Backgrounds:
Despite the latest progresses of early reperfusion, myocardial infarction (MI) remains a leading cause of chronic heart failure (CHF). Left ventricular (LV) assist device (VAD) mechanically unloads LV, thus myocardial oxygen consumption (MVO2). Theoretical analysis indicates that the partial VAD (p-VAD) where LV remains ejecting decreases preload (EDV) while increases afterload (ESV), thereby marginally decreases MVO2. In contrast, total LVAD (t-VAD) where LV no longer ejects, markedly decreases ESV as well as EDV, thus markedly reduces MVO2. We examined whether t-VAD in ischemia reperfusion (IR) could reduce the infarct size and prevent heart failure in the long term.
Methods:
First, in normal dogs, we examined the impact of p-VAD and t-VAD on MVO2 by Fick principle (coronary flow and arterial venous O2 difference). Second, we occluded the left anterior descending coronary artery for 3 hours and reperfused. We started transvascular LVAD (Impella®) from 1 hour after ischemia to 1 hour after reperfusion. We compared cardiac function, infarct size and hormones 1 month after ischemia among 3 groups, control group (IR, n=8), p-VAD (n=6), and t-VAD (n=6).
Results:
t-VAD markedly decreased MVO2 (p<0.05, Figure 1). 1 month after ischemia, t-VAD normalized LV end-systolic elastance (IR: 6.5±3.2, p-VAD: 9.7±1.3, t-VAD: 12.8±5.1 mmHg/ml, p<0.05) and reduced LV end-diastolic pressure (16.5±2.7, 6.4±2.9, 4.4±1.5 mmHg, p<0.05), and NT proBNP (3391±1364, 2084±348, 1632±228 pg/ml, p<0.05) indicating the successful prevention of heart failure. t-VAD markedly reduced the infarct size by more than 80% relative to IR (p<0.05, Figure 2) despite the fact that it started 1 hour after the onset of ischemia.
Conclusions:
Transvascular total left ventricular unloading for acute myocardial infarction strikingly reduces the MI size and prevents heart failure in the chronic phase. It might serve as a new therapeutic strategy in the management of patients with acute MI.