Right Ventricular Septal Pacing Preserves Long-Term Left Ventricular Function Via Minimizing Pacing-Induced Left Ventricular Dyssynchrony in Patients With Normal Baseline QRS Duration

Abstract

ecent clinical studies have demonstrated that longterm right ventricular apical (RVA) pacing imposes a risk of heart failure, ventricular arrhythmias, and cardiac death. 1-5 RVA pacing causes left ventricular (LV) mechanical dyssynchrony because of altered ventricular excitation that bypasses the His-Purkinje system. 6-9 Longterm RVA pacing results in LV dilatation associated with asymmetric LV hypertrophy, 10,11 regional myocardial perfusion defects 12-14 and a decrease in the LV ejection fraction (LVEF). 12,15,16 Pacing on the right ventricular (RV) septum, RV outflow tract and His or para-His bundle has been introduced as a potentially favorable alternative to RVA pacing to preserve a more physiologic ventricular activation. 8 However, previous investigations of alternative pacing sites have yielded inconsistent results, 17-23 which may be attributable, in part, to the fact that the pacing site was determined on a topological rather than functional basis. 24 Indeed, acute hemodynamic studies have demonstrated that individual optimization of the RV pacing sites could preserve LV performance in patients without LV dysfunction, and that there are substantial individual variations in the optimal pacing sites. 25,26 The paced QRS duration seems to be a practical indicator for determining the optimal RV pacing site. 14,19,22,23 However, information on the most appropriate pacing site to preserve long-term LV function is still limited.To address this issue, we investigated the effect of RV septal (RVS) pacing guided by QRS morphology on longterm LV mechanical synchronicity and function in patients with normal QRS duration and preserved LV function at baseline. Methods PatientsWe retrospectively studied 55 patients (22 men, 32 women; 70±10 years) undergoing dual-chamber pacemaker implantation for advanced atrioventricular block (AVB; n=33) or sinus node dysfunction (SND, n=22). In 40 patients (n=24 for AVB, n=16 for SND), pace mapping was carried out at the junction between the upper and middle segments of the RV septum using a hand-shaped stylet under fluoroscopy

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

“…Moreover, patients in the RVAP group had significantly more inter and intraventricular dyssynchrony than did the controls, and patients in the RVSP group had comparable values to those obtained from the control group (Flevari et al, 2009;Verma et al, 2010;Cano et al, 2010). In contrast; Takemoto et al (Takemoto et al, 2009) have revealed that, RVS pacing caused a significant increase in the interventricular mechanical delay (IVMD) compared with AAI pacing, which indicates that the onset of the LV activation is delayed even during RVS pacing. These authors explained that, such an increase in interventricular dyssynchrony may be a result of the initial impulse propagation through a slow muscular conduction region.…”

“…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.…”

“…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).…”

“…The ideal ventricular pacing site should resemble the normal activation and synchronicity of ventricular activation observed with an undamaged conduction system. 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.…”

“…In the remaining patients, there was no difference in QRS duration. Many recent studies have compared the mechanic synchrony between septal pacing and RVA pacing (Schwaab et al, 1999;Yu et al, 2007;Flevari et al, 2009;Ng et al, 2009;Takemoto et al, 2009;Leong et al, 2010;Cano et al, 2010;Yoshikawa et al, 2010) and have showed a more inter and intraventricular synchrony with septal pacing than apical pacing immediately after implantation and at midterm (after 6 to 12 months of follow-up), excepted for the study of Ng et al (Ng et al, 2009). Moreover, patients in the RVAP group had significantly more inter and intraventricular dyssynchrony than did the controls, and patients in the RVSP group had comparable values to those obtained from the control group (Flevari et al, 2009;Verma et al, 2010;Cano et al, 2010).…”