Right Ventricular Septum Research Articles

Hemodynamic effect of rv apex vs rv septum pacing in a monoventricular and biventricular configuration in patients with heart failure

Hemodynamic effect of rv apex vs rv septum pacing in a monoventricular and biventricular configuration in patients with heart failure

Hemodynamic effect of RV apex vs RV septum pacing in a monoventricular and biventricular configuration in patients with heart failure

Hemodynamic effect of RV apex vs RV septum pacing in a monoventricular and biventricular configuration in patients with heart failure

In situ Ca 2+ dynamics of Purkinje fibers and its interconnection with subjacent ventricular myocytes

Purkinje fibers play essential roles in impulse propagation to the ventricles, and their functional impairment can become arrhythmogenic. However, little is known about precise spatiotemporal pattern(s) of interconnection between Purkinje-fiber network and the underlying ventricular myocardium within the heart. To address this issue, we simultaneously visualized intracellular Ca 2+ dynamics at Purkinje fibers and subjacent ventricular myocytes in Langendorff-perfused rat hearts using multi-pinhole type, rapid-scanning confocal microscopy. Under recording of electrocardiogram at room temperature spatiotemporal changes in fluo3-fluorescence intensity were visualized on the subendocardial region of the right-ventricular septum. Staining of the heart with either fluo3, acetylthiocholine iodide (ATCHI), or di-4-ANEPPS revealed characteristic structures of Purkinje fibers. During sinus rhythm (about 60 bpm) or atrial pacing (up to 3 Hz) each Purkinje-fiber exhibited spatiotemporally synchronous Ca 2+ transients nearly simultaneously to ventricular excitation. Ca 2+ transients in individual fibers were still synchronized within the Purkinje-fiber network not only under high-K + (8 mM) perfusion-induced Purkinje-to-ventricular (P–V) conduction delay, but also under unidirectional, orthodromic P–V block produced by 10-mM K + perfusion. While spontaneous, asynchronous intracellular Ca 2+ waves were identified in injured fibers of Purkinje network locally, surrounding fibers still exhibited Ca 2+ transients synchronously to ventricular excitation. In summary, these results are the first demonstration of intracellular Ca 2+ dynamics in the Purkinje-fiber network in situ. The synchronous Ca 2+ transients, preserved even under P–V conduction disturbances or under emergence of Ca 2+ waves, imply a syncytial role of Purkinje fibers as a specialized conduction system, whereas unidirectional block at P–V junctions indicates a substrate for reentrant arrhythmias.

Usefulness of a ventricular extrastimulus from the summit of the ventricular septum in diagnosis of septal accessory pathway in patients with supraventricular tachycardia

To compare usefulness of a ventricular extrastimulus (VES) from the right ventricular (RV) apex versus the RV septum in patients with a septal accessory pathway (AP), VES was applied from the RV apex and the summit of the RV septum in patients with septal APs. A VES from the RV apex and from the summit was diagnostic of the presence of an AP in 13 of 28 patients (83%) and in 10 of 12 patients, respectively (46% p <0.05), and VES proved an AP as a part of the tachycardia circuit in 5 of 28 patients (18%) and 6 of 12 patients, respectively (50%, p <0.05). A VES during His bundle refractoriness from the RV summit increases the diagnostic yield for both the presence of an AP and its participation in the tachycardia circuit with respect to RV apical VES.

Septal lead implantation for the reduction of paced QRS duration using passive-fixation leads.

In 120 consecutive patients with standard pacing indications, we tested the feasibility of RV septal lead implantation technique guided by surface ECG and the degree to which this technique reduces paced QRS duration compared to RV apical stimulation when passive-fixation leads are used. During implantation, an ECG was recorded with a paper speed of 100 mm/s using the orthogonal Frank leads, and QRS was measured from the earliest to the latest deflection in any of the Frank leads. Pace-mapping of the septum was performed until QRS was minimal. The lead was attached, where QRS, pacing threshold, lead impedance, and EGM amplitude provided the best compromise. An average of 3.7 +/- 2.5 attempts (range 1-18, median 7) was needed until a final implantation site was found. There were no technical problems during implantation. QRS could be reduced by 5-55 ms (mean delta QRS 19 +/- 11 ms) in 83 (69%) of 120 patients. In 22 (18%) patients, QRS was identical with apical and septal pacing, and in 15 (13%) patients, QRS was 5-20 ms (10 +/- 4) longer despite septal stimulation. Average QRS was significantly shorter during septal pacing compared with apical pacing (151 +/- 20 vs 162 +/- 23 ms, P < 0.001). There was a tendency towards greatest QRS reduction when the high septum was stimulated (22 +/- 11 ms reduction) as compared with mid- (18 +/- 11 ms) or apical parts of the RV septum (16 +/- 10 ms). QRS reduction was most likely if apical QRS width was > 170 ms (P = 0.0002), and there was an inverse correlation between apical QRS and delta QRS (r = 0.53, P < 10(-7)). During a mean follow-up of 14 months, there was no pacing or sensing problem and no lead dislodgment occurred.

