Insights from preclinical ultra high-density electroanatomical sinus node mapping.

AIMS Although sinus node modification by catheter ablation is an established therapy for the treatment of inappropriate sinus tachycardia, there is incomplete understanding of sinus node anatomy and function but also limited electroanatomical mapping data. Recently, an automatic, ultra high-resolution mapping system has been presented to accurately and quickly identify right atrial (RA) geometry and activation patterns but detailed assessment of sinus node activation has not been performed which was one aim of this study. Preclinical experiences are compared with previous sinus node mapping studies in animals and humans, and potential clinical implications for catheter ablation are discussed. METHODS AND RESULTS In anaesthetized and ventilated 14 pigs, 30 endocardial and 2 eipcardial RA maps were generated using the Rhythmia™ mapping system without complications and earliest activation sites (EAS) and sinus break-out (SBO) were determined. At baseline, EAS and SBO were located anterior to the middle (n = 6) or lower third (n = 8) of the crista terminalis exhibiting a unicentric activation pattern in all cases. Conduction pathways were directed anterior, posterior, superior, or inferior with substantial inter-individual variation in direction, pathway distance, and conduction time. Orciprenaline, propranolol, or amiodarone shifted endocardial activation with considerable variation between animals with inconsistent patterns. Multicentric activation was found in one case after orciprenaline infusion. Sequential endocardial and epicardial high-density mapping of the RA was performed in two animals and showed a high congruence of the sinus node activation in the endo- and the epicardial map. CONCLUSION Ultra high-density mapping allows fast, simple, and very detailed assessment of sinus node activation. Future studies are clearly needed to evaluate novel mapping and ablation strategies for an improved understanding of sinus node disease and better outcomes.

[1]  J. Goldberger,et al.  Epicardial/Endocardial Sinus Node Ablation After Failed Endocardial Ablation for the Treatment of Inappropriate Sinus Tachycardia , 2014, Journal of cardiovascular electrophysiology.

[2]  P. Tchou,et al.  Three-dimensional nonfluoroscopic mapping and ablation of inappropriate sinus tachycardia. Procedural strategies and long-term outcome. , 2002, Journal of the American College of Cardiology.

[3]  Tushar Sharma,et al.  Rapid High Resolution Electroanatomical Mapping: Evaluation of a New System in a Canine Atrial Linear Lesion Model , 2012, Circulation. Arrhythmia and electrophysiology.

[4]  H. Pak,et al.  Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation. , 2013, Circulation journal : official journal of the Japanese Circulation Society.

[5]  P. Sanders,et al.  High‐Density Mapping of the Sinus Node in Humans: Role of Preferential Pathways and the Effect of Remodeling , 2010, Journal of cardiovascular electrophysiology.

[6]  Siew Yen Ho,et al.  High Density Endocardial Mapping of Shifts 
 in the Site of Earliest Depolarization During Sinus Rhythm and Sinus Tachycardia , 2003, Pacing and clinical electrophysiology : PACE.

[7]  P. Sanders,et al.  Remodeling of Sinus Node Function in Patients With Congestive Heart Failure: Reduction in Sinus Node Reserve , 2004, Circulation.

[8]  F. Morady,et al.  Radiofrequency catheter ablation of inappropriate sinus tachycardia guided by activation mapping. , 2000, Journal of the American College of Cardiology.

[9]  R B Schuessler,et al.  Primary negativity does not predict dominant pacemaker location: implications for sinoatrial conduction. , 1995, The American journal of physiology.

[10]  D. Sánchez-Quintana,et al.  Sinus node revisited in the era of electroanatomical mapping and catheter ablation , 2005, Heart.

[11]  G. Lanza,et al.  Beta-Blockers and Ivabradine in Chronic Heart Failure: From Clinical Trials to Clinical Practice , 2014, American Journal of Cardiovascular Drugs.