Physiology and Practicality of Left Ventricular Septal Pacing

Left ventricular septal pacing (LVSP) and left bundle branch pacing (LBBP) have been introduced to maintain or correct interventricular and intraventricular (dys)synchrony. LVSP is hypothesised to produce a fairly physiological sequence of activation, since in the left ventricle (LV) the working myocardium is activated first at the LV endocardium in the low septal and anterior free-wall regions. Animal studies as well as patient studies have demonstrated that LV function is maintained during LVSP at levels comparable to sinus rhythm with normal conduction. Left ventricular activation is more synchronous during LBBP than LVSP, but LBBP produces a higher level of intraventricular dyssynchrony compared to LVSP. While LVSP is fairly straightforward to perform, targeting the left bundle branch area may be more challenging. Long-term effects of LVSP and LBBP are yet to be determined. This review focuses on the physiology and practicality of LVSP and provides a guide for permanent LVSP implantation.

Ventricular Pre-excitation Causing Left Ventricular Dysfunction Partially Reverted After Ablation of the Accessory Pathway

Ventricular pre-excitation is one of the rarest causes of cardiomyopathy induced or mediated by arrhythmia. Right accessory pathways, specifically with left bundle branch block pattern, can cause ventricular dysfunction, since abnormal ventricular activation resulting from anterograde atrioventricular conduction can cause atrioventricular, interventricular, and intraventricular dyssynchrony, with asynchronous contraction of the ventricular wall and mitral regurgitation. An asymptomatic patient, with ventricular pre-excitation with left bundle branch block and moderate ventricular dysfunction at echocardiography, was described. The electrophysiological study demonstrated an accessory route of anterior location and with an anterograde refractory period of 600 ms, successfully performing radiofrequency ablation and substantial improvement of ventricular function.

Pacemaker syndrome

Pacemaker syndrome (PMS) is a constellation of symptoms and signs provoked by haemodynamic and biohumoural modifications secondary to ‘any modification of the temporal sequence of atrial and ventricular contraction’ induced by artificial pacing. This clinical entity was early described after the development of artificial pacing but it still lacks a definite characterization. In particular, several mechanisms may induce PMS beyond ventriculoatrial retrograde conduction in a patient with single-chamber pacing, with the interplay of patient characteristics, device hardware/programming, and pharmacological therapy. The contemporary concept of PMS is strictly connected with the idea of ‘physiological pacing’ for which PMS represent the negative extreme. Moreover, any improvement in cardiac pacing provides additional data on PMS such as atrioventricular timing, intraventricular dyssynchrony, and heart rate adaptation.