Right Ventricular Performance and Mass by Use of Cine MRI Late After Atrial Repair of Transposition of the Great Arteries

The long-term adaptation of the right ventricle after atrial repair of transposition of the great arteries (TGA) remains a subject of major concern. Cine magnetic resonance imaging (MRI), with its tomographic capabilities, allows unique quantitative evaluation of both right and left ventricular function and mass. Our purpose was to use MRI and an age-matched normal population to examine the typical late adaptation of the right and left ventricles after atrial repair of TGA. Cine MRI was used to study ventricular function and mass in 22 patients after atrial repair of TGA. Images were obtained in short-axis sections from base to apex to derive normalized right and left ventricular mass (RVM and LVM, g/m2), interventricular septal mass (IVSM, g/m2), RV and LV end-diastolic volumes (EDV, mL/m2), and ejection fractions (EF). Results 8 to 23 years after repair were compared with analysis of 24 age- and sex-matched normal volunteers and revealed markedly elevated RVM, decreased LVM and IVSM, normal RV size, and only mildly depressed RVEF. Only 1 of 22 patients had clinical RV dysfunction, and this patient had increased RVM. Cine MRI allows quantitative evaluation of both RV and LV mass and function late after atrial repair of TGA. Longitudinal studies that include these measurements should prove useful in determining the mechanism of late RV failure in these patients. On the basis of these early data, inadequate hypertrophy does not appear to be the cause of late dysfunction in this patient group.

Effects of aortic constriction during experimental acute right ventricular pressure loading. Further insights into diastolic and systolic ventricular interaction.

Acute right ventricular (RV) hypertension may result in hemodynamic collapse. The associated reduction in left ventricular (LV) end-diastolic volume is thought to result from reduced RV output (secondary to RV ischemia) and adverse direct ventricular interaction. Aortic constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an increased coronary perfusion pressure. We hypothesized that altered ventricular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction. We instrumented nine dogs with ultrasonic dimension crystals to measure RV segment length, septum-to-RV free wall and septum-to-LV free wall diameters, and LV anterioposterior diameter. Catheter-tipped manometers were used to measure LV and RV pressures. Pericardial pressure was measured with flat, liquid-containing balloon transducers. Inflatable cuff constrictors were placed on the pulmonary artery (PA) and aorta, and a flow probe was placed on the PA. The right coronary artery (RCA) was perfused independently by a roller pump calibrated for flow. During moderate PA constriction, while RCA pressure was maintained at control level, RCA flow did not change significantly (15.8 +/- 6.2 to 16.9 +/- 11.5 mL/min) and was similar during severe PA constriction (18.6 +/- 9.8 mL/min). During severe PA constriction, RV stroke volume decreased from a control value of 10.3 +/- 4.9 to 2.3 +/- 1.4 mL/beat (P < .05). When aortic constriction was added while RCA pressure was maintained at control level, there was an increase in RV stroke volume to 4.5 +/- 2.0 mL/beat (P < .05) with no associated change in RCA flow (17.8 +/- 9.5 mL/min). However, pressure-dimension loops clearly demonstrated changes in diastolic and systolic ventricular interaction; with aortic constriction, there was a large increase in the transeptal pressure gradient associated with a rightward septal shift. During either isolated severe PA constriction or simultaneous severe PA and aortic constriction, RCA flow was increased until RCA pressure was approximately equal to that in the aorta. This produced an increase in RCA flow of 50% (P < .05); however, this increase in coronary flow was ineffective in improving any measure of RV function. In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.

992-111 Minimum Interelectrode Distance to Avoid Interactions Between Coexistent Transvenous Pacemaker and Defibrillator Systems

The coexistence of a dual-chamber (or ventricular) permanent pacemaker (PM) and a non-thoracotomy (NT) ICD may result in ICD nondetection of ventricular fibrillation during uninhibited ventricular pacing. This is important in light of the frequent concomitant use of both devices. Guidelines to avoid this interaction, specifically the minimum safe distance between the 2 electrodes, have not been established. In 33 pts with coexistent PM and NT-lCD, we measured the shortest distance from the PM electrodes to the ICD sensing electrodes using a tridimensional coordinate system on PA and lateral chest radiographs. Pts were extensively tested post-implant for potential deleterious device-to-device interaction. In 5 pts (15%), the ICD was inappropriately inhibited by asynchronous ventricular pacing during ventricular fibrillation. In this “Interaction Group”, the mean shortest distance from the PM electrodes to the ICD sensing electrodes was significantly shorter than in the “Non-Interaction Group” (1.6 cm vs. 3.4 cm. p = 0.03, Mann-Whitney test). Four out of 10 (40%) systems with shortest interelectrode distance &lt; 2.0 cm demonstrated interaction, while this occurred in only 1 of 23 (4%) systems with shortest interelectrode distance ≥ 2.0 cm (p = 0.02, Fisher's Exact test). 1. A distance of at least 2.0 cm between the PM electrodes and the ICD sensing electrodes will avoid deleterious interactions in the vast majority of pts. 2. The use of at least one active-fixation lead will facilitate achievement of this target interelectrode distance by allowing stable lead positioning in the RV outflow tract or septum. 3. Careful lead positioning does not obviate the need for intra- and postoperative testing to identify potentially life-threatening device-to-device interaction.

