Silent myocardial ischemia

Abstract

Silent ischemia is an intriguing phenomenon, and the idea that silent ischemia is causally related to serious or fatal cardiac events is certainly biologically plausible given the striking parallels in the circadian patterns of myocardial ischemia, MI and sudden death, and their reduction by β blockade. Histopathological studies also give credence to the idea that recurrent ischemia may cause irreversible myocardial changes related to the development of scarred or fibrotic myocardium, which would act as an ideal substrate for the development of life-threatening arrhythmias, or lead to the development of congestive cardiac failure. But patient-based studies supporting the development of heart failure or arrhythmic disturbance related to the detection of ischemia are lacking. There is a wealth of data, however, regarding the association, or lack thereof, with other cardiac outcomes. Although silent ischemia (either on ambulatory monitoring or exercise testing) in the general population is associated with a higher relative risk of hard cardiac events, poor sensitivity and specificity make these tests poor screening tools. Ambulatory ECG monitoring in particular has never made its way into mainstream practice in this capacity. In stable angina or in the stable convalescent period after MI, silent ischemia detected on ambulatory monitoring, although of prognostic value in highly select populations and mostly with a positive exercise test, does not add to information from clinical assessment and exercise testing regarding the likelihood of death or infarction. Ischemia on exercise ECG or during other stress testing techniques does predict the likelihood of future hard cardiovascular events. This is greatly influenced by functional capacity and the threshold at which the ischemia develops, but far less so by the concurrent occurrence of pain during the test. The situation is different for acute coronary syndromes, including ST elevation MI, in which ongoing transient ischemia, irrespective of whether or not it is silent, is associated with an increased risk of infarction and death. The increase in risk is proportional to the duration of ischemia. Furthermore, transient ischemia may identify patients with the most to gain from treatment with antithrombotic therapy, making continuous ECG monitoring an extremely useful tool in this clinical scenario. The study of silent ischemia has illuminated our understanding of many of the pathophysiological processes underlying the natural history of coronary disease and enhanced our knowledge and practice of cardiology. Over the years it has become apparent that the detection of ischemia, whether silent or symptomatic, may be of considerable diagnostic and prognostic importance when the clinical population to be studied is clearly defined (Figure 5). Furthermore, careful selection not only of the population for study but also of the techniques for its detection are necessary for the search for silent ischemia to achieve its maximal clinical utility.