Rapid Right Ventricular Pacing Research Articles

Rapid right ventricular pacing for balloon valvuloplasty in congenital aortic stenosis: A systematic review.

BACKGROUNDBalloon aortic valvuloplasty (BAV) is a well-established treatment modality for congenital aortic valve stenosis.AIMTo evaluate the role of rapid right ventricular pacing (RRVP) in balloon stabilization during BAV on aortic regurgitation (AR) in pediatric patients.METHODSA systematic review of the MEDLINE, Cochrane Library, and Scopus databases was conducted according to the PRISMA guidelines (end-of-search date: July 8, 2020). The National Heart, Lung, and Blood Institute and Newcastle-Ottawa scales was utilized for quality assessment.RESULTSFive studies reporting on 72 patients were included. The studies investigated the use of RRVP-assisted BAV in infants (> 1 mo) and older children, but not in neonates. Ten (13.9%) patients had a history of some type of aortic valve surgical or catheterization procedure. Before BAV, 58 (84.0%), 7 (10.1%), 4 (5.9%) patients had AR grade 0 (none), 1 (trivial), 2 (mild), respectively. After BAV, 34 (49.3%), 6 (8.7%), 26 (37.7%), 3 (4.3%), patients had AR grade 0, 1, 2, and 3 (moderate), respectively. No patient developed severe AR after RRVP. One (1.4%) developed ventricular fibrillation and was defibrillated successfully. No additional arrhythmias or complications occurred during RRVP.CONCLUSIONRRVP can be safely used to achieve balloon stability during pediatric BAV, which could potentially decrease AR rates.

Right Ventricular Systolic Function and Cardiac Resynchronization Therapy

Objectives: The aim of this study was to investigate the influence of right ventricular (RV) dysfunction on the response to cardiac resynchronization therapy (CRT) and the impact of CRT on RV function in a beagle model of heart failure (HF). Methods: Twenty-one beagles were implanted with transvenous cardiac pacemakers and underwent rapid RV pacing for 2 weeks at 260 bpm to induce HF. Dogs were subsequently divided into three groups that were either treated with bi-ventricular pacing (CRT group) or untreated (control group and HF group). Echocardiographic images were acquired at baseline, before CRT, and 4 weeks after CRT. Results: Left ventricular systolic function and synchrony (left ventricular internal dimensions, left ventricular end systolic volume [LVESV], left ventricular ejection fraction [LVEF], septal-to-posterior wall motion delay [SPWMD], and aorta pre-ejection interval and the pulmonary artery pre-ejection interval [|APEI-PPEI|]) were significantly improved in the CRT group compared with the HF group. RV myocardial performance index (MPI) and pulmonary artery systolic pressure deteriorated with left ventricular dysfunction and improved after CRT. RV outflow ESV, standard deviation of time to minimum systolic volume (Tmsv), and Tmsv% decreased in the CRT group compared with the HF group. LVESV, LVEF, SPWMD, and |APEI-PPEI| were significantly different between responders and nonresponders, while there was no difference about RV functional parameters. Conclusions: RV function deteriorated with left ventricular dysfunction and improved after CRT. RV function did not significantly influence the response to CRT.

The "hidden" concealed left-sided accessory pathway: An uncommon cause of SVT in young people.

Concealed left-sided accessory pathways (CLAP) are a cause of supraventricular tachycardia (SVT) in the young. Most are mapped with right ventricular (RV) apical/outflow pacing. Rarely, alternative means of mapping are required. We review our experience from three pediatric electrophysiology (EP) centers with a rare form of "hidden" CLAP. All patients<21 years undergoing EP study from 2008 to 2014 with a "hidden" CLAP (defined as an accessory pathway [AP] for which RV pacing at cycle lengths [CL] stable for mapping did not demonstrate eccentric retrograde conduction) were included. preexcitation. Demographic, procedural, and follow-up data were collected. A total of 23 patients met the criteria (median age, 14.3 years [range 7-21], weight, 51kg [31-99]). 21 (96%) had SVT and one AFIB (4%). APs were adenosine sensitive in 7/20 patients (35%) and VA conduction was decremental in six (26%). CLAP conduction was demonstrable with orthodromic reentrant tachycardia in all patients, with RV extrastimulus testing in seven (30%) and with rapid RV pacing (<CL 300) in three (13%). Left ventricular (LV) pacing demonstrated CLAP conduction in 17/17 (100%) patients in whom it was used. All 23 CLAPs were successfully ablated (100%) via transseptal approach with radiofrequency energy. Specific ablation techniques included: 16 (70%) during LV paced rhythm, four (17%) during orthodromic reciprocating tachycardia (ORT; 3/4 ventricular entrained), and three (13%) with brief rapid RV pacing. There were no complications. At 18 months (range 3-96), there was one recurrence (4%). Some CLAPs are only demonstrable with LV pacing, entrained ORT, or rapid RV pacing. LV pacing facilitated preferential AP conduction, allowing for mapping while maintaining stable hemodynamics.

