124-4) Useful for stable and unstable angina, as well coronary vasospasm. Combination with other antianginal agents is beneficial, but verapamil should be administered very cautiously or not at all to pts on beta blockers or disopyramide (additive effects on LV dysfunction). Use sustained-release, not short-acting, calcium antagonists; the latter increase coronary mortality.
Aspirin 80–325 mg/d reduces the incidence of MI in chronic stable angina, following MI, and in asymptomatic men. It is recommended in pts with CAD in the absence of contraindications (GI bleeding or allergy). Consider clopidogrel (75 mg/d) for aspirin-intolerant individuals.
Mechanical Revascularization
Percutaneous Coronary Intervention (PCI) Includes percutaneous transluminal angioplasty (PTCA) and/or stenting. Performed on anatomically suitable stenoses of native vessels and bypass grafts; more effective than medical therapy for relief of angina. Has not been shown to reduce risk of MI or death; should not be performed on asymptomatic or only mildly symptomatic individuals. With PCI initial relief of angina occurs in 95% of pts; however, with PTCA stenosis recurs in 30–45% within 6 months (more commonly in pts with initial unstable angina, incomplete dilation, diabetes, or stenoses containing thrombi). If restenosis occurs, PTCA can be repeated with success and risks like original procedure. Potential complications include dissection or thrombosis of the vessel and uncontrolled ischemia or CHF. Complications are most likely to occur in pts with CHF, long eccentric stenoses, calcified plaque, female gender, and dilation of an artery that perfuses a large segment of myocardium with inadequate collaterals. Placement of an intracoronary stent in suitable pts reduces the restenosis rate to 10–30% at 6 months. PCI has also been successful in some pts with recent total coronary occlusion (<3 months).
Coronary Artery Bypass Surgery (CABG) For angina refractory to medical therapy or when the latter is not tolerated (and when lesions are not amenable to PCI) or if severe CAD is present (left main, three-vessel disease with impaired LV function). CABG is preferred over PTCA in diabetics with CAD in ³2 vessels because of better survival.
The relative advantages of PTCA and CABG are summarized in Table 122-3.

Table 122-3 Comparison of Revascularization Procedures in Multivessel Disease

Includes (1) new onset (<2 months) of severe angina, (2) angina at rest or with minimal activity, (3) recent increases in frequency and intensity of chronic angina, (4) recurrent angina within several days of acute MI without reelevation of cardiac enzymes.


Admit to continuous ECG-monitored floor.

Identify and treat exacerbating factors (hypertension, arrhythmias, CHF, acute infection).

Anticoagulation: IV heparin (aim for PTT 2 × control) or low-molecular- weight heparin (e.g., enoxaparin 1 mg/kg SC bid) × 3–5 d; plus aspirin 325 mg/d. In high-risk patients (Fig. 122-2) add GpIIb/IIIa inhibitor [e.g., eptifibatide, 180 µg/kg, then 2 (µg/kg)/min].

FIGURE 122-2. Management algorithm for unstable angina. CCSC, Canadian Cardiovascular Society classification; CCU, coronary care unit; CABG, coronary artery bypass grafting; PCI, percutaneous coronary intervention. (Modified from E Braunwald et al, Circulation 90: 613, 1994.)

Rule out MI by ECG and cardiac enzymes.

Maximize therapy with oral nitrates, beta blockers (to reduce heart rate to 50–70 beats per min). Reserve use of calcium antagonists for those with refractory pain.

For refractory pain: IV TNG (begin at 10 µg/min); titrate dosage to alleviate pain, but maintain systolic bp ³100 mmHg.

Refractory unstable angina warrants coronary arteriography and possible PCI or CABG. If symptoms are controlled on medical therapy, a predischarge exercise test should be performed to assess need for coronary arteriography.

Intermittent focal spasm of coronary artery; often associated with atherosclerotic lesion near site of spasm. Chest discomfort is similar to angina but more severe and occurs typically at rest, with transient ST-segment elevation. Acute infarction or malignant arrhythmias may develop during spasm-induced ischemia. Evaluation includes observation of ECG (or ambulatory Holter monitor) for transient ST elevation; diagnosis confirmed at coronary angiography using provocative (e.g., IV acetylcholine) testing. Treatment consists of long-acting nitrates and calcium antagonists. Prognosis is better in pts with anatomically normal coronary arteries than those with fixed coronary stenoses.
Myocardial ischemia that develops without anginal symptoms; detected by Holter monitoring or exercise electrocardiography; occurs mainly in pts who also have symptomatic ischemia but is sometimes demonstrated in totally asymptomatic individuals. Management is guided by exercise electrocardiography, often with radionuclide scintigraphy, to assess severity of myocardial ischemia. Pts with evidence of severe silent ischemia are candidates for coronary arteriography. It has not been demonstrated that pts with silent ischemia without marked abnormalities on exercise testing require chronic anti-ischemic therapy. However, aspirin and lipid-lowering therapy (if LDL > 130 mg/dL) are recommended.

For a more detailed discussion, see Selwyn AP, Braunwald E: Ischemic Heart Disease, Chap. 244 p. 1399; and Baim DS: Percutaneous Coronary Revascularization, Chap. 245, p. 1410, in HPIM-15.


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