There is growing evidence that, in patients with coronary artery disease, the majority of transient ischemic events are not associated with angina pectoris or its equivalents. The mechanism responsible for painless ischemia has not been clearly elucidated; while a generalized decrease in sensitivity to algogenic stimuli or cardiac afferent denervation may play a role in some patients, other and more complex mechanisms modulating the peripheral and central coding and transmission of cardiac pain could be accountable. Differentiation between patients with silent myocardial ischemia and those with predominantly symptomatic disease cannot be reliably achieved on the basis of coronary angiographic findings or the duration and extent of the ischemic periods even though development of symptoms would appear more likely in those with severe and diffuse anatomical lesions. Nevertheless, the problem remains that totally asymptomatic individuals are apparently subject to the risk of sudden cardiac death, and myocardial infarction not substantially different from that of symptomatic patients are exposed. Consequently, with regard to the potential economic and logistic implications, the issue of identification of such persons is not merely of academic relevance and should be investigated diligently. Moreover, as for patients with clear-cut symptoms, therapeutic strategies should be defined individually on the basis of pathophysiological and prognostic considerations.