Pathophysiology of myocardial hibernation. Implications for the use of dobutamine echocardiography to identify myocardial viability.

Since the pioneering works of Tennant and Wiggers, it has been known that total ischaemia leads to a prompt cessation of contraction and eventually results in the appearance of cell damage and irreversible myocardial necrosis. Accordingly, in the minds of many cardiologists, the discovery of an abnormal regional contraction in a patient with coronary artery disease had long been equated with the presence of irreversible myocardial necrosis. However, with the advent of recanalisation treatment, evidence progressively accumulated that prolonged regional “ischaemic” dysfunction did not always arise from irreversible tissue damage and, to some extent, could be reversed by the restoration of blood flow. These observations have led to the speculation that chronically jeopardised myocardium, which is often referred to as “hibernating”, could spontaneously downgrade its contractile function and minimise its energy requirements to prevent the appearance of irreversible tissue damage. 4 5 During the past decade, the pathophysiology of the hibernating myocardium has received considerable attention and has fostered the development of several new modalities aimed at predicting the return of left ventricular function after revascularisation. Among these modalities, dobutamine stress echocardiography has recently emerged as a safe, non-invasive, and accurate way of identifying viable myocardium. It is the purpose of this paper to review some of the more recent advances in the understanding of the pathophysiology of chronic myocardial hibernation and the use of dobutamine echocardiography to identify viable myocardium. Emphasis will be placed on regional perfusion–contraction matching in both the experimental and the clinical setting, on the peculiar morphological changes that have been shown to occur in the hibernating myocardium, on the determinants of mechanical reversibility after restoration of adequate coronary patency, and on the presence of recruitable inotropic reserve.