J Interv Card Electrophysiol DOI 10.1007/s10840-014-9917-8
Phrenic nerve stimulation in cardiac resynchronization therapy Ghassan Moubarak & Abdeslam Bouzeman & Jacky Ollitrault & Frederic Anselme & Serge Cazeau
Received: 9 February 2014 / Accepted: 7 May 2014 # Springer Science+Business Media New York 2014
Abstract In cardiac resynchronization therapy (CRT), the electrical impulse delivered by the left ventricular (LV) lead may incidentally cause phrenic nerve stimulation (PNS). The purpose of this state-of-the-art review is to describe the frequency, risk factors, and clinical consequences of PNS and to present the most recent options to successfully manage PNS. PNS occurs in 2 to 37 % of implanted patients and is not always detected in the supine position during implantation. Lateral and posterior veins are at higher risk of PNS than anterior veins, and apical positions are at higher risk of PNS than basal positions. The management of PNS discovered during implantation may include mapping the course of the target vein in order to find a PNS-free site, targeting another vein if available, and pacing with alternative configurations before changing the lead location. Non-invasive options for management of post-operative PNS depend on the difference between PNS and LV stimulation thresholds and include reducing the LV pacing output, automatic determination of LV stimulation threshold and minimal output delivery by the device, increasing the pulse duration, and electronic repositioning. New quadripolar leads allow to pace from different cathodes, and the multiple pacing configurations available have proved superior to bipolar leads in mitigating PNS. This electronic repositioning addresses almost all of the clinically relevant PNS and should markedly reduce the need for invasive lead repositioning or CRT abandon, which is actually the last option for 2 % of patients. G. Moubarak (*) : A. Bouzeman : J. Ollitrault : S. Cazeau Department of Pacing and Interventional Electrophysiology, Groupe Hospitalier Paris Saint-Joseph, 185, rue Raymond Losserand, 75014 Paris, France e-mail: [email protected] F. Anselme Department of Cardiology, Rouen University Hospital, Rouen, France
Keywords Cardiac resynchronization therapy . Phrenic nerve stimulation . Electronic repositioning . Quadripolar lead
1 Introduction Cardiac resynchronization therapy (CRT) is effective in diminishing mortality and morbidity in heart failure patients with reduced ejection fraction and wide QRS [1, 2]. Left ventricular stimulation (LVS) is delivered epicardially by placing a lead in a coronary sinus tributary, and the quality of resynchronization is dependent, among other factors, on the anatomical site of stimulation. The electrical impulse may incidentally capture the left phrenic nerve (PN) causing ipsilateral hemidiaphragmatic contractions. The purposes of this review are to describe the frequency, risk factors, and clinical consequences of phrenic nerve stimulation (PNS) and to present the most recent options to successfully manage PNS.
2 Anatomy of the left phrenic nerve and its relationship with LV lead The left PN originates from the cervical plexus and terminates at the diaphragm behind the apex of the left ventricle (LV). In an examination of 22 human cadavers, the left PN descended on the fibrous pericardium along one of three courses [3]: over the anterior surface of the left ventricle (18 %), over the lateral margin of the left ventricle (59 %), and in a posteroinferior direction (23 %). In another examination of nine hearts, the course was lateral in seven and anterior in two [4]. The anterior, lateral, and posteroinferior courses can bring the PN in close proximity to the great cardiac vein, left obtuse marginal vein, and posterior vein, respectively. These anatomical considerations explain the higher prevalence of PNS with leads implanted in posterolateral veins
J Interv Card Electrophysiol
compared to anterior veins [5–7]. It is also be possible that the pacing stimulus delivered from posterior sites may cause direct diaphragmatic contraction rather than PNS, but this assertion remains to be proven. The distance between cardiac veins and PN is variable, depending on the amount of adipose tissue adherent to the pericardium, and is less than 3 mm between the left obtuse marginal vein and the PN in 43 % of cases with a lateral course [4]. The PNS threshold is linearly correlated with the distance from LV cathode to PN [8], with farther distances resulting in a lower probability of PNS. Another anatomical determinant for PNS is the LV electrode spacing, with shorter spacing causing less PNS [9]. In an acute canine study using a decapolar electrophysiologic catheter performing bipolar pacing with the electrode closest to the PN as the cathode, PNS thresholds varied according to the electrode spacing. Compared with a bipolar electrode spacing of 20 mm (a standard for most current bipolar leads), pacing with 1 and 2 mm bipolar electrode spacing resulted in a PNS threshold increase of 5.5±2.2 V (p=0.003) and 2.8±1.7 V (p2 V, the prevalence is much higher (24.2 % at follow-up including 12.3 % symptomatic [15]). 3.3 LV lead position Lateral and posterior veins are at higher risk of PNS than anterior veins. Biffi et al. reported that PNS was exclusively observed in lateral or posterolateral veins [7]. In another study, the hazard ratio for PNS for lateral leads vs. anterior leads was 4.12 (p=0.005) and posterior leads vs. anterior leads was 2.89 (p=0.048) [6]. Albertsen et al. [5] observed PNS in 4.2 % of leads in an anterior vein vs. 11.4 % of leads in a lateral or posterior vein (p=0.001). Apical positions are at higher risk of PNS than basal positions. The mid-apical position, as opposed to mid-basal, was the only predictor in multivariable analysis of PNS at lateral or posterolateral sites (odds ratio 4.23, 95 % confidence interval 2.03–8.81, p
