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Background While ventricular-based timing modes are known to cause elevated atrial pacing above the lower rate when intrinsic atrioventricular (AV) conduction is shorter than programmed AV delay, there is one case report in 2015 by Jafri et al. where rapid atrial pacing was induced in an Abbott device set DDI with a lower rate of 90 by an unsensed premature atrial complex and slow intrinsic AV conduction allowing pacemaker 'crossover.' Case summary We present a very unusual case of rapid atrial pacing at >180 b.p.m. due to a perfect storm of events that we believe has not been previously reported. A patient with a St. Jude Abbott DCPPM set DDDR had an atrial tachyarrhythmia causing a mode switch to DDIR, which uses ventricular-based timing. This was followed by a period of rapid atrial pacing that terminated spontaneously. Discussion This phenomenon depended on an initial atrial tachyarrhythmia causing a mode switch to DDIR. In addition, the set lower rate would not have led to a short enough calculated ventriculo-atrial interval (VAI), but because rate responsive pacing was enabled, the calculated VAI was short enough to promote the crossover in setting of slow AV conduction and allow the rapid atrial pacing. Understanding this unique mechanism requires careful attention to pacemaker timing cycles and appreciation of the limitations of device programming. While it appears that a similar phenomenon was reported once in the literature, we believe that this episode of rapid atrial pacing was even more serendipitous due to the unlikely series of events required for its inception. [ABSTRACT FROM AUTHOR]

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Previous studies indicated long non-coding RNAs (lncRNAs) participated in the pathogenesis of atrial fibrillation (AF). However, little is known about the role of lncRNAs in AF-induced electrical remodeling. This study aimed to investigate the regulatory effect of lncRNA GAS5 (GAS5) on the electrical remodeling of neonatal rat cardiomyocytes (NRCMs) induced by rapid pacing (RP). RNA microarray analysis yielded reduced GAS5 level in NRCMs after RP. RT-qPCR, western blot, and immunofluorescence yielded downregulated levels of Nav1.5, Kv4.2, and Cav1.2 after RP, and whole-cell patch-clamp yielded decreased sodium, potassium, and calcium current. Overexpression of GAS5 attenuated electrical remodeling. Bioinformatics tool prediction analysis and dual luciferase reporter assay confirmed a direct negative regulatory effect for miR-27a-3p on lncRNA-GAS5 and HOXa10. Further analysis demonstrated that either miR-27a-3p overexpression or the knockdown of HOXa10 further downregulated Nav1.5, Kv4.2, and Cav1.2 expression. GAS5 overexpression antagonized such effects in Nav1.5 and Kv4.2 but not in Cav1.2. These results indicate that, in RP-treated NRCMs, GAS5 could restore Nav1.5 and Kv4.2 expression via the miR-27a-3p/HOXa10 pathway. However, the mechanism of GAS5 restoring Cav1.2 level remains unclear. Our study suggested that GAS5 regulated cardiac ion channels via the GAS5/miR-27a-3p/HOXa10 pathway and might be a potential therapeutic target for AF. [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation (AF) is frequently seen in patients with a volume-loaded left atrium (LA) such as mitral valve regurgitation (MR). Previous animal models have incomplete relevance to human AF associated with MR. Methods: A novel experimental model with a combination of volume loading of LA by creating a shunt from the subclavian artery to pulmonary artery and electrical remodeling induced by continuous rapid LA pacing was designed and the electrophysiological effects were examined in 10 canines. Five weeks after the shunt surgery, the entire atrial epicardium was mapped during sustained AF with form-fitted electrode patches with 246 bipolar electrodes and a three-dimensional dynamic mapping system to characterize the induced AF. Results: Three animals died of severe heart failure and pacing failure occurred in one. Remaining six animals were subjected to the analysis. The LA diameter increased progressively after the shunt surgery. Sustained AF was induced after 3 weeks of continuous rapid LA pacing in all animals. The activation maps revealed repetitive focal activations arising from the pulmonary veins, right or left atrial regions, and reentrant activations in the RA, which patterns of atrial activations are the same as those seen in human AF. Conclusion: The animal model with a combination of LA volume load and electrical remodeling was relevant to human AF associated with LA volume load. Studies using the present model may provide further knowledges of AF and may be useful in examining the effects of pharmacological and non-pharmacological therapies. [ABSTRACT FROM AUTHOR]

