Evidence for concealed fasciculo-ventricular connections as revealed by His bundle pacing.

BACKGROUND: It is almost 100 years ago since Mahaim described the so-called paraspecific connections between the ventricular conduction axis and the crest of the muscular ventricular septum, believing such pathways to be ubiquitous. These pathways, however, have yet to be considered as potential pathways for septal activation during His bundle pacing. MATERIALS: So as to explore the hypothesis that specialised septal pathways might provide the substrate for septal activation during His bundle pacing, we compared the findings from 22 serially sectioned histological datasets and 34 different individuals undergoing His bundle pacing. RESULTS: We found histologically specialised pathways connecting the branching component of the atrioventricular conduction axis with the crest of the muscular ventricular septum in almost four-fifths of the histological datasets. In 32 of 34 patients undergoing His bundle pacing, the QRS complex closely resembled published images of known conduction through fasciculo-ventricular pathways. In only two patients was a delta wave not seen at any pacing voltages. Capture of these connections varied according to pacing voltage, a finding which correlated with the distance of the pathways from the site of penetration of the ventricular conduction axis. Ventricular activation times remained normal in the presence of the delta wave at higher pacing voltage but were prolonged at lower voltages. CONCLUSIONS: Our histologic findings confirm fasciculo-ventricular connections, initially described by Mahaim as being paraspecific, are likely ubiquitous. Analysis of 12-lead electrocardiograms leads us to conclude that fasciculo-ventricular pathways, concealed during sinus rhythm, become manifest with His bundle pacing.

Effect of His bundle pacing on right bundle branch block located distal to site of pacing.

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.

Voltage dependent conduction abnormalities in His bundle pacing in patients without His Purkinje system disease.

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.

Outcomes with physiologic His bundle pacing in patients with narrow QRS complex.

BACKGROUND: 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. OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Effect of Nonselective His Bundle Pacing on Delayed Myocardial Activation in Left-axis Deviation and Left Bundle Branch Block.

It has been suggested that nonselective His bundle pacing (NS-HBP) corrects terminal conduction delay in right bundle branch block by early excitation of the right ventricular free wall. A similar analysis of NS-HBP, in patients with left bundle branch block (LBBB) and left-axis deviation (LAD) has not been done. Therefore, we compared the baseline QRS parameters in LAD and LBBB during NS-HBP and selective HBP (S-HBP). In LAD patients (n = 16), NS-HBP normalized the QRS axis from -35° ± 10° to 30° ± 34° (p < 0.01) and increased the lead 1 voltage (L1V) from 0.55 ± 0.3 mV to 0.88 ± 0.2 mV (p < 0.001) without increasing the peak lateral wall activation time (PLWAT) (p = not significant). In 23 of 41 LBBB patients, NS-HBP decreased the prolonged PLWAT by 73 ms (p < 0.0001), resolved the mid-QRS notch, normalized the QRS axis, and increased the L1V from 0.5 ± 0.3 mV to 1.15 ± 0.3 mV (p < 0.0001). In the remaining 18 LBBB patients, NS-HBP did not resolve the mid-QRS notch; however, the peak septal activation time decreased by 45 ms (p < 0.0001), PLWAT decreased by 53 ms (p < 0.0001), L1V increased from 0.5 ± 0.3 mV to 0.87 ± 0.4 mV (p < 0.0001), and the QRS axis normalized. All patients who developed S-HBP at lower pacing showed uncorrected LBBB (n = 6) or LAD (n = 7). In conclusion, NS-HBP, which causes myocardial activation in advance of simultaneously initiated S-HBP, results in a paced QRS complex with a normal axis and shorter activation times and restores the L1V in patients with LAD and LBBB. In some patients, a mid-QRS notch was seen with NS-HBP, which suggests fusion with S-HBP, which conducts without LBBB correction. A higher L1V in association with a shorter PLWAT and a normal QRS axis suggests that a more organized degree of left ventricular activation occurs with NS-HBP as compared to LBBB.