Cardiac vanilloid receptor-1 afferent depletion enhances stellate ganglion neuronal activity and efferent sympathetic response to cardiac stress.

Afferent fibers expressing the vanilloid receptor 1 (VR1) channel have been implicated in cardiac nociception; however, their role in modulating reflex responses to cardiac stress is not well understood. We evaluated this role in Yorkshire pigs by percutaneous epicardial application of resiniferatoxin (RTX), a toxic activator of the VR1 channel, resulting in the depletion of cardiac VR1-expressing afferents. Hemodynamics, epicardial activation recovery intervals, and in vivo activity of stellate ganglion neurons (SGNs) were recorded in control and RTX-treated animals. Stressors included inferior vena cava or aortic occlusion and rapid right ventricular pacing (RVP) to induce dyssynchrony and ischemia. In the epicardium, stellate ganglia, and dorsal root ganglia, immunostaining for the VR1 channel, calcitonin gene-related peptide, and substance P was significantly diminished by RTX. RTX-treated animals exhibited higher basal systolic blood pressures and contractility than control animals. Reflex responses to epicardial bradykinin and capsaicin were mitigated by RTX. Cardiovascular reflex function, as assessed by inferior vena cava or aortic occlusion, was similar in RTX-treated versus control animals. RTX-treated animals exhibited resistance to hemodynamic collapse induced by RVP. Activation recovery interval shortening during RVP, a marker of cardiac sympathetic outflow, was greater in RTX-treated animals and exhibited significant delay in returning to baseline values after cessation of RVP. The basal firing rate of SGNs and firing rates in response to RVP were also greater in RTX-treated animals, as was the SGN network activity in response to cardiac stressors. These data suggest that elimination of cardiac nociceptive afferents reorganizes the central-peripheral nervous system interaction to enhance cardiac sympathetic outflow. NEW & NOTEWORTHY Our work demonstrates a role for cardiac vanilloid receptor-1-expressing afferents in reflex processing of cardiovascular stress. Current understanding suggests that elimination of vanilloid receptor-1 afferents would decrease reflex cardiac sympathetic outflow. We found, paradoxically, that sympathetic outflow to the heart is instead enhanced at baseline and during cardiac stress.

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

It is now well recognized that heart failure (HF) patients with left bundle branch block (LBBB) derive substantial clinical benefits from cardiac resynchronization therapy (CRT), and LBBB has become one of the important predictors for CRT response. The conventional tachypacing-induced HF model has several major limitations, including absence of stable LBBB and rapid reversal of left ventricular (LV) dysfunction after cessation of pacing. Hence, it is essential to establish an optimal model of chronic HF with isolated LBBB for studying CRT benefits. In the present study, a canine model of asynchronous HF induced by left bundle branch (LBB) ablation and 4 weeks of rapid right ventricular (RV) pacing is established. The RV and right atrial (RA) pacing electrodes via the jugular vein approach, together with an epicardial LV pacing electrode, were implanted for CRT performance. Presented here are the detailed protocols of radiofrequency (RF) catheter ablation, pacing leads implantation, and rapid pacing strategy. Intracardiac and surface electrograms during operation were also provided for a better understanding of LBB ablation. Two-dimensional speckle tracking imaging and aortic velocity time integral (aVTI) were acquired to validate the chronic stable HF model with LV asynchrony and CRT benefits. By coordinating ventricular activation and contraction, CRT uniformed the LV mechanical work and restored LV pump function, which was followed by reversal of LV dilation. Moreover, the histopathological study revealed a significant restoration of cardiomyocyte diameter and collagen volume fraction (CVF) after CRT performance, indicating a histologic and cellular reverse remodeling elicited by CRT. In this report, we described a feasible and valid method to develop a chronic asynchronous HF model, which was suitable for studying structural and biologic reverse remodeling following CRT.