Previous studies indicated long non-coding RNAs (lncRNAs) participated in the pathogenesis of atrial fibrillation (AF). However, little is known about the role of lncRNAs in AF-induced electrical remodeling. This study aimed to investigate the regulatory effect of lncRNA GAS5 (GAS5) on the electrical remodeling of neonatal rat cardiomyocytes (NRCMs) induced by rapid pacing (RP). RNA microarray analysis yielded reduced GAS5 level in NRCMs after RP. RT-qPCR, western blot, and immunofluorescence yielded downregulated levels of Nav1.5, Kv4.2, and Cav1.2 after RP, and whole-cell patch-clamp yielded decreased sodium, potassium, and calcium current. Overexpression of GAS5 attenuated electrical remodeling. Bioinformatics tool prediction analysis and dual luciferase reporter assay confirmed a direct negative regulatory effect for miR-27a-3p on lncRNA-GAS5 and HOXa10. Further analysis demonstrated that either miR-27a-3p overexpression or the knockdown of HOXa10 further downregulated Nav1.5, Kv4.2, and Cav1.2 expression. GAS5 overexpression antagonized such effects in Nav1.5 and Kv4.2 but not in Cav1.2. These results indicate that, in RP-treated NRCMs, GAS5 could restore Nav1.5 and Kv4.2 expression via the miR-27a-3p/HOXa10 pathway. However, the mechanism of GAS5 restoring Cav1.2 level remains unclear. Our study suggested that GAS5 regulated cardiac ion channels via the GAS5/miR-27a-3p/HOXa10 pathway and might be a potential therapeutic target for AF.

TAVI is an established therapy for patients with severe aortic stenosis. Rapid or control pacing is necessary for TAVI, and most centers are familiar with right ventricular (RV) pacing. Although there are several reports on the efficacy and safety of LV pacing, they are still few. In addition, LV pacing has not been studied for different LV guidewires. Our aim is to study the effectiveness of left ventricular (LV) pacing and the thresholds of LV guidewires in patients who underwent transcatheter aortic valve implantation (TAVI). We retrospectively analyzed 252 consecutive patients who underwent trans-femoral TAVI (TF-TAVI) with LV pacing in our institute between December 2017 and November 2020. We excluded 48 patients from the total cohort due to TAVI with RV pacing, and the remaining 204 patients were analyzed (52 males, mean age 85 ± 5 years). Among them, 202 patients (99.0%) had successful LV pacing. In the two patients with failed LV pacing, SAFARI2™ Small was used. The CONFIDA™ group (n = 34) showed a significantly lower threshold than the SAFARI2™ group (n = 163) (median 3.0 vs. 5.0 V; P = 1.1 × 10–7). LV pacing with Lunderquist® was successful in all patients (n = 7). LV pacing in TAVI was an effective and safe strategy. CONFIDA™ wire may be particularly well suited for LV pacing in TAVI. [ABSTRACT FROM AUTHOR]

We report a case of revascularization of the right coronary artery via the epicardial collateral, for which we used transcoronary rapid pacing to obtain cardiac standstill while puncturing the distal chronic total occlusion (CTO) cap. To our knowledge, this is the first case in which this technique has been used in CTO. (Level of Difficulty: Advanced.)

Cardiac tamponade is a life-threatening complication during transcatheter aortic valve implantation (TAVI), often caused by perforation of the right ventricle (RV) by the temporary pacemaker used for rapid pacing during valve deployment. We aimed to assess the feasibility of performing rapid pacing while maintaining inflation of the pacing lead balloon in the RV during TAVI. Among 749 consecutive patients who underwent TAVI with SAPIEN XT valves between October 2013 and July 2015, 726 treated using rapid pacing with a transvenous balloon-tip lead were enrolled in our study, and were stratified into three groups according to the extent of balloon inflation in the RV as follows: full inflation (n = 100), partial inflation (n = 196), and deflation (n = 430). We compared the following clinical outcomes: pacing lead-related RV perforation, rapid pacing failure, valve malpositioning due to rapid pacing failure, device success, and 30-day mortality. Pacing lead-related RV perforation occurred only in patients in the deflation group (6 cases, 1.4%), but the differences among the groups were not statistically significant (p = 0.13). Rapid pacing failure, but no valve malpositioning, occurred most frequently in patients in the full inflation group (4.0% vs. 0.5% in the other groups, p = 0.004). The rate of device success (> 94%) and the 30-day mortality (2.0%) were similar among the three groups. Partial inflation of the balloon of the pacing lead may reduce the risk of RV perforation without increasing the risk of pacing failure or valve malpositioning. [ABSTRACT FROM AUTHOR]

