The basic aspect of cell behaviour that is the clue for viability recognition by stress echo is regional function. By definition, the function is depressed both in viable and in necrotic segments. However, only viable segments retain a contractile reserve; which can be evoked by an inotropic challenge, either cathecolaminic or flow-mediated, as consistently shown by several experimental studies. This is the basis of viability recognition by pharmacological stress echocardiography. Both dobutamine and dipyridamole exploit the same pathophysiological principle: viable tissue has a residual contractile reserve, which can be elicited by an appropriate inotropic stimulus. With dobutamine, the stimulus is a beta-receptor mediated effect on myocardial cell, which is later matched by an increase in flow. With dipyridamole, the primary stimulus is an adenosine A2-receptor mediated effect on the coronary arteriole smooth muscle cell, leading to an increase in flow. At that point, the increase in function is to be expected on the basis of the known relationship between myocardial contractility and coronary perfusion. From the technical point of view, the "viability window" is dose-related with dobutamine, and time-related with dipyridamole--where the same dose is associated to an early inotropic phase followed by a later ischemic response. In spite of the different pathophysiological background and technical modalities, dobutamine and and dipyridamole have shown a similar sensitivity and specificity for prediction of viability, with an overall accuracy only marginally lower than resting thallium. The practical, clinical impact of these observations is still blunted by relatively small numbers of observations in highly selected populations including a limited number of patients and studies in very few centers.(ABSTRACT TRUNCATED AT 250 WORDS)