CardiothoracicBiventricular pacing improves left ventricular function by 2-D strain in right ventricular failure
Introduction
Acute right ventricular (RV) failure is a well-recognized problem after acute pulmonary embolism, after cardiac transplantation, during pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension, and during surgical correction of congenital heart disease. Registry data from the International Society of Heart and Lung Transplantation show that, despite advances in perioperative management, RV dysfunction accounts for 50% of all cardiac complications and 19% of all early deaths in patients after heart transplantation [1]. Current therapies for the failing RV are limited to preload optimization, vasopressors and vasodilators to adjust afterload, and inotropic support to improve contractility [2]. Mechanical circulatory assistance is available for end-stage RV failure.
Clinical studies have demonstrated that pathologic increases in pulmonary pressures not only affect the RV, but also worsen left ventricular (LV) synchrony and function and alter function of the interventricular septum. Dohi et al. [3] used speckle-tracking echocardiography (STE) to demonstrate LV regional dyssynchrony with paradoxical motion of the interventricular septum in patients with chronic RV pressure overload (RVPO). Takamura et al. [4] showed that acute pulmonary embolism reduces LV strain in patients. They concluded that coordination of radial LV wall motion plays a key role in the short-term regulation of cardiac output (CO) in patients with acute pulmonary embolism.
These observations suggest that resynchronization therapy based on biventricular pacing (BiVP) might be of value in RVPO. However, there is little experience with cardiac pacing in acute RV failure [5]. Preliminary studies report improved hemodynamics with temporary atrial-RV pacing in patients with RV dysfunction and after surgery for congenital heart defects [6], [7]. Our laboratory demonstrated in a pig model of critical pulmonary stenosis that sequential BiVP with RV pre-excitation can improve CO by more than 20% [8]. Potential mechanisms include increased RV contractility, improved RV and LV synchrony [9], and enhanced LV geometry and fractional shortening [10]. We have not, however, explored the effects of pacing on LV synchrony and radial strain.
STE is a novel strain imaging technique that quantifies regional LV deformation and synchrony [11]. Radial strain has been useful in assessing the response to BiVP and has been recognized as an accurate and noninvasive measure of cardiac function and mechanical synchrony [12], [13]. In the current study, we apply STE to define the effects of BiVP in a RVPO model, seeking mechanisms that may be of value in clinical studies.
Section snippets
Experimental protocol
All animal studies were performed according to the National Institutes of Health Guide for the Care and Use of Laboratory Animals. The experimental protocol was approved by the Columbia University Institutional Animal Care and Use Committee. Five male pigs (40–50 kg) were anesthetized intramuscularly with atropine (0.02 mg/kg), ketamine (20 mg/kg), and xylazine (0.5 mg/kg) and subjected to oral endotracheal intubation. They were mechanically ventilated with a rate- and volume-regulated
Results
RVPO approximately doubled average RV peak systolic pressures from baseline, with a tendency toward septal wall flattening. Table 1 presents optimum AVDs and VVDs during RVPO. Optimum AVD ranged from 120 to 180 ms. Optimum VVD was +40 to +80 ms. CO increased by 8.6% with BiVP compared to LVP (0.96 ± 0.26 L/min versus 0.89 ± 0.27 L/min; P = 0.05 by ANOVA). CO during RVP (0.93 ± 0.27 L/min) was higher than LVP but lower than BiVP, a difference that was not statistically significant. Table 2
Discussion
Our results demonstrate that pre-excitation of the “failing” RV benefits the “nonfailing” LV through improved LV intraventricular synchrony and increased free wall radial strain. These findings enhance our understanding of optimal pacemaker programming during acute RV failure due to RVPO.
A 106-msec delay between anterior septal and posterior wall contraction during LVP demonstrates that inappropriate myocardial activation can cause dyssynchronous contraction. Dyssynchronous contraction wastes
Conclusion
Both BiVP (RV-first pacing) and RVP restore intraventricular synchrony and increase regional LV function compared to LVP during acute RVPO. RV pre-excitation unloads the RV, reducing the duration of anterior septal wall contraction and homogenizing LV wall timings. Functional benefit is found primarily in the opposing LV free wall. STE is able to assess regional timing and function during RVPO, defining acute responses to BiVP. The present data could support future clinical trials of BiVP or
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Cited by (2)
Resynchronization therapy for right ventricular failure: Restoring harmony in left ventricular contractility
2013, Journal of Surgical ResearchEffects of biventricular pacing on left heart twist and strain in a porcine model of right heart failure
2013, Journal of Surgical ResearchCitation Excerpt :During both AVD and VVD variations, free wall RS significantly correlated with increases in CO. This supports our previous study analyzing the effects of BiVP during RVPO [16] and acute LV volume overload [12] that found greater RS changes in the free wall than in the septum. Our findings are in contrast, however, with other studies that found that CRT improved septal RS and decreased lateral RS [29,30].