Thoracic endovascular aortic repair (TEVAR) for aortic pathologies requires sufficient landing zone of ideally more than 25 mm for safe anchoring of the stent-graft and prevention of endoleaks. In the aortic arch and at the thoracoabdominal transition, landing zone length is usually limited by the offspring of the major aortic side-branches. Exact deployment of the stent-graft to effectively use the whole length of the landing zone and to prevent occlusion of one of the side-branches is key to successful TEVAR. There are numerous techniques described to lower blood pressure and to reduce or eliminate aortic impulse to facilitate exact deployment of stent-grafts including pharmacologic blood pressure lowering, adenosine-induced asystole, inflow occlusion, and rapid pacing. Aim of this review was to assess the current literature to identify which of the techniques is best suited to prevent displacement and allow for precise placement of the stent-graft and safe balloon-molding. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) play a key role in various pathological processes like atrial fibrillation (AF). However, the mechanisms remain unclear. Herein, this study was undertaken to probe the roles of ADAM10 and its targeting miR-520d in rapid pacing-induced apoptosis in atrial myocytes. In this study, the atrial myocytes grew adherently with irregular morphology. Immunofluorescence showed that more than 90% of atrial myocytes were α-sarcomeric actin (α-SCA) positive, indicating that the primary cells were positive for α-SCA staining and atrial myocytes were successfully isolated. The pacing atrial myocyte model was established after rapid pacing stimulation and we found the rapid pacing stimulation caused elevated ADAM10 and suppressed miR-520d. CCK-8 assay was applied for evaluation of cell viability, TUNEL staining for assessment of cell apoptosis and dual-luciferase reporter gene assay for verification of the targeting relationship between miR-520d and ADAM10. Overexpression of miR-520d or silencing of ADAM10 could enhance cell viability and reduce cell apoptosis in the rapid pacing-induced atrial myocytes. ADAM10 was a target gene of miR-520d. MiR-520d negatively targeted ADAM10, thereby promoting cell viability and inhibiting apoptosis in rapid pacing atrial myocyte model. In summary, miR-520d enhances atrial myocyte viability and inhibits cell apoptosis in rapid pacing-induced AF mouse model through negative mediation of ADAM10. [ABSTRACT FROM AUTHOR]

Background: The effect of myocardial injury (MI) post-transcatheter aortic valve implantation (TAVI) on clinical outcomes is controversial. This study aimed to evaluate the effect of MI severity on clinical outcome and left ventricle function 30 days post-TAVI and determine MI post-TAVI predictors.Methods: Overall, 138 consecutive patients who underwent successful transfemoral TAVI using SAPIEN3 and diagnosed using echocardiography and computed tomography were analyzed. High-sensitivity cardiac troponin T (TnT) was evaluated at baseline, immediately, and at 24, 48, and 72 h post-TAVI. Echocardiography findings and N-terminal pro-B-type natriuretic peptide (Nt-pro BNP) levels were evaluated 30 days post-TAVI.Results: Mean age and STS score were 84.4 ± 3.5 years and 6.4 ± 3.2%, respectively. All cases showed severe aortic valve stenosis. Peri-procedural MI was observed in 48 of 100 patients (48.0%). Patients were grouped into MI (n = 48) and non-MI (n = 52), without significant difference in characteristics. Pre-balloon aortic valvuloplasty rate and total pacing time were significantly higher in MI vs non-MI. Total rapid pacing time (TRPT) was an independent predictor for MI (OR 1.06; 95% CI 1.01-1.16; p = 0.04). Echocardiography and Nt-pro BNP changes 30 days post-TAVI were similar between groups.Conclusion: Peri-procedural MI, assessed by TnT changes, was observed in 48% of patients. The MI was not associated with overt cardiac dysfunction, and the recovery of left ventricular function and Nt-pro BNP level occurred similarly by 30 day post-TAVI between both groups. In multivariate analysis, TRPT was associated with MI after SAPIEN3 implantation.Trial Registration Number: UMIN000036669. [ABSTRACT FROM AUTHOR]

