Combining total support pLVAD with intravenous vagal nerve stimulation significantly reduced myocardial oxygen consumption compared to pLVAD alone (42.6 vs 65.3 ml/min/100g, p<0.01).
Does combining intravenous vagal nerve stimulation with a percutaneous left ventricular assist device reduce myocardial oxygen consumption and left ventricular work in a healthy canine model?
The addition of intravenous vagal nerve stimulation to total pLVAD support significantly enhances left ventricular unloading and reduces myocardial oxygen consumption in a healthy canine model.
Absolute Event Rate: 42.6% vs 65.3%
p-value: p=<0.01
Abstract Background Percutaneous left ventricular assist devices (pLVADs) reduce left ventricular (LV) workload and myocardial oxygen consumption (MVO₂) in a flow-dependent manner. We previously demonstrated that total pLVAD support, where LV ejection ceases, decreased MVO₂ by 56% compared to no LVAD support and limited infarct size in a canine ischemia-reperfusion model. Given that MVO₂ is linearly correlated with the product of LV workload and heart rate (HR), we hypothesized that inducing bradycardia during total pLVAD support would further reduce MVO₂. While various drugs can induce bradycardia, sustained HR reduction can sometimes lead to problematic hemodynamics, particularly in acute heart failure. Therefore, we developed an intravenous vagal nerve stimulation (iVNS) catheter capable of rapidly reducing HR by stimulating the right vagal nerve at the superior vena cava level. Purpose This study aimed to evaluate the impact of combining total support pLVAD with iVNS on hemodynamics, LV work, and MVO₂. Methods Under general anesthesia, healthy beagle dogs (n=3) underwent biventricular volume measurement using ultrasonic sonomicrometry, combined with biventricular pressure measurement to obtain pressure-volume (PV) loops. A pLVAD and an iVNS catheter were inserted as shown in Figure 1A. The pLVAD was adjusted to the total support condition. PV loops were recorded under three conditions: before pLVAD insertion, pLVAD alone, and pLVAD with iVNS (inducing 10% reduction in HR). Furthermore, in healthy beagle dogs (n=8), we measured hemodynamic parameters and LV MVO₂ (calculated from arterial and coronary sinus oxygen saturation, hemoglobin levels, and left coronary artery blood flow) at each condition. Results Figure 1B demonstrates the representative bi-ventricular PV loops under three conditions. The pLVAD support initially reduced the LV-PV area, and the addition of iVNS shifted it left-downward further. The pLVAD caused a rightward shift in the right ventricular PV loop, while iVNS had no notable effect on it. This trend was consistent across all three dogs. As shown in Figure 2, combining iVNS with pLVAD significantly reduced HR and MVO₂ (65.3±31.9 vs. 42.6±23.2 ml/min/100g of LV mass, p0.01) without affecting mean arterial pressure. Consistent with PV loop analysis, iVNS further lowered LV systolic pressure and left atrial pressure. These results suggest that iVNS enhanced the LV unloading effect of total pLVAD support, as evidenced by a significant reduction in HR and MVO₂ per beat (0.53±0.22 vs. 0.41±0.22 ml/min/100g/beat, p=0.039). Conclusion Combining total support pLVAD and iVNS successfully achieved powerful LV unloading and over 30% greater MVO₂ reduction than total pLVAD, without adversely affecting hemodynamics. This combined approach, enabling both hemodynamic fine-tuning and maximal MVO₂ reduction, has the potential to serve as a lifesaving tool for acute conditions such as myocardial infarction and acute heart failure.
Hiraki et al. (Sat,) conducted a other in Healthy (n=11). Intravenous vagal nerve stimulation (iVNS) combined with total support pLVAD vs. Total support pLVAD alone was evaluated on Myocardial oxygen consumption (MVO2) (p=<0.01). Combining total support pLVAD with intravenous vagal nerve stimulation significantly reduced myocardial oxygen consumption compared to pLVAD alone (42.6 vs 65.3 ml/min/100g, p<0.01).