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Right Ventricular Apex (right + ventricular_apex)
Selected AbstractsLong-Term Mechanical Consequences of Permanent Right Ventricular Pacing: Effect of Pacing SiteJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2010DARRYL P. LEONG M.B.B.S. Optimal Right Ventricular Pacing,Introduction: Long-term right ventricular apical (RVA) pacing has been associated with adverse effects on left ventricular systolic function; however, the comparative effects of right ventricular outflow tract (RVOT) pacing are unknown. Our aim was therefore to examine the long-term effects of septal RVOT versus RVA pacing on left ventricular and atrial structure and function. Methods: Fifty-eight patients who were prospectively randomized to long-term pacing either from the right ventricular apex or RVOT septum were studied echocardiographically. Left ventricular (LV) and atrial (LA) volumes were measured. LV 2D strain and tissue velocity images were analyzed to measure 18-segment time-to-peak longitudinal systolic strain and 12-segment time-to-peak systolic tissue velocity. Intra-LV synchrony was assessed by their respective standard deviations. Interventricular mechanical delay was measured as the difference in time-to-onset of systolic flow in the RVOT and LV outflow tract. Septal A' was measured using tissue velocity images. Results: Following 29 ± 10 months pacing, there was a significant difference in LV ejection fraction (P < 0.001), LV end-systolic volume (P = 0.007), and LA volume (P = 0.02) favoring the RVOT-paced group over the RVA-paced patients. RVA-pacing was associated with greater interventricular mechanical dyssynchrony and intra-LV dyssynchrony than RVOT-pacing. Septal A' was adversely affected by intra-LV dyssynchrony (P < 0.05). Conclusions: Long-term RVOT-pacing was associated with superior indices of LV structure and function compared with RVA-pacing, and was associated with less adverse LA remodeling. If pacing cannot be avoided, the RVOT septum may be the preferred site for right ventricular pacing. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1120-1126) [source] Timing of Depolarization and Contraction in the Paced Canine Left Ventricle:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003Experiment, Model Introduction: For efficient pump function, contraction of the heart should be as synchronous as possible. Ventricular pacing induces asynchrony of depolarization and contraction. The degree of asynchrony depends on the position of the pacing electrode. The aim of this study was to extend an existing numerical model of electromechanics in the left ventricle (LV) to the application of ventricular pacing. With the model, the relation between pacing site and patterns of depolarization and contraction was investigated. Methods and Results: The LV was approximated by a thick-walled ellipsoid with a realistic myofiber orientation. Propagation of the depolarization wave was described by the eikonal-diffusion equation, in which five parameters play a role: myocardial and subendocardial velocity of wave propagation along the myofiber cm and ce; myocardial and subendocardial anisotropy am and ae; and parameter k, describing the influence of wave curvature on wave velocity. Parameters cm, ae, and k were taken from literature. Parameters am and ce were estimated by fitting the model to experimental data, obtained by pacing the canine left ventricular free wall (LVFW). The best fit was found with cm= 0.75 m/s, ce= 1.3 m/s, am= 2.5, ae= 1.5, and k= 2.1 × 10,4 m2/s. With these parameter settings, for right ventricular apex (RVA) pacing, the depolarization times were realistically simulated as also shown by the wavefronts and the time needed to activate the LVFW. The moment of depolarization was used to initiate myofiber contraction in a model of LV mechanics. For both pacing situations, mid-wall circumferential strains and onset of myofiber shortening were obtained. Conclusion: With a relatively simple model setup, simulated depolarization timing patterns agreed with measurements for pacing at the LVFW and RVA in an LV. Myocardial cross-fiber wave velocity is estimated to be 0.40 times the velocity along the myofiber direction (0.75 m/s). Subendocardial wave velocity is about 1.7 times faster than in the rest of the myocardium, but about 3 times slower