Ischaemic heart disease (IHD) is the largest single cause of death and the most frequent cause of heart failure in Australia and the western world. There have been relatively recent advances in the management of IHD in the acute setting with thrombolysis, anti-platelet therapy and primary angioplasty, and in the chronic setting with surgical and percutaneous revascularisation procedures. Despite these advances many patients remain debilitated either because of failed, inadequate or delayed mechanical or pharmacological reperfusion therapy in the acute setting, or because of unsuitable coronary anatomy or co morbidities that may preclude revascularisation for chronic coronary artery disease (CAD).
After an acute myocardial infarction (AMI), necrotic, normal and viable myocardium may occur together in the infarct zone, the proportions of which will vary according to a number of factors including the duration of coronary occlusion, the extent of collateral blood supply and the occurrence of pre-infarct ischaemia (preconditioning).
Viable myocardium is that which will improve its function after restoration of blood supply. The benefits of restoration of blood supply to viable myocardium result in improvement in regional myocardial function and may confer a survival advantage. Much effort has been expended on developing clinical tests (such as dobutamine echocardiography, nuclear medicine tests and positron emission tomography) that can be used to identify viable myocardium. Although the aim of these viability tests is to predict which tissue will improve functionally with revascularisation, the surrogates used in this prediction differ, and it is not surprising therefore that the sensitivity and specificity of viability tests differ. For the purpose of the present studies, dobutamine echocardiography (DbE) was used to identify viable myocardium.
Whether restoration of blood supply to viable tissue confers more benefit than improvement in regional function and a possible survival advantage is not known. Furthermore, little is known about the medical treatment of viable myocardium, and whether this tissue that is metabolically active may benefit from drug therapy. In the first study presented, we investigated the effect of revascularisation of viable myocardium on left ventricular (LV) remodelling. Seventy patients with CAD and LV dysfunction were studied, 31 of whom were revascularised. Standard DbE was performed and LV volumes and ejection fraction (EF) were measured by three-dimensional echocardiography at baseline and again after an average of 40 weeks. Revascularised patients had significant improvements in end systolic volume (ESV) and EF's compared to those treated medically. However, there was no relationship between the amount of viable myocardium and remodelling in either revascularised or medically treated groups.
In the second study presented, we sought to assess whether an infusion of glucose insulin and potassium (GIK), would have a functional benefit in patients with chronic ischaemic LV dysfunction. Dobutamine echocardiography was performed on thirty patients with chronic ischaemic LV dysfunction; these patients were then recalled for a 4-hour infusion of GIK. The effect of GIK on regional function was compared to that of dobutamine, myocardial velocities and tissue displacement were measured in each segment at rest and after dobutamine and GIK, left ventricular volumes and EF's were measured using three-dimensional reconstructions of the left ventricle.
Wall motion score index improved with dobutamine (1.8±0.4 to 1.6±0.4, p<0.001) and GIK (1.8±0.4 to 1.7±0.4, p<0.001), and the increment in wallmotion score index (WMSI) was similar with DbE and GIK. Myocardial tissue velocity increased significantly with dobutamine (2.5±1.8 to 3.2±2.2 cm/s, p<0.01), and GIK, (3.0±1.6 to 3.5±1.7 cm/s, p<0.001) in normal, viable and scarred segments. Furthermore GIK resulted in a significant improvement in ESV, which was confined to patients with viable myocardium. GIK had no significant effect on pulse rate, mean arterial pressure, and serum nor-adrenaline and lactate levels. Serum adrenalin did increase significantly with GIK but this was not above basal resting levels. When compared to dobutamine; GIK had a sensitivity of 55% and specificity of 95% for identifying segments that were classified as viable by DbE.
While previous studies have focused on the relationship between viability and functional outcome after revascularisation, this work shows that revascularisation is not mandatory for recovery of function, and that recovery is not limited to recovery or improvement of resting wall motion abnormalities.