Assessment of viability

Abstract

Ischaemic left ventricular (LV) dysfunction due to coronary artery disease (CAD) is steadily increasing as a consequence of the ageing of the population and of improved survival of patients with acute coronary syndromes and currently represents the first cause of heart failure (HF). Myocardial function is dependent on blood supply, as anaerobic reserve is minimum due to a nearly maximal arteriovenous oxygen extraction. At rest, myocardial blood flow remains normal even in the presence of severe coronary artery stenosis (up to 85% diameter stenosis) by coronary autoregulation. In the presence of transstenotic pressure gradient due to epicardial coronary stenosis, arteriolar dilatation maintains normal myocardial flow at rest but with a progressive reduction in flow reserve. When arteriolar dilatation is maximal, autoregulation is exhausted and myocardial ischaemia develops. The limit of autoregulation depends on myocardial oxygen demand and is influenced by heart rate. Tachycardia increases oxygen demand and supply is reduced because of a decreased diastolic perfusion time. In the presence of acute ischaemia, there is a close relation between subendocardial perfusion and transmural function. Indeed, the contribution of subendocardium to myocardial thickening largely exceeds the contribution of the subepicardium. Akinesia can therefore result from subendocardial ischaemia and transmural ischaemia is not necessary. This chapter looks at how viability of the different techniques for treating myocardial dysfunction is assessed.