Avaliação dos resultados tardios da operação de derivação cavo-pulmonar bidirecional, no tratamento paliativo de cardiopatias congênitas com câmara ventricular única

No periodo de marco de 1990 a janeiro de 1994, 17 pacientes com idades de 1 a 13 anos (media: 7 anos), portadores de cardiopatias congenitas com câmara ventricular unica funcionante, foram submetidos a operacao de derivacao cavo-pulmonar bidirecional. Nove pacientes tinham atresia tricuspide (AT), 7 do tipo lb, 1 tipo le e 1 tipo Mb. Cinco pacientes tinham dupla via de entrada ventricular tipo ventriculo direito (DVEVD); 2 com comunicacao interventricular(CIV) multipla+hipoplasiado VD; 1 com atresia pulmonar com septo interventricular integro (APc/SIVI). Nove (52,9%) pacientes tinham operacoes paliativas previas. A operacao foi realizada com auxilio da circulacao extracorporea (CEC) em 12 (70,5%) casos e mediante derivacao do fluxo sanguineo da veia cava superior (VCS) para o atrio direito (AD) em 5 (29,5%) casos. Em todos os casos a VCS foi anastomosada a arteria pulmonar direita (APD), interrompendo o fluxo sanguineo para o pulmao, fechando a valva pulmonar e ligando a derivacao de Blalock-Taussig pervio. Houve 3 (17,6%) obitos no pos-operatorio imediato (POI) e 2 (14,2%) no pos-operatorio tardio (POT). Doze (70,5%) pacientes estao em acompanhamento clinico, com um tempo de evolucao de 2 a 46 meses. Um paciente foi submetido ao 2o tempo da operacao, tunelizando a veia cava inferior (VCI) para a APD, com sucesso. A avaliacao do fluxo da derivacao cavo-pulmonar bidirecional esta sendo realizada pela ecodopplercardiografia e ressonância nuclear magnetica e a perfusao pulmonar mediante cintilografia radioisotopica. A indicacao do 2o tempo da operacao obedece a propria evolucao clinica e avaliacao da saturacao arterial durante a cicioergometria. A derivacao cavo-pulmonar bidirecional permite uma adaptacao progressiva do fluxo venoso para o pulmao, diminuindo a sobrecarga de volume do ventriculo, preparando o paciente para a derivacao venosa total.

Differential Regional Function of the Right Ventricle During the Use of a Left Ventricular Assist Device

The use of a left ventricular assist device (LVAD) as a bridge to transplant is associated with a 52% incidence of RV failure requiring additional inotropic or mechanical support (RVAD). This study evaluated the differential performance of the RV free wall and septum to identify the need for additional RV support. Cross-sectional views of the RV were obtained immediately before, and 1 hr after, Novacor LVAS implantation in 12 consecutive patients using transesophageal echocardiography. Each image was divided into a free wall portion (FW) and a septal portion (SP) by grids drawn from the center of gravity of the end-diastolic endocardial outline to the junction between the FW and the SP. Percentage change between preimplant and postimplant for RV ejection fraction (RVEF), fractional area change for the FW (FAC-FW) and the SP (FAC-SP), and fractional shortening of the FW to SP distance (F-S) is reported for patients based upon the need for RV support: minimal (Group 1), maximal (Group 2). After LVAS implantation, patients showed a reduction in SP fractional area change. However, this reduction was most pronounced in Group 2. The degree of SP impairment may explain the mechanism of RV failure in patients on an LVAD.

