- Angina
- Symptoms
- Physical Examination
- Laboratory ECG
- Stress Testing
- Coronary Arteriography
- Prinzmetal's Variant Angina (Coronary Vasospasm)
Angina pectoris, the most common clinical manifestation of coronary artery disease (CAD), results from an imbalance between myocardial O2 supply and demand, most often due to atherosclerotic coronary artery obstruction. Other major conditions that upset this balance and result in angina include aortic valve disease (Chap. 116 Valvular Heart Disease), hypertrophic cardiomyopathy (Chap. 117 Cardiomyopathies and Myocarditis and coronary artery spasm (see below).
Angina is typically associated with exertion or emotional upset; relieved quickly by rest or nitroglycerin (Chap. 33 Chest Pain). Major risk factors are cigarette smoking, hypertension, hypercholesterolemia (↑LDL; ↓HDL), diabetes, obesity, and family history of CAD before age 55.
Often normal; arterial bruits or retinal vascular abnormalities suggest generalized atherosclerosis; S4 is common. During acute anginal episode, other signs may appear: e.g., an S4, diaphoresis, rales, and a transient murmur of mitral regurgitation due to papillary muscle ischemia.
May be normal between anginal episodes or show old infarction (Chap. 113 Electrocardiography). 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.
Enhances diagnosis of CAD; 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. Exercise testing with radionuclide, echocardiographic, or magnetic resonance imaging increases sensitivity and specificity and is particularly useful if baseline ECG abnormalities prevent interpretation of test. 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, pharmacologic stress with IV dipyridamole, adenosine, regadenoson, or dobutamine can be performed in conjunction with radionuclide or echocardiographic imaging (Table 123-1 Stress Testing Recommendations). Pts with LBBB on baseline ECG should be referred for adenosine or dipyridamole radionuclide imaging, which is most specific for diagnosis of CAD in this setting.
The prognostic utility of coronary calcium detection (by electron-beam or multidetector CT) in the diagnosis and management of CAD continues to be defined.
Some pts do not experience chest pain during ischemic episodes with exertion (“silent ischemia”) but are identified by transient ST-T-wave abnormalities during stress (see below).
Major indications are (1) angina refractory to medical therapy, (2) markedly positive exercise test (≥2-mm ST-segment depression, onset of ischemia at low workload, or ventricular tachycardia 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 noninvasive tests are not diagnostic.
The role of noninvasive coronary imaging techniques (CT and MR angiography) continues to be defined.
| TREATMENT | ||
Chronic Stable Angina(Fig. 123-1. Algorithm for Management of Ischemic Heart Disease) GENERAL
DRUG THERAPYSublingual 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 >10 min despite 2-3 TNG, pt should report promptly to nearest medical facility for evaluation of possible acute coronary syndrome. Long-Term Angina SuppressionThe following classes of drugs are used, frequently in combination. Long-Acting NitratesMay be administered by many routes (Table 123-2 Examples of Commonly Used Nitrates); start at the lowest dose and frequency to limit tolerance and side effects of headache, light-headedness, tachycardia. Beta BlockersAll have antianginal properties; β1-selective agents are less likely to exacerbate airway or peripheral vascular disease (see Table 119-2 Oral Drugs Commonly Used in Treatment of Hypertension). 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 AntagonistsUseful for stable and unstable angina, as well coronary vasospasm (see Table 119-2 Oral Drugs Commonly Used in Treatment of Hypertension). Combination with other antianginal agents is beneficial, but verapamil should be administered cautiously to pts on beta blockers (additive effects on slowing heart rate). Use sustained-release, not short-acting, calcium antagonists; the latter are associated with increased coronary mortality. RanolazineFor pts who continue to experience stable angina despite the above standard medications, consider addition of ranolazine (500-1000 mg PO bid), which reduces anginal frequency and improves exercise capacity without affecting blood pressure or heart rate. Ranolazine is contraindicated in hepatic impairment, in pts with prolongation of the QTc interval, or in combination with drugs that inhibit its metabolism (e.g., ketoconazole, macrolide antibiotics, HIV protease inhibitors, diltiazem, and verapamil). Aspirin81-162 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. The addition of an ACE inhibitor is recommended in pts with CAD and LV ejection fraction <40%, hypertension, diabetes, or chronic kidney disease. MECHANICAL REVASCULARIZATIONUsed in conjunction with, not as replacement for, risk factor modification and medical therapies. Percutaneous Coronary Intervention (PCI)Technique of balloon dilatation, usually with intracoronary stent implantation. 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 in chronic stable angina; should not be performed on asymptomatic or only mildly symptomatic individuals. With PCI initial relief of angina occurs in 95% of pts; however, restenosis develops in 30-45% following balloon dilatation alone, in ∼20% after bare metal stenting, but in <10% after drug-eluting stent (DES) implantation. Late stent thrombosis may occur rarely in pts with DES; it is diminished by prolonged antiplatelet therapy (aspirin indefinitely and a platelet P2Y12 receptor antagonist for a minimum of 12 months). Coronary Artery Bypass Graft (CABG)Appropriately used 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 (e.g., left main, three-vessel disease with impaired LV function). In type 2 diabetics with multivessel CAD, CABG plus optimal medical therapy is superior to medical therapy alone in prevention of major coronary events. The relative advantages of PCI and CABG are summarized in Table 123-3 Comparison of Revascularization Procedures in Multivessel Disease. |
Prinzmetal's Variant Angina (Coronary Vasospasm) 
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 for transient ST elevation during discomfort; diagnosis confirmed at coronary angiography using provocative (e.g., IV acetylcholine) testing. Primary treatment consists of long-acting nitrates and calcium antagonists. Prognosis is better in pts with anatomically normal coronary arteries than in those with fixed coronary stenoses.