Phrenic nerve stimulation in cardiac resynchronization therapy Ghassan Moubarak & Abdeslam Bouzeman & Jacky Ollitrault & Frederic Anselme & Serge Cazeau
Received: 9 February 2014 / Accepted: 7 May 2014 # Springer Science+Business Media New York 2014
Abstract In cardiac resynchronization therapy (CRT), the electrical impulse delivered by the left ventricular (LV) lead may incidentally cause phrenic nerve stimulation (PNS). The purpose of this state-of-the-art review is to describe the frequency, risk factors, and clinical consequences of PNS and to present the most recent options to successfully manage PNS. PNS occurs in 2 to 37 % of implanted patients and is not always detected in the supine position during implantation. Lateral and posterior veins are at higher risk of PNS than anterior veins, and apical positions are at higher risk of PNS than basal positions. The management of PNS discovered during implantation may include mapping the course of the target vein in order to find a PNS-free site, targeting another vein if available, and pacing with alternative configurations before changing the lead location. Non-invasive options for management of post-operative PNS depend on the difference between PNS and LV stimulation thresholds and include reducing the LV pacing output, automatic determination of LV stimulation threshold and minimal output delivery by the device, increasing the pulse duration, and electronic repositioning. New quadripolar leads allow to pace from different cathodes, and the multiple pacing configurations available have proved superior to bipolar leads in mitigating PNS. This electronic repositioning addresses almost all of the clinically relevant PNS and should markedly reduce the need for invasive lead repositioning or CRT abandon, which is actually the last option for 2 % of patients. G. Moubarak (*) : A. Bouzeman : J. Ollitrault : S. Cazeau Department of Pacing and Interventional Electrophysiology, Groupe Hospitalier Paris Saint-Joseph, 185, rue Raymond Losserand, 75014 Paris, France e-mail: [email protected] F. Anselme Department of Cardiology, Rouen University Hospital, Rouen, France
Keywords Cardiac resynchronization therapy . Phrenic nerve stimulation . Electronic repositioning . Quadripolar lead
1 Introduction Cardiac resynchronization therapy (CRT) is effective in diminishing mortality and morbidity in heart failure patients with reduced ejection fraction and wide QRS [1, 2]. Left ventricular stimulation (LVS) is delivered epicardially by placing a lead in a coronary sinus tributary, and the quality of resynchronization is dependent, among other factors, on the anatomical site of stimulation. The electrical impulse may incidentally capture the left phrenic nerve (PN) causing ipsilateral hemidiaphragmatic contractions. The purposes of this review are to describe the frequency, risk factors, and clinical consequences of phrenic nerve stimulation (PNS) and to present the most recent options to successfully manage PNS.
2 Anatomy of the left phrenic nerve and its relationship with LV lead The left PN originates from the cervical plexus and terminates at the diaphragm behind the apex of the left ventricle (LV). In an examination of 22 human cadavers, the left PN descended on the fibrous pericardium along one of three courses [3]: over the anterior surface of the left ventricle (18 %), over the lateral margin of the left ventricle (59 %), and in a posteroinferior direction (23 %). In another examination of nine hearts, the course was lateral in seven and anterior in two [4]. The anterior, lateral, and posteroinferior courses can bring the PN in close proximity to the great cardiac vein, left obtuse marginal vein, and posterior vein, respectively. These anatomical considerations explain the higher prevalence of PNS with leads implanted in posterolateral veins
J Interv Card Electrophysiol
compared to anterior veins [5–7]. It is also be possible that the pacing stimulus delivered from posterior sites may cause direct diaphragmatic contraction rather than PNS, but this assertion remains to be proven. The distance between cardiac veins and PN is variable, depending on the amount of adipose tissue adherent to the pericardium, and is less than 3 mm between the left obtuse marginal vein and the PN in 43 % of cases with a lateral course [4]. The PNS threshold is linearly correlated with the distance from LV cathode to PN [8], with farther distances resulting in a lower probability of PNS. Another anatomical determinant for PNS is the LV electrode spacing, with shorter spacing causing less PNS [9]. In an acute canine study using a decapolar electrophysiologic catheter performing bipolar pacing with the electrode closest to the PN as the cathode, PNS thresholds varied according to the electrode spacing. Compared with a bipolar electrode spacing of 20 mm (a standard for most current bipolar leads), pacing with 1 and 2 mm bipolar electrode spacing resulted in a PNS threshold increase of 5.5±2.2 V (p=0.003) and 2.8±1.7 V (p2 V, the prevalence is much higher (24.2 % at follow-up including 12.3 % symptomatic [15]). 3.3 LV lead position Lateral and posterior veins are at higher risk of PNS than anterior veins. Biffi et al. reported that PNS was exclusively observed in lateral or posterolateral veins [7]. In another study, the hazard ratio for PNS for lateral leads vs. anterior leads was 4.12 (p=0.005) and posterior leads vs. anterior leads was 2.89 (p=0.048) [6]. Albertsen et al. [5] observed PNS in 4.2 % of leads in an anterior vein vs. 11.4 % of leads in a lateral or posterior vein (p=0.001). Apical positions are at higher risk of PNS than basal positions. The mid-apical position, as opposed to mid-basal, was the only predictor in multivariable analysis of PNS at lateral or posterolateral sites (odds ratio 4.23, 95 % confidence interval 2.03–8.81, p