than as found in Purkinje fibers. Furthermore, model and experiment agreed in the following respects. (1) Ventricular pacing decreased both systolic pressure and ejection fraction relative to natural sinus rhythm. (2) In early depolarized regions, early shortening was observed in the isovolumic contraction phase; in late depolarized regions, myofibers were stretched in this phase. Maps showing timing of onset of shortening were similar to previously measured maps in which wave velocity of contraction appeared similar to that of depolarization. (J Cardiovasc Electrophysiol, Vol. 14, pp. S188-S195, October 2003, Suppl.) [source] Site-Specific Arrhythmogenesis in Patients with Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2003HIROSHI MORITA M.D. Introduction: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. Methods and Results. Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. Conclusion: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.(J Cardiovasc Electrophysiol, Vol. 14, pp. 373-379, April 2003) [source] Relationship between the Duration of the Basal QRS Complex and Electrical Therapies for Ventricular Tachycardias among ICD PatientsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2010JAVIER JIMÉNEZ-CANDIL M.D., Ph.D. Background:,In implantable cardioverter-defibrillators (ICD) patients, the duration of the basal QRS complex (QRSd) is not associated with a greater risk of developing ventricular tachyarrhythmias. QRSd could be inversely related to the effectiveness of antitachycardia pacing (ATP) because it may be associated with longer conduction times of the paced-impulses and hence, with a greater propensity to require shocks to terminate ventricular tachycardias (VTs). Methods:,We followed 216 ICD patients (pacing site: right ventricular apex; QRSd , 100: 34%) for 21 ± 12 months. ICD programming was standardized. QRSd was determined on the electrocardiogram (50 mm/s) at device implantation. Results:,Five hundred and fifty-one VTs (cycle length: 329 ± 35 ms) occurred in 67 patients (36% had a QRSd , 100 ms). ATP terminated 86% of VTs and 11% needed shocks. Mean ATP efficiency per patient was 83%. QRSd was significantly correlated with the probability of successful ATP (C-coefficient: 0.66), the best cut-off point being 100 (sensitivity and specificity of 91% and 49%). Patients with QRSd , 100 had a higher ATP effectiveness (98% vs 75%; P = 0.003) and fewer VTs terminated by shocks (1% vs 23%; P = 0.003). By logistic regression, QRSd > 100 remained as an independent predictor of receiving shocks to terminate VTs (P = 0.01). According to Kaplan-Meier analysis, the occurrence of VTs was similar regardless of the QRSd (30% vs 38%; P = 0.2), but the incidence of shock due to VTs was higher in patients with a QRSd > 100 (19% vs 7%; P = 0.01). Conclusion:,Since QRSd is a negative and independent predictor of effective ATP, ICD patients with QRSd > 100 ms require shocks more frequently to terminate VTs. (PACE 2010; 596,604) [source] Exact Location of the Branching Bundle in the Living HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009MASAMITSU ADACHI M.D., Ph.D. Aims: The His bundle electrogram is believed to reflect the exact location of the His bundle. However, the distinction between distal His bundle potential and proximal right bundle branch potential is challenging. The aim of this study was to pinpoint the location of the branching point of the His bundle, and to compare that site with the site of recording of the largest His bundle electrogram (LH) during sinus rhythm. Methods: We hypothesized that the site of earliest His activation (EH) during retrograde conduction via the left bundle branch is the branching point. We studied 15 nonconsecutive patients (mean age = 40 ± 22 years; eight men). We performed a programmed stimulation from right ventricular apex until retrograde right bundle branch block appeared. At that point we measured (1) the distance between antegrade LH site and retrograde EH site and (2) the atrial-to-ventricular amplitude ratio (A/V ratio) at both sites. Results: EH was recorded at the proximal electrode of the His bundle catheter in all patients. Mean distance between EH and LH was 9.8 ± 2.5 mm. The mean A/V ratios at the EH site and the LH site were 1.01 ± 0.42 and 0.08 ± 0.06, respectively. Discussion: This study showed that the EH site is