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[Display omitted] [ABSTRACT FROM AUTHOR]

In patients with narrow QRS complex, both ventricular and biventricular pacing is associated with increased cardiac morbidity and mortality. This risk is not decreased by ventricular pacing avoidance algorithms, which cause nonphysiologic atrioventricular (AV) delays. This study aimed to report outcomes in patients with narrow QRS complex when the paced complex is in normal range and physiologic AV delays are programmed. In 196 patients with QRS duration of 92 ± 10 ms, permanent pacing was done at the site of the His bundle electrogram. The pacemakers were then programmed to maintain physiologic AV delays and to increase heart rates in response to exercise. Patients received usual care and were observed for 3 years. The paced complex exhibited a delta wave, and the ventricular activation time, QRS axis, and lead I voltage remained in normal range. Physiologic programming resulted in His bundle pacing burden of 92%. In patients with decreased ejection fraction, there was significant improvement in left ventricular function, left ventricular dilation, and mitral regurgitation (P <.003). In patients with normal ejection fraction, left ventricular function remained normal without new valvular abnormalities. The 3-year all-cause mortality was 10%, and there was no increase in heart failure admissions. In patients with narrow QRS complex, when paced QRS morphology is maintained in normal range and AV dyssynchrony is avoided, His bundle pacing is associated with low all-cause mortality and improvement in abnormal echocardiographic parameters. The paced QRS morphology and physiologic AV delays may be important factors to evaluate in future trials of conduction system pacing. [Display omitted] [ABSTRACT FROM AUTHOR]

[Display omitted] [ABSTRACT FROM AUTHOR]

Background: It is generally accepted that bundle branch block (BBB) may be corrected simply by selective His bundle pacing (S-HBP) distal to site of block. However, clinical HBP is often non-selective (NS), the site of block unknown and moving the HB lead is not always an option. Thus, while correction of right (R) BBB in NS-HBP has been reported, its mechanism is unknown.Methods: Threshold testing was done during His bundle pacing in 39 patients with RBBB. We compared NS-HBP and S-HBP and analyzed the role of pacing voltage and capture threshold of the parallel pathway, in partially or completely correcting RBBB.Results: During NS-HBP, higher pacing voltage completely corrected RBBB in 22/35 patients as compared to 5/18 patients at lower voltage. Remaining patients showed incomplete correction of RBBB. NS-HBP group with lower capture threshold of 1.3 ± 0.5 V completely resolved RBBB in 9/14 vs 3/11 patients in NS-S HBP group with higher capture threshold of 2.4 ± 0.8 V. QRS activation time in NSHBP was 91 ± 8 ms (baseline 97 ± 7 ms p = ns). S-HBP resolved RBBB in only 1/21 patients.Conclusions: 1.) Lack of correction with S-HBP suggests that RBBB was distal to site of HBP and yet was corrected with NS-HBP. 2.) Voltage dependent correction of RBBB in NS-HBP suggests that conduction via a specialized parallel pathway maintains normal ventricular activation time. 3.) Correction of RBBB in all patients with NS-HBP, suggests that conduction block was either bypassed or right ventricular free wall pre-excited by conduction via parallel pathway. [ABSTRACT FROM AUTHOR]

Background: During His bundle (HB) pacing, the active fixation of HB lead may cause disruption of the enclosed conduction fibers and cause conduction delay. His Purkinje conduction delays have been shown to revert to normal with higher voltage pacing.Objective: To determine if conduction delays seen with penetrative HB pacing are voltage dependent and can resolve with higher stimulus voltage.Methods: In 17 patients undergoing HBP, the effect of voltage on a composite His Purkinje system-ventricular activation time (hVAT) as well as electrocardiographic (ECG) evidence of conduction delay, was systematically evaluated.Results: There was highly significant prolongation of hVAT indicative of conduction delay in 13/17 patients. ECG changes of rightward delay were also seen in 9/13 patients. Both types of delays we manifest at lower voltages and we uniquely resolved by higher stimulation voltage. A pre-excitation like abnormality was also seen in 15/17 patients. This conduction abnormality was manifest at higher voltage without prolongation of hVAT. In 6/15 patients the pre-excitation like abnormality ceased at lower voltage.Conclusion: HB pacing is associated with evidence of significant conduction delay noted at low voltage, which resolves with higher stimulation voltage. The more common pre-excitation like abnormality appears to occur at high voltage and, in of itself, does not appear to prolong hVAT. [ABSTRACT FROM AUTHOR]