Abstract
Ramp studies are utilized for speed optimization of continuous flow left ventricular assist devices (CF-LVADs). We here report the utility of combined left and right heart catheterization during a ramp study to ensure a comprehensive understanding of the hemodynamic implications on both ventricles. Pressure-volume loop (PV loop) monitoring uncovered compromised systolic and mildly compromised right ventricular (RV) function with increasing LVAD speeds, despite improvement in left ventricular unloading. These findings informed patient management and highlight the potential utility of PV loop monitoring as an adjunct to left and right heart catheterization during ramp studies of next generation LVADs.
Introduction
Mechanical circulatory support (MCS) has become a cornerstone of heart failure management both as bridge to transplant and destination therapy [1]. In particular, continuous flow left ventricular assist devices (CF-LVADs) with fully magnetically levitated impellers have emerged as next-generation technology endowed with enhanced hemocompatibility [2–4]. To ensure appropriate left ventricular (LV) unloading, initial efforts have established a ramp protocol for speed optimization relying on echocardiography [5] and right heart catheterization (RHC) [6]. RV dysfunction and right-sided heart failure have been reported with CF-LVAD support, in part attributed to interventricular interactions. However, predicting RV response can be complicated due to a multitude of possible interventricular interactions [7]. In addition, the identification of RV dysfunction with LVAD can be challenging with traditional hemodynamic parameters. In this context, RV PV loops provide added benefit in the assessment of RV function in LVAD patients [8]. Our group introduced a catheterization protocol combining both left heart catheterization (LHC) and RHC to provide unique insights into LV unloading and right ventricular (RV) function [9]. We here utilized PV loop monitoring with the RHC/LHC protocol during speed optimization for a patient with a HeartMate 3 (Abbott Laboratories, Inc, Chicago, IL) LVAD in the setting of residual mitral regurgitation (MR).
Case Report
A 68-year-old male with ischemic cardiomyopathy underwent implantation of a HeartMate 3 LVAD as destination therapy two years prior to presentation. His clinical course was complicated by stent thrombosis in the right coronary artery requiring urgent percutaneous coronary intervention early after implantation. The patient presented with intermittent NYHA class III symptoms. Transthoracic echocardiography was notable for moderate RV systolic dysfunction and moderate MR. To evaluate the etiology of his dyspnea, he underwent an LHC/RHC ramp study. Evaluation of the RV was aided by a conductance catheter system for pressure-volume loops utilizing 3D echocardiography for baseline RV volumes. At the baseline speed of 5300 rpm, right atrial pressure was 16 mmHg (Figure 1A), mean pulmonary artery (PA) pressure was 26 mmHg, and pulmonary capillary wedge pressure was 15 mmHg (V-waves to 18 mmHg). LV end-diastolic pressure (EDP) was 14 mmHg and cardiac index (CI) was 2.01 L/min/m2. By both PV-loop analysis and 3D echo, his RV ejection fraction (EF) was 36% (Figure 1B; Figure 2). RV contractility (+dP/dt) was 188 mmHg/s (Figure 1C). The end-systolic pressure-volume relationship (ESPVR) of the RV was 0.16 mmHg/mL (Figure 1D; Figure 2) and arterial elastance (EA) was 0.34 mmHg/mL when estimating V0 as 0 mmHg and 0 mL. Trends in hemodynamics with ramp (5300 to 5800 rpms) revealed progressive unloading of the LV (LVEDP 9 mmHg; Figure 1E) with a decrease in mean PA pressure (23 mmHg) as expected. Additionally, ramp (5300 to 5800 rpms) revealed an adverse trend for ventricular-arterial coupling assessed as the ratio of arterial elastance and end-systolic elastance (Figure 1F). However, there was a clear trend toward worsening of all markers of RV systolic function, including RVEF (−6% [−17% reduction]; Figure 1B), RV ESPVR (−0.035 mmHg/mL [−22%]; Figure 1D), and RV +dP/dt (−38 mmHg/s [−20%]; Figure 1C), despite no increase in RA pressure (Figure 1A) or RVEDP (Figure 2). Due to reduced stroke volume and end-systolic pressure, RV EA increased by 0.033 mmHg/mL (+10%) despite the decrease in PA pressure. As a result, there was no appreciable net increase in CI (+ 0.04 L/min/m2) with increased speed. Consequently, inotropic therapy was advised to support RV function and the LVAD speed was increased to outcompete his mitral regurgitation.
Figure 1.
Impact of increasing LVAD speed on (A) right atrial pressure (B) right ventricular ejection fraction (RVEF) (C) right ventricular contractility (D) right ventricular end-systolic pressure-volume relationship (E) left ventricular end-diastolic pressure (F) Ventricular-arterial coupling estimated as arterial elastance/end-systolic elastance.
Figure 2.
Right ventricular pressure-volume loop with a HeartMate 3 speed of 5300 and 5800 rpm in a patient with mitral regurgitation.
Discussion
The impact of mechanical LV unloading on RV systolic and diastolic functional parameters is complex and still being elucidated, especially in the setting of fully magnetically levitated LVADs. The limited available studies using RHC in ramp protocols for next-generation devices have suggested that a multitude of interventricular interaction-mediated outcomes are possible, including no interactions, systolic-diastolic interactions, and diastolic interactions [7]. We leveraged LHC/RHC to better assess hemodynamic changes across the circulatory circuit during ramp optimization. In this patient, although increasing speed improved LV unloading with a trend towards worse ventricular-arterial coupling, there was an associated compromise in RV systolic performance. Despite decreasing PA pressures (RV afterload), PV loop assessment documented a drop in RV stroke volume and contractility with ramping of LVAD speeds, provided added diagnostic insight, and informed an alternate management strategy. The addition of PV loop monitoring in this context may also provide a unique opportunity in assessing need for mechanical RV support. Subsequently, this approach may be beneficial in guiding titration of RV/LV support and should be further studied.
Conclusion
The hemodynamic findings in the present case illustrate that even in the presence of residual MR, RV systolic function may be jeopardized by increasing LVAD speed. Thereby, this case highlights the need to further study the utility of PV loop monitoring, in tandem with LHC/RHC to assess hemodynamics during speed optimization trials in the setting of fully magnetically levitated LVADs.
Acknowledgments
A.G. was supported by the National Institute of General Medical Sciences (T32GM145408).
There are no conflicts of interest to disclose and no sources of funding.
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