located approximately 10-mm proximal to the LH site. The mean A/V ratio at the EH site during sinus rhythm is approximately 1.0. These observations suggest that the majority of His potentials reflect proximal right bundle activation. Before delivering radiofrequency energy in the para-Hisian area, attention should be paid to the presence of a His potential and to the A/V ratio, rather to the amplitude of the His electrogram. [source] Delayed Cardiac Perforation by Defibrillator Lead Placed in the Right Ventricular Outflow Tract Resulting in Massive Pericardial EffusionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2008ERNEST W. LAU M.D. A 76-year-old man received a dual-chamber implantable cardioverter defibrillator (ICD), with the defibrillator lead positioned within the right ventricular outflow tract. The lead parameters at the time of implantation were satisfactory and the postprocedure chest X-ray showed the leads were in place. The patient was cardioverted from atrial fibrillation during defibrillation threshold testing and commenced on anticoagulation immediately. One month post implantation, he experienced multiple ventricular tachycardia episodes all successfully treated with antitachycardia pacing and shocks by his ICD, but he fell and hit his chest against a hard surface during one of these attacks. He developed a massive pericardial effusion and computed tomography confirmed cardiac perforation by the defibrillator lead. Pericardiocentesis was performed and the defibrillator lead replaced with a different model positioned at the right ventricular apex. The patient made an uneventful recovery. The management and avoidance of delayed cardiac perforation by transvenous leads were discussed. [source] Does Size Really Matter?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2008A Comparison of the Riata Lead Family Based on Size, Its Relation to Performance Background: Recently, the performance and safety of smaller diameter implantable cardioverter defibrillator (ICD) leads has been questioned. The purpose of this analysis was to determine the impact of size on lead performance and perforation rates by comparing the performance of 7 French (7F) and 8 French (8F) leads with similar design characteristics implanted by a single operator. Methods: Patients implanted with a Riata 1580 (8F) or 7000 (7F) series leads (St. Jude Medical, Sylmar, CA, USA) over a 2-year period were evaluated to compare performance and perforation rates. Results: There were 357 Riata 8F leads and 357 Riata 7F leads implanted in 714 patients. Follow-up ranged from 1 to 24 months. The 8F leads were implanted in the right ventricular apex more often than were 7F leads (129 or 37% vs 72 or 20%, P < 0.0001). Oversensing that did not result in therapy occurred in 2 pts (0.56%) with 8F leads and 1 pt. (0.28%) with a 7F lead (P = 0.56). Oversensing with therapy occurred once in both groups (0.28%, P = NS). One perforation occurred in each group (0.28%, P = NS). Both occurred in leads that were implanted in the right ventricular apex (P = 0.02). Conclusions: The performance of St. Jude Medical 7F and 8F Riata leads was similar. The incidence of lead-related adverse events was within or below the low end of published acceptable ranges for ICD lead perforation and sensing anomalies. Perforations were less likely to occur in leads that were implanted in nonapical positions. [source] Effect of Right Ventricular Apex Pacing on the Tei Index and Brain Natriuretic Peptide in Patients with a Dual-Chamber PacemakerPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2006HITOSHI ICHIKI Background: Asynchronous electrical activation induced by right ventricular apex (RVA) pacing can cause various abnormalities in left ventricular (LV) function, particularly in the context of severe LV dysfunction or structural heart disease. However, the effect of RVA pacing in patients with normal LV and right ventricular (RV) function has not been fully elucidated. The aim of this study was to characterize the effects of RVA pacing on LV and RV function by assessing isovolumic contraction time and isovolumic relaxation time divided by ejection time (Tei index) and by assessing changes in plasma brain natriuretic peptide (BNP). Methods: Doppler echocardiographic study and BNP measurements were performed at follow-up (mean intervals from pacemaker