Is Right Ventricular Outflow Tract Pacing Superior to Right Ventricular Apex Pacing in Patients with Normal Cardiac Function?

Abstract

Background: Whether right ventricular outflow tract (RVOT) pacing is superior to right ventricular apex (RVA) pacing in terms of ventricular synchrony, cardiac function, and remodeling in patients with normal cardiac function is still unknown. Hypothesis: Right ventricular outflow tract pacing is superior to RVA pacing in patients with normal cardiac function. Methods: A total of 96 consecutive patients with high or third-degree atrial ventricular block were enrolled and randomized into 2 groups: RVOT pacing group (n = 48) and RVA pacing group (n = 48). Tissue Doppler imaging (TDI) and 2D echocardiography were performed to study left ventricular (LV) systolic and diastolic synchrony, LV volumes, and function. Results: There were no significant differences in baseline characteristics between the 2 groups. Left ventricular systolic asynchrony is more severe in the RVA pacing group than in the RVOT pacing group (P < 0.05), while diastolic synchrony is not significantly (NS) different between the 2 groups after pacing. There were no significant differences with respect to the mean myocardial systolic (Sm) and early diastolic velocities (Em), LV ejection fraction, LV end-diastolic and systolic volume in the 2 groups at 12 months of follow-up (all NS). Conclusions: Although RVOT pacing caused more synchronous LV contraction compared with RVA pacing, it had no benefit over RVA pacing in aspect of preventing cardiac remodeling and preserving LV systolic function after 12 months of pacing in patients with normal cardiac function.

Permanent Cardiac Pacing in Adults with High Grade Atriovetricular Block and Preserved Left Ventricular Function: Optimal Mode and Site of Pacing

“…Previous investigations of alternative pacing sites have yielded inconsistent results (Mera et al, 1999;Giudici et al, 1997;Bourke et al, 2002;Victor et al, 2006;Kypta et al, 2008;Dabrowska-Kugacka et al, 2009;Tse et al Europace 2009;Victor et al, 1999) which may be attributable, in part, to the fact that the pacing site was determined on a topological rather than functional basis (Giudici & Karpawich, 1999). Many previous studies (Schwaab et al, 1999;Victor et al, 2006;Yu et al, 2007;Ng et al, 2009;Takemoto et al, 2009;Tse et al, Europace 2009, Gong et al, 2009Leong et al, 2010;Schwaab et al, 2001), have showed that septal pacing induced shorter paced QRS duration than RVA pacing did. These results indicated that RVS pacing resulted in better electric synchrony compared with RVA pacing.…”

“…The RV septal pacing also resulted in shorter isovolumic relaxation than RV apical pacing (Yu et al, 2007), implicating better diastolic function that has been invasively demonstrated by Kolettis et al (Kolettis et al, 2000) at the cardiac catheterization laboratory. In fact despite the beneficial features of reducing electrical and mechanical dyssynchrony , different studies failed to demonstrate a positive effect on indices of LV structure and 85 function and did not confirm the above mentioned clinical outcomes, at least during the 3-18 months after implantation (Bourke et al, 2002;Victor et al, 2006;Kypta et al, 2008;Dabrowska-Kugacka et al, 2009;Gong et al, 2009;Cano et al, 2010) Kypta et al (Kypta et al, 2008) randomized 98 patients with atrioventricular block (AVblock) undergoing pacemaker implantation to positioning the ventricular lead in the high or mid septum (n =53) or in the apex (n = 45) of the right ventricle. The Changes of N-terminal pro-brain natriuetic peptide (BNP) levels, LVEF, and exercise capacity from baseline to 18 months were statistically not different between septal and apical stimulation.…”

“…Right Ventricular Apical permanent pacing could have negative hemodynamic effects. Initially, attention was directed to RV outflow tract/septum pacing and His/para-Hisian pacing in patients with LV dysfunction ( Mera et al, 1999;Schwaab et al, 1999;Buckingham et al, 1997;Buckingham et al, 1998;de Cock et al, 1998) and latter in preserved LV function patients (Giudici et al, 1997;Karpawich & Mital, 1997;Kolettis et al, 2000;Bourke et al, 2002;Tse et al, 2002;Occhetta et al, 2006;Victor et al, 2006;Yu et al, 2007;Kypta et al, 2008;Flevari et al, 2009;Ng et al, 2009;Dabrowska-Kugacka et al, 2009;Takemoto et al, 2009;Gong et al, 2009;Rosso et al, 2010;Verma et al , 2010;106:806-9;Leong et al, 2010;Cano et al,. 2010;Yoshikawa et al, 2010) while subsequently biventricular stimulation began to emerge as an appealing alternative proposal (Yu et al, 2009;Simantirakis et al, 2009;Doshi et al, 2005).…”

“…A pacing site that is in closer proximity with the proximal portion of His bundle at the RV septum should lead to a narrower QRS which in turn might reflect a lesser degree of activation delay compared with RVA pacing (Mera et al, 199;Schwaab et al, 1999;Tse et al, 2002) and less dyssynchrony, as demonstrated by multiple echocardiographic techniques (Tse et, 2002;Flevari et al, 2009;Takemoto et al, 2009;Gong et al, 2009;Leong et al, 2010;Cano et al, 2010). Pacing on the right ventricular (RV) septum, at high (septal RVOT pacing) (Giudici et al, 1997;Kolettis et al, 2000;Bourke et al, 2002;Tse et al, 2002;Dabrowska-Kugacka et al, 2009;Gong et al, 2009;Leong et al, 2010;Yoshikawa et al, 2010), mid (Yu et al, 2007;Cano et al, 2010;Muto et al, 2007) or lower (Flevari et al, 2009) septal pacing position has been introduced as a potentially favorable alternative to RVA pacing to preserve a more physiologic ventricular activation. Previous investigations of alternative pacing sites have yielded inconsistent results (Mera et al, 1999;Giudici et al, 1997;Bourke et al, 2002;Victor et al, 2006;Kypta et al, 2008;Dabrowska-Kugacka et al, 2009;Tse et al Europace 2009;Victor et al, 1999) which may be attributable, in part, to the fact that the pacing site was determined on a topological rather than functional basis (Giudici & Karpawich, 1999).…”

“…Authors measured dyssynchrony by different indices (Flevari et al, 2009;Takemoto et al, 2009;Gong et al, 2009;Leong et al, 2010;Yoshikawa et al, 2010) and available parameters quantifying intraventricular dyssynchrony could not contain all information of dyssynchrony. A positive and statistically significant correlation was found between the paced QRS duration and global dyssynchrony (Victor et al, 2006;Flevari et al 2009;Takemoto et al, 2009;Muto et al, 2007).…”