Background: High-grade or complete atrioventricular block (AVB) requiring permanent pacemaker (PPM) implantation is a known complication of transcatheter aortic valve replacement (TAVR). Wenckebach AVB induced by rapid atrial pacing (RAP) after TAVR was previously demonstrated in an observational analysis to be an independent predictor for PPM. We sought to investigate the utility of both pre- and post-TAVR RAP in predicting PPM implantation., Methods: In a single-center, prospective study, 421 patients underwent TAVR with balloon-expandable valves (BEV) between April 2020 and August 2021. Intraprocedural RAP was performed in patients without a pre-existing pacemaker, atrial fibrillation/flutter, or intraprocedural complete AVB to assess for RAP-induced Wenckebach AVB. The primary outcome was PPM within 30 days after TAVR., Results: RAP was performed in 253 patients, of whom 91.3% underwent post-TAVR RAP and 61.2% underwent pre-TAVR RAP. The overall PPM implantation rate at 30 days was 9.9%. Although there was a numerically higher rate of PPM at 30 days in patients with RAP-induced Wenckebach AVB, it did not reach statistical significance (13.3% vs. 8.4%, p = 0.23). In a multivariable analysis, RAP-induced Wenckebach was not an independent predictor for PPM implantation at 30 days after TAVR. PPM rates at 30 days were comparable in patients with or without pre-TAVR pacing-induced Wenckebach AVB (11.8% vs. 8.2%, p = 0.51) and post-TAVR pacing-induced Wenckebach AVB (10.2% vs. 5.8%, p = 0.25)., Conclusion: In patients who underwent TAVR with BEV, there were no statistically significant differences in PPM implantation rates at 30 days regardless of the presence or absence of RAP-induced Wenckebach AVB. Due to conflicting results between the present study and the prior observational analysis, future studies with larger sample sizes are warranted to determine the role of RAP during TAVR as a risk-stratification tool for significant AVB requiring PPM after TAVR., (© 2023 Wiley Periodicals LLC.)

BackgroundWe sought to determine whether right ventricular stunning could be detected after supply (during coronary balloon occlusion [BO]) and supply/demand ischemia (induced by rapid pacing [RP] during transcatheter aortic valve replacement) in humans. Methods and ResultsTen subjects with single‐vessel right coronary artery disease undergoing percutaneous coronary intervention with normal ventricular function were studied in the BO group. Ten subjects undergoing transfemoral transcatheter aortic valve replacement were studied in the RP group. In both, a conductance catheter was placed into the right ventricle, and pressure volume loops were recorded at baseline and for intervals over 15 minutes after a low‐pressure BO for 1 minute or a cumulative duration of RP for up to 1 minute. Ischemia‐induced diastolic dysfunction was seen 1 minute after RP (end‐diastolic pressure [mm Hg]: 8.1±4.2 versus 12.1±4.1, P

Background: Supernormal conduction (SNC) of the human ventricular myocardium has been reported, but its mechanism remains controversial. Methods: We recorded monophasic action potentials during rapid ventricular pacing from the right ventricular endocardium in 24 patients with supraventricular tachyarrhythmias who underwent catheter ablation. Results: In 7 of 24 patients, shortening of the QRS duration was observed at a pacing cycle length ≤400 ms and lengthening of the QRS duration was observed in 3. Conclusions: Shortening of the QRS duration during rapid ventricular pacing was observed in the patients.

Background The aim of the present study was to investigate whether transfemoral implantation of the Acurate neo transcatheter heart valve without pre-dilation is feasible. Methods Between December 2014 and December 2016, 294 patients were treated with the Acurate neo prosthesis at our center. Of these, 72 cases were performed without pre-dilation. The decision to omit pre-dilation was at the discretion of the operator, preferably in the case of mild to moderate aortic valve calcification (AVC). Propensity matching (1:1) resulted in 48 cases in each group. Main outcomes of interest were device success according to VARC-2 criteria, residual aortic regurgitation (AR) ≥ 2°, and rate of post-dilation. Results Median [IQR] age in patients without pre-dilation was 82.7 years [78.6–85.6], STS score was 4.6% [3.4–6.1], and AVC-score was 1436 AU [1043–1682] with mild and moderate AVC in 63.9% and 36.1% of cases, respectively. Device success was achieved in 94.4% of cases, post-dilation was necessary in 26.4%, and one (1.4%) patient had moderate AR. In the matched population, there were no differences regarding device success, rate of AR ≥ 2°, need for post-dilation, and post-procedural mean gradient, but the group without pre-dilation had shorter procedure (34.0 min [27.0–38.8] vs. 43.0 min [34.3–52.0]; p < 0.001) and fluoroscopy times (7.4 min [5.7–9.0] vs. 9.9 min [7.9–13.5]; p < 0.001). Conclusion In select patients with mild to moderate AVC, transfemoral implantation of the Acurate neo without pre-dilation is feasible and safe. This allows for a straightforward procedure that may be performed without rapid pacing in the majority of cases. [ABSTRACT FROM AUTHOR]

