Porth's Essentials of Pathophysiology, 4e

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Circulatory Function

U N I T 5

Silent Myocardial Ischemia Silent myocardial ischemia occurs in the absence of anginal pain. The factors associated with asymptomatic ischemia appear to be the same as those responsible for angina: impaired blood flow from the effects of coro- nary atherosclerosis or vasospasm. Silent myocardial ischemia affects three populations—persons who are asymptomatic without other evidence of CAD, per- sons who have had a myocardial infarct and continue to have episodes of silent ischemia, and persons with angina who also have episodes of silent ischemia. 21 The reason for the painless episodes of ischemia is unclear. The ischemic episodes may be shorter and involve less myocardial tissue than those producing pain. Another explanation is that persons with silent angina have defects in pain threshold or pain transmission, or an autonomic neuropathy with sensory denervation. For example, asymptomatic ischemia is observed in persons with diabetes mellitus, probably the result of autonomic neuropathy, which is a common complication of diabe- tes. 21 Silent myocardial ischemia makes up a significant proportion of all STEMIs in the elderly. Variant (Vasospastic) Angina Variant angina, also known as vasospastic or Prinzmetal angina, is caused by coronory artery spasm. The causes of variant angina are not completely understood, but a combination of pathologic processes may be respon- sible. Endothelial dysfunction, hyperactive sympathetic nervous system responses, defective handling of cal- cium by vascular smooth muscle, or altered nitric oxide production may all contribute. 21 In some persons it is associated with hypercontractility of vascular smooth muscle, as well as with migraine headaches or Raynaud phenomenon. Unlike stable angina that occurs with exertion or stress, variant angina usually occurs during rest or with minimal exercise and frequently occurs noc- turnally (between midnight and 8 am ). Rhythm disturbances often occur when the pain is severe, and most persons are aware of their presence dur- ing an attack. Electrocardiographic changes are transient and include ST-segment elevation or depression, T-wave peaking, and inversion of U waves. Persons with variant angina who have serious arrhythmias during spontane- ous episodes of pain are at a higher risk of sudden death. 23 Diagnosis andTreatment The diagnosis of chronic ischemic heart disease is based on a detailed pain history, the presence of risk factors, inva- sive and noninvasive studies, and laboratory studies. It is important to rule out non-coronary causes of chest pain, such as esophageal reflux or musculoskeletal disorders. Noninvasive testing for chronic stable angina includes ECG, echocardiography, exercise stress testing, nuclear imaging studies, computed tomography (CT) scan, and possibly cardiac magnetic resonance imaging (MRI). Because the resting ECG is often normal, exercise testing is important for evaluating persons with angina. Although noninvasive testing is valuable in the diagnosis of chronic

stable angina, cardiac catheterization and coronary arteri- ography are often needed for a definitive diagnosis. 21 The treatment goals for stable angina are directed toward symptom reduction and prevention of myocar- dial infarction through nonpharmacologic strategies, pharmacologic therapy, and coronary interventions. Nonpharmacologic methods are aimed at symptom control and lifestyle modifications to reduce risk factors for coronary disease. They include smoking cessation in persons who smoke, stress reduction, a regular exercise program, limiting dietary intake of foods high in cho- lesterol and saturated fats, weight reduction if obesity is present, and avoidance of cold or other stresses that produce vasoconstriction. Immediate cessation of activ- ity often is sufficient to abort the onset of anginal pain. Sitting down or standing quietly may be preferable to lying down because these positions decrease preload by producing pooling of blood in the lower extremities. Pharmacologic agents used in the treatment of chronic stable angina include nitrates, beta blockers, and calcium channel blockers. 22 Nitrates, both short- and long-acting, are vasodilators used in the treatment of chronic stable angina and in silent myocardial ischemia. Nitrates exert their effect mainly through a decrease in venous return to the heart with a resultant decrease in intraventricu- lar volume. Arterial pressure also decreases. Decreased intraventricular pressure and volume are associated with decreased wall tension and myocardial oxygen require- ment. Although they are not vasodilators, beta blockers are extremely useful in management of angina associated with effort. The benefits of beta blockers are due primar- ily to their hemodynamic effects—decreased heart rate, blood pressure, and myocardial contractility—which decrease myocardial oxygen requirements at rest and dur- ing exercise. The calcium channel–blocking agents, also called calcium antagonists, block activated and inactivated L-type calcium channels in cardiac and smooth muscle. The therapeutic effects of the calcium channel blockers result from coronary and peripheral artery dilation and from decreased myocardial metabolism associated with the decrease in myocardial contractility. Percutaneous coronary intervention relieves symptoms for patients with chronic stable angina, but does not appear to extend the life span. Coronary artery bypass grafting is usually indi- cated in patients with double- or triple-vessel disease. 22

SUMMARY CONCEPTS

■■ Coronary artery disease is a disorder of impaired coronary blood flow, usually caused by atherosclerosis. ■■ The acute coronary syndromes (ACS) include unstable angina/non-ST elevation myocardial infarction (UA/NSTEMI) and ST elevation myocardial infarction (STEMI), which differ in severity based on the absence or presence of electrocardiograph ST segment changes.