Dr Sakata was awarded the Best in Research Award by the A-CURE Faculty as the author of the highest-scoring abstract from all abstract submissions.
At the 6th Annual A-CURE Symposium, Dr Sakata showed preclinical evidence that mechanical left ventricular (LV) unloading increases coronary perfusion of the infarct area.1 Study data suggested that mechanical LV unloading is more beneficial in post-MI patients with high diastolic pressure associated with increased LV stiffness and in those with worse cardiac contractility.1 However, there are other factors that are thought to increase coronary flow with LV unloading, including low cardiac output, low dP/dtmax, high left atrial pressure, high pulmonary capillary wedge pressure and high LV end-diastolic pressure. The exact mechanism by which LV unloading influences coronary flow remains to be determined.
It is within this context that Dr Sakata set out the hypothesis of his study that aimed to investigate how mechanical LV unloading increases coronary flow by modifying LV diastole. MI was induced in five Yorkshire pigs by mid-left anterior descending (LAD) coronary artery occlusion for 90 minutes followed by reperfusion for 60 minutes before the Impella CP was initiated to perform mechanical LV unloading. The pigs were catheterised to enable coronary pressure and flow monitoring. Coupled LV pressure and coronary flow–pressure data gated by the ECG were collected from each animal.
Dr Sakata presented the study results: diastolic LV pressure was lower and the proportion of the diastolic phase was extended in the unloaded compared with control group; coronary pressure fluctuated less and was consistently higher throughout the cardiac cycle with unloading; and coronary flow was higher throughout diastole in the unloaded group. Although the correlation was not significant, coronary flow tended to increase with lower LV end-diastolic pressure.
Dr Sakata used wave intensity analysis to quantify the forces that create individual pressure and velocity waves within the coronary artery circulation to determine the contributors to these observed changes. Dr Sakata set out the four types of forces as forward and backward pushing waves, and forward and backward suction waves. The pushing wave is the dominant forward-travelling pushing wave and is created in the proximal aortic root by LV ejection; the backward-travelling pushing wave is created in the distal side by compression of the myocardial vasculature. The backward-travelling suction wave is caused by relief of myocardial microcirculatory compression.2
Dr Sakata explained that, in simple terms, the total wave intensity is the sum of backward and forward wave intensities, which can also be calculated by changes in pressure and flow. In his study, Dr Sakata focused on the backward suction wave and the backward pushing wave because these waves are the beginning and end of the coronary wave form.2 The results of Dr Sakata’s study demonstrate that the magnitude of the forward wave intensity was lower with LV unloading due to less variation in coronary pressure created by continuous pump flow in the aortic root. In addition, the results show that the duration between the backward suction wave and the backward pushing wave was extended with LV unloading, with the effect of prolonging the duration of the relaxation–contraction period.
Dr Sakata summarised the mechanism of increased coronary flow speculated from his study as follows: the implementation of the Impella CP affects coronary haemodynamics by pump suction and pump flow effects. Suction in the LV works as LV unloading lowers diastolic LV pressure, and the continuous pump flow creates a constant and high coronary pressure. Together, these two phenomena modify myocardial relaxation and contraction, leading to a prolonged diastolic phase. The resulting extended diastolic phase increases coronary flow during diastole. Dr Sakata recognised that further studies are needed to verify these mechanisms.
Dr Sakata concluded that mechanical LV unloading decreased LV pressure and extended the diastolic period, leading to increased coronary flow throughout diastole in the infarcted heart.