Aim Rapid pacing ( RP) is a regularly used model to induce heart failure in dogs. The aim of the study was to evaluate Ca2+ handling, left ventricular ( LV) contractile response during Ca2+ administration compared to exercise, as well as oxygen consumption and mechanical efficiency after 48 h of RP. Methods Fifty-three mongrel dogs were instrumented to measure LV pressure, LV fractional shortening, regional wall thickening and coronary blood flow. Contractile reserve was measured with isoproterenol and intravenous ( IV) Ca2+ administration. To assess the function of the sarcoplasmic reticulum ( SR), post-extrasystolic potentiation ( PESP) and SR Ca2+ uptake were measured. A graded treadmill test was performed in baseline and after RP ( n = 14). In a separate group of animals ( n = 5), myocardial performance and oxygen consumption were measured using a wide range of loading conditions. Results Left ventricular contractility was significantly decreased upon cessation of pacing. The contractile response to isoproterenol was blunted compared to a preserved response to IV Ca2+. Post-extrasystolic potentiation was slightly increased after RP. Maximal velocity ( Vmax) of SR Ca2+ uptake was unchanged. Contractile response during exercise is attenuated after RP. External work is reduced, whereas oxygen consumption is preserved, provoking a reduced mechanical efficiency. Conclusion Forty-eight-hours RP provokes a reversible LV dysfunction, while the SR function and response to exogenous Ca2+ are preserved. This is compatible with an intracellular functional remodelling to counteract Ca2+ overload provoked by RP. Left ventricular dysfunction is accompanied by a reduced contractile reserve, but an unchanged oxygen consumption, illustrating an alteration in oxygen utilization. [ABSTRACT FROM AUTHOR]

Remodeling of atrial electrophysiology and structure is the primary feature of atrial fibrillation (AF). Evidence suggests that abnormalities in the expression levels of embryological cardiovascular development-associated transcription factors, including Nkx2.5, are crucial for the development of AF. Rat atrial myocardial cells (AMCs) in culture dishes were placed in an electric field and stimulated. Transmission electron microscopy was used to observe the ultrastucture prior to and following rapid pacing. The action potential durations and effective refractory periods were measured. RT-PCR and western blotting were performed to investigate the effect of rapid pacing on the expression levels of ion channel and nuclear proteins in AMCs. Nkx2.5 short interfering RNA (siRNA) transfection was performed. Through this in vitro rat AMC culture and rapid pacing model, it was demonstrated that rapid pacing shortened the action potential and downregulated the expression levels of L-type calcium and potassium channels. Expression levels of Nkx2.5 and cardiac ankyrin repeat protein (CARP) were significantly upregulated by rapid pacing at the mRNA and protein levels. siRNA-mediated Nkx2.5 silencing attenuated the rapid pacing-induced downreglation of ion channel levels. These results suggest that the Nkx2.5/CARP signaling pathway contributes to the early electrical remodeling process of AF. [ABSTRACT FROM AUTHOR]

Alterations to the expression L-type calcium channels (LTCCs) and Kv4.3 potassium channels form the possible basis of atrial electrical remodeling during rapid pacing. The mitogen-activated protein kinase (MAPK) pathway is affected by increases in cytoplasmic Ca2+, and therefore represents an attractive candidate for the regulation and mediation of Ca2+-induced ion channel remodeling. The present study aimed to investigate alterations to the ion channel-MAPK axis, and to determine its influence on ion channel remodeling during atrial fibrillation. Rat atrial myocytes were isolated, cultured, and in vitro rapid pacing was established. Intracellular Ca2+ signals were monitored using the Fluo-3/AM Ca2+ indicator. Verapamil, PD98058 and SB203580 were added to the culture medium of various groups at specific time-points. The mRNA expression levels of LTCC-α1c and Kv4.3 potassium channels were detected by reverse transcription-polymerase chain reaction. Western blotting was performed to determine the expression levels of channel and signaling proteins. The results demonstrated that fast pacing significantly increased the intracellular Ca2+ concentration in atrial myocytes, whereas treatment with verapamil markedly inhibited this increase. In addition, verapamil significantly antagonized the rapid pacing-induced activation of extracellular signal-regulated kinase (ERK) and p38MAPK. These results indicated that the MAPK pathway may have an important role in the opening of LTCCs, and alterations to MAPK molecule expression could affect the expression and remodeling of ion channels. [ABSTRACT FROM AUTHOR]