Tolerance of Rapid Right Ventricular Pacing during Thoracic Endovascular Aortic Repair

The objective of this retrospective study was to evaluate the tolerance of rapid right ventricular pacing (RRVP) compared with that of the traditional methods of hypotension used during thoracic endovascular aortic repair (TEVAR). From January 2002 to December 2012, we retrospectively included all the patients treated with TEVAR by comparing the 2 groups: patients operated with RRVP (RRVP+) and those operated without RRVP (RRVP-). The characteristics of the population and the procedures were recorded. The rates of complications were compared up to 1 year. Sixty-one patients were operated. Treated pathologies were multiple with 19 aneurysms, 14 false aneurysms, 12 isthmic ruptures, 11 dissections, 3 coarctations, and 2 endoleaks. Twenty-four patients were RRVP+ and 37 patients were RRVP-. Mortality rates at 1 month in groups RRVP+ and RRVP- were of 0% and 2.7%, respectively (P = 1), and reintervention rates were 0% and 13.5%, respectively (P = 0.15). Three peroperative rhythm disorders (12.5%) were observed in the RRVP+ group including 2 ventricular fibrillations and 1 atrial fibrillation, both reduced without complications. One pacemaker was implanted for atrioventricular block in the RRVP- group. In the RRVP+ group, 83.3% of the patients presented a rise in troponin Ic (TnI) >0.04 ng/mL in 72 hours compared with 40.5% of the patients in the RRVP- group (P = 0.0013), with a spontaneously favorable evolution. No coronary syndrome was observed at 1 year with a mortality rate of 10.8% in the RRVP- group vs. 0% in the RRVP+ (P = 0.15). In spite of a frequent moderate rise of TnI at the time of RRVP, this technique does not present more complications at 1 year than the use of a chemical hypotension. It thus seems an interesting alternative for selected patients, in trained teams.

Inadvertently Developed Ventricular Fibrillation during Electrophysiologic Study and Catheter Ablation: Incidence, Cause, and Prognosis

Background and ObjectivesVentricular fibrillation (VF) can inadvertently occur during electrophysiologic study (EPS) or catheter ablation. We investigated the incidence, cause, and progress of inadvertently developed VF during EPS and catheter ablation.Subjects and MethodsWe reviewed patients who had developed inadvertent VF during EPS or catheter ablation. Patients who developed VF during programmed ventricular stimulation to induce ventricular tachycardia or VF were excluded.ResultsInadvertent VF developed in 11 patients (46.7±9.3 years old) among 2624 patients (0.42%); during catheter ablation for atrial fibrillation (AF) in nine patients, frequent ventricular premature beats (VPBs) in one, and Wolff-Parkinson-White (WPW) syndrome were observed in one. VF was induced after internal cardioversion in six AF patients due to incorrect R-wave synchronization of a direct current shock. Two AF patients showed spontaneous VF induction during isoproterenol infusion while looking for AF triggering foci. The remaining AF patient developed VF after rapid atrial pacing to induce AF, but the catheter was accidentally moved to the right ventricular (RV) apex. A patient with VPB ablation spontaneously developed VF during isoproterenol infusion. The focus of VPB was in the RV outflow tract and successfully ablated. A patient with WPW syndrome developed VF after rapid RV pacing with a cycle length of 240 ms. Single high energy (biphasic 150-200 J) external defibrillation was successful in all patients, except in two, who spontaneously terminated VF. The procedure was uneventfully completed in all patients. At a mean follow-up period of 17.4±15.5 months, no patient presented with ventricular arrhythmia.ConclusionAlthough rare, inadvertent VF can develop during EPS or catheter ablation. Special caution is required to avoid incidental VF during internal cardioversion, especially under isoproterenol infusion.

