Clinical aspects of silent myocardial ischemia in patients with angina and other forms of coronary heart disease

Abstract

Silent myocardial ischemia is defined as objective evidence of myocardial ischemia occurring in the absence of symptoms in a patient who has either coronary artery disease or spasm. The largest number of patients with silent myocardial ischemia identified to date are those with effort angina, in whom silent episodes are at least three to four times as frequent as painful episodes. Since episodes of silent myocardial ischemia are not alarming to the patient and are likely to escape detection, their clinical importance must reside in their association with morbid events of ischemic heart disease. In fact, silent myocardial ischemia can result in silent myocardial infarction, sudden death, or other events. The detection of these episodes has the potential to provide clinicians with a more complete understanding of all the ischemic processes occurring in patients with angina or other forms of coronary disease. Silent myocardial ischemia can be detected by a variety of methods. Transient ischemic-type electrocardiographic abnormalities that occur without symptoms and that have been recorded during exercise testing or by means of ambulatory, coronary care unit, or telemetry monitoring may be used to document silent myocardial ischemia. Reversible left ventricular wall motion abnormalities without symptoms, observed at rest or during exercise radionuclide angiography, 2-D echocardiography, or contrast angiography, may also be used to document silent myocardial ischemia. However, only ambulatory electrocardiographic monitoring provides long-term evaluation that documents repeated episodes of silent myocardial ischemia outside of the laboratory. Controlled studies, directed specifically at preventing silent myocardial ischemia and/or its consequences in patients with angina, are limited. It has been determined, however, that both hourly administration of sublingual nitroglycerin and intravenous administration of isosorbide dinitrate are effective. Other studies examining the effects of beta blockers (propranolol, atenolol, and labetalol) in the treatment of angina have shown that their use also results in a reduced frequency of silent episodes, but that a large number of episodes persist. It has been observed that verapamil alone and nifedipine, either alone or in combination with a beta blocker, appear to significantly decrease silent myocardial ischemia in patients with angina. A major limitation of these studies is that treatment was not specifically titrated to reduce or eliminate silent myocardial ischemia. Recent studies from our laboratory suggest that if the dosing is modified, calcium channel blockers, as well as beta blockers, are effective in preventing silent myocardial ischemia in patients with angina. We also have found that percutaneous transluminal coronary angioplasty and coronary artery bypass grafting appear to be effective treatment for this condition. Thus, it can be seen that silent myocardial ischemia is a major problem for both patients and clinicians. Nevertheless, results using currently available methods, although limited, suggest that the problem can be detected and successfully managed in certain patient groups, particularly in those patients with angina pectoris.