Background: Rapid pacing during balloon aortic valvuloplasty (BAV) or transcatheter aortic valve replacement (TAVR) is an important step allowing for proper valve position and effective implantation while avoiding valve pop-up or ventricular complications. There are different regimes for rapid pacing during BAV/TAVR, some of which will be presented here1 . Materials and methods: Literature database PubMed has been reviewed yielding a total of 49 research articles related to rapid pacing during BAV/TAVR in the period of 2009 to 2021. Collected articles were assessed and reappraised to extrapolate different pacing options. Literature overview: Rapid pacing during BAV/TAVR can be achieved by insertion of a temporary transvenous pacemaker, reprogramming the existing permanent pacemaker in situ, or over-the-wire (OTW) pacing1 (Figure 1). The latter further includes different protocols. The most utilized OTW pacing protocol is based on the pacing circuit consisting of a positive pole attached to the wire in the left ventricle (isolated with the catheter), while a negative pole is attached to the femoral subcutaneous tissue over the needle. However, while the described protocol offers an attractive and simple set-up, it carries a risk of contact loss, inadequate pacing, or possibly insufficient post-implantation pacing2. Therefore, we present our modification of the OTW pacing scheme which allows for a safer procedure and bail-out options if necessary (Figure 1). Contrary to the conventional OTW scheme, our protocol includes the attachment of a negative pole to a wire in the inferior vein cava (5 French femoral sheath). This allows for stable contact, adequate length of the negative electrode, and quick bail-out insertion of a temporary transvenous pacemaker if necessary. Conclusions: Rapid pacing during BAV/TAVR is an important procedural step, and different methods have been described to achieve this. Modification of the existing protocol may lead to additional benefits and a more convenient procedure. [ABSTRACT FROM AUTHOR]

Objective To identify the risk factors of prolonged hemodynamic compromise caused by rapid pacing for valve deployment during transcatheter aortic valve implantation. Design A retrospective study. Setting Academic hospital. Participants Forty-seven patients with severe aortic stenosis who underwent transcatheter aortic valve implantation. Interventions The time after the end of rapid pacing until systolic arterial pressure and SvO 2 recovery (systolic arterial pressure>90 mmHg and SvO 2 >65%) was defined as “the hemodynamic recovery time” and was measured from online anesthetic charts. The total study population was divided into 2 groups according to the recovery time (third quartile in all patients; 33 and 14 patients in the early and delayed recovery groups, respectively). Subsequently, the factors associated with prolonged hemodynamic compromise after rapid pacing for valve deployment were identified by univariate and multivariate analyses. Measurements and Main Results Multivariate analysis identified left ventricular end-diastolic diameter (odds ratio, 0.774; 95% confidence interval, 0.608-0.915) and SvO 2 (odds ratio, 0.748; 95% confidence interval, 0.590-0.868) as independent factors associated with prolonged hemodynamic compromise after rapid pacing for valve deployment. Conclusions SvO 2 and left ventricular end-diastolic diameter were found to be significant independent predictors of prolonged hemodynamic compromise immediately after rapid pacing for valve deployment during transcatheter aortic valve implantation. [ABSTRACT FROM AUTHOR]

Background Supernormal conduction (SNC) of the human ventricular myocardium has been reported, but its mechanism remains controversial. Methods We recorded monophasic action potentials during rapid ventricular pacing from the right ventricular endocardium in 24 patients with supraventricular tachyarrhythmias who underwent catheter ablation. Results In 7 of 24 patients, shortening of the QRS duration was observed at a pacing cycle length ≤400 ms and lengthening of the QRS duration was observed in 3. Conclusions Shortening of the QRS duration during rapid ventricular pacing was observed in the patients. [ABSTRACT FROM AUTHOR]