Effects of Tolvaptan on Systemic and Renal Hemodynamic Function in Dogs with Congestive Heart Failure

We investigated the effects of tolvaptan, a vasopressin V(2)-receptor antagonist, on diuretic response and systemic and renal hemodynamic characteristics in conscious dogs with congestive heart failure (CHF). We also compared these effects with those of furosemide, a loop diuretic. CHF was induced by rapid right-ventricular pacing at 260 beats/min for at least 3 weeks, and maintained with a pacing rate of 220-240 beats/min. CHF dogs were orally given tolvaptan (10 mg/kg), furosemide (10 mg/kg) and vehicle in random order during the stable CHF state. Urine excretion, systemic and renal hemodynamic parameters, and plasma hormone levels were measured over 6-hour periods after drug administration. Tolvaptan induced aquaresis with an increase in free water clearance, resulting in a significant increase in serum sodium concentrations and a decrease in cumulative water balance. Tolvaptan also decreased pulmonary capillary wedge pressure without affecting systemic vascular resistance, glomerular filtration rate or renal blood flow. Tolvaptan tended to increase plasma arginine vasopressin concentrations but did not affect plasma renin activity. In contrast, furosemide induced clear saluresis with increased electrolyte excretion, resulting in decreased pulmonary capillary wedge pressure. However, furosemide also decreased serum potassium concentration and increased plasma arginine vasopressin concentrations and plasma renin activity. Tolvaptan elicited a potent aquaretic response and reduced the cardiac preload without unfavorable effects on systemic or renal hemodynamics, the renin-angiotensin-aldosterone system, or the sympathetic nervous system in CHF dogs. Thus, tolvaptan may offer a novel approach to remove excess water congestion from patients with CHF.

PP77. Pulmonary Artery Catheter Directed Rapid Right Ventricular Pacing to Facilitate Precise Deployment of Endografts in the Thoracic Aorta: A Novel Approach

Controlled hypotension is critical for precise deployment of endografts in the thoracic aorta and for safe balloon dilation after deployment. Rapid right ventricular pacing (RRVP) via a transfemoral venous catheter has been reported previously as a technique to facilitate thoracic endograft placement. We describe a novel approach to RRVP using a pulmonary artery catheter (PAC) that is placed during the endograft procedure for hemodynamic monitoring.

Rapid Pacing for Better Placing: Comparison of Techniques for Precise Deployment of Endografts in the Thoracic Aorta

To investigate the safety, efficacy, impact on positioning, and neurocognitive outcomes of 3 conceptually different methods of avoiding the "windsock" effect during thoracic stent-graft placement. A retrospective review was conducted of 70 patients (48 men; mean age 63 years) who underwent elective or emergency stent-graft placement in the thoracic aorta for various pathologies. Twenty-seven patients (18 men; mean age 64+/-12 years) had stent-graft positioning during rapid right ventricular (RV) pacing at 180 to 200 beats per minute. Another 27 patients (18 men; mean age 62+/-12 years) had stent-graft placement under controlled hypotension (<or=45 mmHg) achieved with sodium nitroprusside (3 microg/kg/min). Sixteen patients (12 men; mean age 63+/-14 years) had intermittent cardiac arrest induced by a 0.5-mg/kg adenosine bolus prior to launching the stent-graft. Termination of the endovascular procedure, weaning, and recovery were conducted according to the same routines in all patients. Hemodynamics, landing precision (deviation from planned placement site), cerebral blood flow, and neurocognitive function were compared. Rapid RV pacing (median 12 seconds) was conducted without technical difficulty or delayed recovery in any of the 27 patients. Once rapid pacing ceased, blood pressure recovered within 8 seconds from 22+/-8 mmHg to normal prepacing levels. The level of hypotension was most pronounced in the rapid RV pacing group (20+/-4 mmHg, p<0.001), and the duration of hypotension was also the shortest (20+/-10 seconds, p<0.001) at a pacing rate of 190+/-10 beats per minute. The instantaneous mean flow velocity was lowest (10+/-4 cm/s, p<0.001) and recovery to normal pressure was quickest (within 1 minute) with rapid pacing. Instrumentation for rapid pacing did not prolong the procedure, but shortened it approximately 25 minutes. Moreover, precise positioning at a mean 2+/-2 mm from the predetermined launch site was observed with rapid pacing (p<0.05). There were no differences in postprocedural neurological assessment among groups. Rapid RV pacing is safe in selected patients and in experienced hands. It abbreviates hemodynamic compromise, shortens the endovascular procedure, and may eventually emerge as the preferred method to avoid the windsock effect during stent-grafting. The maneuver, however, requires knowledge of right cardiac anatomy and expertise in selecting patients.