Stimulation of the summit of the right ventricular aspect of the ventricular septum during orthodromic atrioventricular reentrant tachycardia

Application of ventricular premature complexes (VPCs) from the right ventricular (RV) apex during orthodromic atrioventricular (AV) reentrant tachycardia has limitations both in the ability to shorten the succeeding atrial cycle length and in helping to identify accessory pathway location. Stimulation from the summit of the RV aspect of the septum during AV reentrant tachycardia was investigated as a new technique to improve the diagnostic utility of applying VPCs during AV reentrant tachycardia. VPCs were induced during AV reentrant tachycardia at 10 ms decrements in patients with left free wall (n = 15), posteroseptal (n = 5), and right free wall (n = 3) accessory pathways from the RV apex and then from the summit of the RV septum. When the His was refractory, shortening of the atrial cycle length was noted in 13% of patients with left free wall pathways, in 60% of patients with posteroseptal pathways, and in 100% of patients with right free wall pathways with VPCs from the RV apex, and in 47,100 and 100%, respectively, with VPCs from the summit of the septum. When all VPCs were considered, there was a significant shortening of the atrial cycle length in 67% of patients with left free wall pathways when stimulated from the RV apex, which increased to 93% with summit stimulation. An extrastimulus applied on or after the His effected a significant shortening of the atrial cycle length in no patients with left free wall pathways. The mean maximal shortening of the atrial cycle length when the His was refractory was 4 ± 11 and 9 ± 13 ms for left free wall pathways, 29 ± 30 and 40 ± 11 ms for posteroseptal pathways, and 35 ± 15 and 53 ± 35 ms for right free wall accessory pathway from the apex (p = 0.006) and summit (p = 0.0002), respectively. Stimulation of the summit of the RV septum improves the ability of VPCs to shorten the atrial cycle length during AV reentrant tachycardia.

Management of Acute Right Ventricular Failure

The thin-walled right ventricle compensates poorly for any increase in afterload, and its output abruptly decreases with small elevations in pulmonary vascular resistance. In patients who have acute right ventricular (RV) dysfunction following bypass, it is, therefore, important to maintain pulmonary vascular resistance at normal or reduced levels. The location and movement of the RV septum may have a dramatic impact on RV contraction, and abnormalities of left ventricular function all affect RV function. Inadequate intraoperative protection has also been implicated in impaired RV function, and there is some evidence that caution is required during removal of air from the left side of the heart and resumption of ventilation. Volume expansion, pharmacological intervention, and mechanical devices have all been used successfully in patients with RV failure. Volume loading is the basis of treatment when the pulmonary vascular resistance is normal. When this alone is insufficient, or when pulmonary vascular resistance is elevated, inotropic agents may be useful. Clinical reports have demonstrated that amrinone, a member of the new class of inotropic fraction-III phosphodiesterase inhibitors, is an effective agent for the management of RV dysfunction following bypass. Correction of septal wall dislocation may be achieved with intraaortic balloon pumps.

Preload Dependence of Right Ventricular Blood How: I. The Normal Right Ventricle

Right ventricular (RV) failure is commonly treated with intravascular volume expansion to increase the RV–left atrial pressure gradient and improve left-sided filling. As RV pressure rises, chamber distention occurs and wall tension increases. These studies were designed to determine if increased wall tension might impede RV myocardial blood flow in the normal canine right ventricle and thus contribute to RV failure. Hemodynamic data, the septal–RV free wall dimension, and RV myocardial blood flow were obtained at low and high levels of preload and in both the autoregulated and vasodilated (adenosine, 2 mg per kilogram of body weight per minute) states. Elevated filling pressure decreased RV myocardial blood flow in both the autoregulated (0.85 ± 0.18 to 0.67 ± 0.15 ml/min/gm; p < .05) and vasodilated (2.25 ± 0.50 to 0.85 ± 0.25 ml/min/gm; p < .05) states but did not change the transmural distribution of blood flow to the right ventricle. Vasodilator reserve was markedly impaired in the high-preload state. These observations suggest that preload is an important determinant of RV myocardial blood flow. Volume loading to treat RV dysfunction may be limited by impairment of RV myocardial blood flow.

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation: LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.

Right ventricular contractile function in children with congenital heart disease

Indexes of right ventricular (RV) systolic function were evaluated in 41 patients undergoing cardiac catheterization. High-fidelity tracings were used to determine RV pressure, maximal RV dP/dt and the velocity of contractile element shortening at a developed pressure of 10 mm Hg (VCE10). In 14 children with an RV systolic pressure <35 mm Hg, normal RV volume, pulmonary vascular resistance (PVR) <3 units·m 2 and no shunts (our normal group), mean (± Standard deviation) RV dP/dt was 437 ± 116 mm Hg·s −1 and VCE10 was 1.15 ± 0.33 muscle length·S −1. In patients with RV systolic hypertension due to valvular pulmonary stenosis or isolated increases in PVR, mean values for RV dP/dt and VCE10 were significantly (p <0.05) greater than the normal values. In patients with a ventricular septal defect, RV hypertension and normal PVR, VCE10 was normal but RV dP/dt was significantly elevated. Children with chronic RV volume overload had normal RV contractile indexes. No patient in any group had values for RV dP/dt or VCE10 that were less than normal (mean normal — 2 Standard deviations). This study establishes for the first time the indexes of RV isovolumic systole in children. It also shows that RV contractile function is preserved in young patients with chronic RV pressure or volume overload who do not have overt congestive heart failure.