implantation, 44 ± 75 months) in 76 patients with dual chamber pacemakers (sick sinus syndrome, n = 30; atrioventricular block, n = 46) without structural heart disease. Patients were classified based on frequency of RVA pacing, as determined by 24-hour ambulatory electrocardiogram (ECG) that was recorded just before echocardiographic study: pacing group, n = 46 patients with RVA pacing ,50% of the time, percentage of ventricular paced 100 ± 2%; sensing group, n = 30, patients with RVA pacing <50% of the time, percentage of ventricular paced 3 ± 6%. Results: There was no significant difference in mean heart rate derived from 24-hour ambulatory ECG recordings when comparing the two groups (66 ± 11 bpm vs 69 ± 8 bpm). LV Tei index was significantly higher in pacing group than in sensing group (0.67 ± 0.17 vs 0.45 ± 0.09, P < 0.0001), and the RV Tei index was significantly higher in pacing group than in sensing group (0.34 ± 0.19 vs 0.25 ± 0.09, P = 0.011). Furthermore, BNP levels were significantly higher in pacing group than in sensing group (40 ± 47 pg/mL vs 18 ± 11 pg/mL, P = 0.017). With the exception of LV diastolic dimension (49 ± 5 mm vs 45 ± 5 mm, P = 0.012), there were no significant differences in other echocardiographic parameters, including left atrium (LA) diameter (35 ± 8 mm vs 34 ±5 mm), LA volume (51 ± 27 cm3 vs 40 ± 21 cm3), LV systolic dimension (30 ± 6 mm vs 29 ± 7 mm), or ejection fraction (66 ± 9% vs 63 ± 11%), when comparing the two groups. Conclusions: These findings suggest that the increase of LV and RV Tei index, LVDd, and BNP are highly correlated with the frequency of the RVA pacing in patients with dual chamber pacemakers. [source] Underestimation of Pacing Threshold as Determined by an Automatic Ventricular Threshold Testing AlgorithmPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2006WILLIAM H. SAUER In this case report, we describe markedly different pacing thresholds determined by a manual threshold test and the automatic Ventricular Capture Management algorithm. The discrepancy in pacing threshold values reported was due to the difference in the AV intervals used with the different testing methods. We propose that the differences in right ventricular dimensions with altered diastolic filling periods affected the threshold in this patient with a new passive fixation lead in the right ventricular apex. [source] Relation Between the Pacing Induced Sequence of Activation and Left Ventricular Pump Function in AnimalsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2002FRITS W. PRINZEN PRINZEN, F.W., et al.: Relation Between the Pacing Induced Sequence of Activation and Left Ventricu-lar Pump Function in Animals. The main goal of this article was to review animal experimental work on the effect of asynchronous activation on ventricular pump function. During normal sinus rhythm and atrial pacing, the Purkinje system contributes significantly to the rapid electrical activation of the ventricles. In contrast, during ventricular pacing the impulse is almost exclusively conducted through the normal myocardium. As a consequence, electrical activation of the ventricles becomes asynchronous and has an abnormal sequence. The abnormal impulse conduction causes considerable disturbances to occur in regional systolic fiber shortening, mechanical work, blood flow, and oxygen consumption; low values occurring in early activated regions and values above normal being present in late activated regions. Many animal studies have now shown that the abnormal electrical activation, induced by ventricular pacing, leads to a depression of systolic and diastolic LV function. Pacing at the right ventricular apex (the conventional pacing site) reduces LV function more than pacing at the high ventricular septum or at LV sites. In canine hearts with experimental LBBB, LV pacing significantly improves LV pump function. Differences in LV pump function between (combinations of) pacing sites are poorly correlated with QRS duration. Therefore, the cause of the depression of LV function during abnormal electrical activation appears to be a combination of the asynchrony and the sequence of activation. These experimental findings justify continuing attention for optimizing the site(s) of ventricular pacing in patients with normal and abnormal ventricular impulse conduction. [source] | ||||||||||