Metabolic and structural abnormalities in dogs with early left ventricular dysfunction induced by incessant tachycardia.

To assess morphologic and metabolic abnormalities in dogs with early left ventricular dysfunction (ELVD) induced by rapid right ventricular pacing (RRVP). 7 Beagles. Plasma carnitine concentrations were measured before and after development of ELVD induced by RRVP. At the same times, transvenous endomyocardial biopsy was performed, and specimens were submitted for determination of myocardial carnitine concentrations and histologic, morphometric, and ultrastructural examination. In 4 dogs in which baseline plasma total carnitine concentration was normal, RRVP induced a decrease in myocardial total and free carnitine concentrations and an increase in myocardial esterified carnitine concentration. In 3 dogs in which baseline plasma total carnitine concentration was low, plasma and myocardial carnitine concentrations were unchanged after pacing. Structural changes associated with pacing included perinuclear vacuolization in 3 dogs. Morphometric analyses indicated there was a decrease in myofiber cross-sectional diameter and area following pacing. Electron microscopy revealed changes in myofibrils and mitochondria following pacing. Results indicated that moderate to severe alterations in myocyte cytoarchitecture are present in dogs with ELVD induced by RRVP and that in dogs with normal plasma carnitine concentrations, myocardial carnitine deficiency may be a biochemical marker of ELVD. Results also indicated that transvenous endomyocardial biopsy can be used to evaluate biochemical and structural myocardial changes in dogs with cardiac disease.

Usefulness of dobutamine stress tests for detection of cardiac abnormalities in dogs with experimentally induced early left ventricular dysfunction.

To determine whether dobutamine stress tests (DST) can be used to detect cardiac dysfunction in dogs with early left ventricular dysfunction (ELVD) induced by rapid right ventricular pacing (RRVP). 7 adult male Beagles. A pacemaker was surgically implanted in each dog at the level of the right ventricular apex. Electrocardiography, Doppler sphygmomanometry, and Doppler echocardiography were performed before and during a DST prior to activation of the pacemaker and every 3 to 4 days during the period of RRVP. Dobutamine stress tests were performed by infusing dobutamine at incremental dosages ranging from 12.5 to 42.5 microg/kg of body weight/min. Clinical signs of congestive heart failure were not observed during the pacing period. However, all dogs developed ELVD associated with significant changes in values for most Doppler echocardiographic variables obtained prior to DST Adverse cardiac effects were not detected during DST. Most Doppler echocardiographic indices of cardiac function were significantly altered in response to dobutamine infusion during the pacing period, compared with prepacing values. However, a dobutamine-induced 2-fold increase in cardiac output was maintained. Dobutamine stress tests can be safely performed in dogs with experimentally induced ELVD. Dobutamine stress tests may be a sensitive, noninvasive diagnostic method, complementary to standard clinical examinations, for detection of early cardiac dysfunction in dogs asymptomatic for dilated cardiomyopathy.

Hormonal response to dobutamine cardiac stress testing in a conscious canine model of early left ventricular dysfunction induced by chronic rate overload

The aims of this study were to investigate (1) hormonal activation before and during dobutamine cardiac stress testing (DST) in a canine model of early left ventricular dysfunction (ELVD) induced by rapid right ventricular pacing (RRVP) and (2) the relationship between this hormonal profile and carnitine concentrations. Before the pacing period, the 6 dogs were assigned to 2 groups according their baseline total plasma carnitine concentration. A DST was performed on each dog before activation of the pacemaker and every 3 to 4 days during development of 3 progressive stages of ELVD (stages 1, 2 and 3). Plasma atrial natriuretic factor (ANF), angiotensin II (ANG II) and endothelin-1 (ET-1) levels were measured at the start and at the end of each DST. Effects of ELVD, DST and plasma carnitine concentration on these measurements were tested. The RRVP induced a significant increase of ANF and ANG II and a non significant trend toward increase of ET-1 in all dogs. Before the pacing period, ANF remained constant during the DST in dogs with normal total plasma carnitine concentration, while it significantly decreased in dogs with low total plasma carnitine concentration. Dobutamine stress testing induced a significant decrease in ANF in all dogs in ELVD. Dobutamine infusion induced a significant increase in ANG II in all dogs before as well as during the pacing period while ET-1 was unchanged. These results suggest that investigation of the hormonal profile before and after a dobutamine challenge might provide important diagnostic information in dogs with asymptomatic or mildly symptomatic cardiac dysfunction of different origins.

Acute effect of L-arginine on hemodynamics and vascular capacitance in the canine pacing model of heart failure.

The effect of L-arginine, 250 mg/kg over 10 min, on hemodynamics and venous function was studied in nine splenectomized dogs under light pentobarbital anesthesia before and after 17 +/- 1 days of rapid right ventricular pacing (RRVP) at 250 beats/min. Chronic RRVP induced mild congestive heart failure with increased mean circulatory filling (Pmcf), right atrial (Pra) and pulmonary capillary wedge pressures (Ppcw), and reduced cardiac output (CO). During the development of heart failure, total vascular compliance assessed from Pmcf-blood volume relationships during circulatory arrest was unchanged, but total vascular capacitance was markedly reduced, with an increase in stressed and reduction in unstressed blood volumes. At baseline but not after RRVP, L-arginine increased CO and reduced pulmonary vascular resistance. There were no significant changes in Pra, Ppcw, or total peripheral resistance. L-Arginine failed to alter total vascular compliance and capacitance or central blood volume in the baseline or failure state. These results do not support the hypothesis that increased Pmcf and reduced total vascular capacitance in the early stages of pacing-induced heart failure are caused by reduced substrate availability for or an endogenous competitive antagonist of NO synthase in venous endothelial cells.

Captopril attenuates pacing-induced acute heart failure by increasing total vascular capacitance.

To study the effects of captopril pretreatment on vascular capacitance in acute heart failure, anesthetized splenectomized dogs were subjected to rapid right ventricular pacing (RRVP) at 250 beats/min for 60 min combined with an intravenous (i.v.) 20-ml/kg volume load of dextran 70 over 10 min. Captopril pretreatment [50 mg every 8 h for 3 days plus 0.5 mg/kg intravenously (i.v.) at induction of anesthesia] attenuated development of acute heart failure associated with RRVP, maintaining normal cardiac output (CO) and pulmonary capillary wedge pressures (PCWP). Total vascular capacitance after a volume load plus RRVP was higher in captopril-pretreated animals (129.8 +/- 3.2 vs. 100.4 +/- 4.8 ml/kg) owing to an increase in unstressed volume (118.6 +/- 3.1 vs. 88.4 +/- 5.6 ml/kg). Arterial capacity and pulmonary (central) vascular capacitance were also increased.

Failure of atrial natriuretic factor to increase with volume expansion in acute and chronic congestive heart failure in the dog.

It remains unclear whether the levels of atrial natriuretic factor (ANF) observed in chronic CHF are appropriate for the magnitude of elevations in atrial pressures. Specifically, it is not known whether acute increases in atrial pressure in CHF can result in further significant increases in circulating ANF. The present study was designed to test the hypothesis that in chronic CHF there is an attenuated relation between circulating ANF and atrial pressure such that the heart is unable to respond to further increases in atrial pressure with appropriate increases in ANF. Cardiovascular hemodynamics and plasma levels of ANF were measured at baseline and after rapid right ventricular pacing (RRVP) to produce acute (n = 10, 25 minutes RRVP) and chronic (n = 7, 14-16 days RRVP) CHF. Acute saline volume expansion was then performed in each group to determine the response of circulating ANF to acute increases in atrial pressure in both acute and chronic CHF. In chronic CHF, right atrial pressure was much higher than in acute CHF (8.5 +/- 0.9 vs. 3.4 +/- 1.3 mm Hg, p less than 0.05); however, circulating ANF was not greater in chronic as compared with acute CHF (385 +/- 73 vs. 500 +/- 89 pg/ml), which is consistent with an attenuated release of ANF in chronic CHF. In response to volume expansion, right atrial pressure increased in both acute (3.4 +/- 1.3 to 12.1 +/- 7 mm Hg) and chronic (8.5 +/- .9 to 13.3 +/- 1.0 mm Hg) CHF.(ABSTRACT TRUNCATED AT 250 WORDS)