Influence of the pericardium on right and left ventricular filling in the dog

We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired distensibility of the left ventricle after stiffening of the right ventricle.

Acute and chronic alterations of right ventricular (RV) wall properties can change left ventricular (LV) performance. We investigated whether and how stiffening of the RV free wall alters LV diastolic distensibility. We used cross-circulated isolated hearts, in which the LV and RV were independently controllable. Stiffness of the RV free wall was altered by intramuscular injections of glutaraldehyde into the RV free wall after right coronary artery ligation. We measured circumferential and longitudinal regional lengths in the septum and LV free wall. During data acquisition, RV volume was held constant. After the RV free wall was stiffened by glutaraldehyde, the LV diastolic pressure-volume relation shifted upward and became steeper. Importantly, stiffening of the RV free wall increased the diastolic regional area in the septum and LV free wall under constant LV volume. The augmented regional dimensions may result in enhanced regional tension under constant LV volume and may be related to the observed increase in LV diastolic intracavitary pressure. The impaired LV diastolic distensibility by stiffening of the RV free wall may be at least partly explained by myocardial stretch, probably due to LV deformation.     

Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload

Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.     

Right bundle branch block pattern after uncomplicated right ventricular outflow tract pacing in a patient with a left sided superior vena cava and corrected tetralogy of Fallot

Usually an electrocardiogram after right ventricular (RV) pacing should yield left bundle branch block (LBBB) pattern. However, the presence of right bundle branch block (RBBB) pattern after pacemaker implantation should alert the physician to a malposition of lead. We report a case of 18-year-old female who underwent dual chamber pacemaker implantation and had RBBB pattern post implantation. Detailed evaluation revealed an uncomplicated right ventricular outflow tract pacing. The possible causes of this abnormal pattern after an uncomplicated RV pacing are also reviewed.     

Quantification of interventricular asynchrony during LBBB and ventricular pacing

The quantification of mechanical interventricular asynchrony (IVA) was investigated. In 12 dogs left bundle branch block (LBBB) was induced by radio frequency ablation. Left ventricular (LV) and right ventricular (RV) pressures were recorded before and after induction of LBBB and during LBBB + LV apex pacing at different atrioventricular (AV) delays. Four IVA measures were validated using computer simulations on experimentally obtained pressure signals. The most robust measure for IVA was the time delay between the upslope of the LV and RV pressure signals (DeltaT(up)), estimated by cross correlation. The induction of experimental LBBB decreased DeltaT(up) from -6.9 +/- 7.0 ms (RV before LV) to -33.9 +/- 7.6 ms (P < 0.05) in combination with a significant decrease of LV maximal first derivative of pressure development over time (dP/dt(max)). During LV apex pacing, DeltaT(up) increased with decreasing AV delay up to +20.9 +/- 14.6 ms (P < 0.05). Interventricular resynchronization (DeltaT(up) = 0 ms) significantly improved LV dP/dt(max) by 15.1 +/- 5.9%. QRS duration increased significantly after induction of LBBB but did not change during LV apex pacing. In conclusion, DeltaT(up) is a reliable measure of mechanical IVA, which adds valuable information concerning the nature of asynchronous activation of the ventricles.     

Diastolic right ventricular filling vortex in normal and volume overload states

Functional imaging computational fluid dynamics simulations of right ventricular (RV) inflow fields were obtained by comprehensive software using individual animal-specific dynamic imaging data input from three-dimensional (3-D) real-time echocardiography (RT3D) on a CRAY T-90 supercomputer. Chronically instrumented, lightly sedated awake dogs (n = 7) with normal wall motion (NWM) at control and normal or diastolic paradoxical septal motion (PSM) during RV volume overload were investigated. Up to the E-wave peak, instantaneous inflow streamlines extended from the tricuspid orifice to the RV endocardial surface in an expanding fanlike pattern. During the descending limb of the E-wave, large-scale (macroscopic or global) vortical motions ensued within the filling RV chamber. Both at control and during RV volume overload (with or without PSM), blood streams rolled up from regions near the walls toward the base. The extent and strength of the ring vortex surrounding the main stream were reduced with chamber dilatation. A hypothesis is proposed for a facilitatory role of the diastolic vortex for ventricular filling. The filling vortex supports filling by shunting inflow kinetic energy, which would otherwise contribute to an inflow-impeding convective pressure rise between inflow orifice and the large endocardial surface of the expanding chamber, into the rotational kinetic energy of the vortical motion that is destined to be dissipated as heat. The basic information presented should improve application and interpretation of noninvasive (Doppler color flow mapping, velocity-encoded cine magnetic resonance imaging, etc.) diastolic diagnostic studies and lead to improved understanding and recognition of subtle, flow-associated abnormalities in ventricular dilatation and remodeling.     

Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

Hypoxia has been reported to alter left ventricular (LV) diastolic function, but associated changes in right ventricular (RV) systolic and diastolic function remain incompletely documented. We used echocardiography and tissue Doppler imaging to investigate the effects on RV and LV function of 90 min of hypoxic breathing (fraction of inspired O(2) of 0.12) compared with those of dobutamine to reproduce the same heart rate effects without change in pulmonary vascular tone in 25 healthy volunteers. Hypoxia and dobutamine increased cardiac output and tricuspid regurgitation velocity. Hypoxia and dobutamine increased LV ejection fraction, isovolumic contraction wave velocity (ICV), acceleration (ICA), and systolic ejection wave velocity (S) at the mitral annulus, indicating increased LV systolic function. Dobutamine had similar effects on RV indexes of systolic function. Hypoxia did not change RV area shortening fraction, tricuspid annular plane systolic excursion, ICV, ICA, and S at the tricuspid annulus. Regional longitudinal wall motion analysis revealed that S, systolic strain, and strain rate were not affected by hypoxia and increased by dobutamine on the RV free wall and interventricular septum but increased by both dobutamine and hypoxia on the LV lateral wall. Hypoxia increased the isovolumic relaxation time related to RR interval (IRT/RR) at both annuli, delayed the onset of the E wave at the tricuspid annulus, and decreased the mitral and tricuspid inflow and annuli E/A ratio. We conclude that hypoxia in normal subjects is associated with altered diastolic function of both ventricles, improved LV systolic function, and preserved RV systolic function.     

Left ventricular effects on right ventricular developed pressure.

The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.     

Factorial phase analysis of ventricular contraction using equilibrium radionuclide angiography images

Factorial phase analysis (FaPI) represents an alternative method to Fourier phase analysis (FoPI) in the evaluation and detection of abnormalities on cardiac contraction patterns, but it has limitations in representing the sequence in abnormal contraction patterns. In this work we propose a modified factorial phase image (FaPIm) that incorporates more complete information regarding the ventricular contraction sequence. In particular, we analyze and evaluate the contribution of the third eigenimage, in the presence of ventricular dyssynchrony, which has not been sufficiently explored in the literature. We have validated the proposed FaPIm using two Equilibrium Radionuclide Angiography (ERNA) sets of images obtained with a dynamic cardiac phantom and with a numerically simulated phantom. Also, we have tested the proposed representation for a control group of 23 normal subjects and for a sample of 15 patients with Complete Left Bundle Branch Block (LBBB). Whereas FoPI allows us to obtain an image that synthesizes ventricular contraction with the smallest dispersion around the mean values, FaPI and FaPIm show that external areas surrounding ventricular cavities present more dephasing than the rest of the ventricular region and contain more detailed information about the progression of contraction. Also, in the presence of an abnormal contraction pattern, the magnitude of the third eigenvalue was greater than the corresponding eigenvalue obtained for normal simulations. The dispersion plots obtained for a normal contraction pattern show that left ventricle (LV) and right ventricle (RV) information overlap. Therefore, when there is a dyssynchrony between LV and RV contraction it becomes necessary to incorporate the information corresponding to the third factor to achieve a clear separation between regions.In the comparison of the indices of control and LBBB populations, FaPIm shows significant differences in five out of six contraction indices, showing its promising value as a clinical tool.     

Left ventricular resynchronization therapy in a canine model of left bundle branch block

Positive responses to left (LV) and biventricular (BV) stimulation observed in heart failure patients with left bundle branch block (LBBB) suggest a possible mechanism of LV resynchronization. An anesthetized canine LBBB model was developed using radio frequency ablation. Before and after ablation, LV pressure derivative over time (dP/dt) and aortic pulse pressure (PP) were assessed during normal sinus rhythm with right ventricle (RV), LV, or BV stimulation combined with four atrioventricular delays in six dogs. In three more dogs, M-mode echocardiograms of septal and LV posterior wall motion were obtained before and after LBBB and during LV stimulation. LBBB caused QRS widening and hemodynamics deterioration. Before ablation, stimulation alone worsened LV dP/dt and PP. After ablation, LV and BV stimulation maximally increased LV dP/dt by 16% and PP by 7% (P < 0.001), whereas little improvement was observed during RV stimulation. M-mode echocardiogram showed that LBBB resulted in a paradoxical septal wall motion that was corrected by LV stimulation. In conclusion, LV and BV stimulation improved cardiac function in a canine LBBB model via resynchronization of LV excitation and contraction.     

A fiduciary marker-based framework to assess heterogeneity and anisotropy of right ventricular epicardial strains in the beating ovine heart

Quantifying ventricular deformation in health and disease is critical to our understanding of normal heart function, heart disease mechanisms, and the effect of medical treatments. Imaging modalities have been developed that can measure ventricular deformation non-invasively. However, because of the small thickness, complex shape, and anatomic position of the right ventricle, using these technologies to determine its deformation remains challenging. Here we develop a first fiduciary marker-based method to assess heterogeneity and anisotropy of right ventricular epicardial strain across the entire free wall. To this end, we combine a high-density array of sonomicrometry crystals implanted across the entire right ventricular epicardial surface with a subdivision surface algorithm and a large deformation kinematics framework. We demonstrate our approach on four beating ovine hearts and present a preliminary regional analysis of circumferential, longitudinal, and areal strain. Moreover, we illustrate maps of the same strains across the entire right ventricular epicardial surface to highlight their spatial heterogeneity and anisotropy. We observe in these animals that RV epicardial strains vary throughout the cardiac cycle, are heterogeneous across the RV free wall, and are anisotropic with larger compressive strains, i.e., contraction, in the longitudinal direction than in the circumferential direction. Average peak compressive strains vary by region between −3.34% and −8.29% in circumferential direction, and −4.02% and −10.57% in longitudinal direction. In summary, we introduce an experimental framework that will allow us to study disease- and device-induced deformations, and long-term consequences of these deformations, including heterogeneous and anisotropic effects.     

Heterogeneous expression of connexin 43 in the myocardium of rabbit right ventricular outflow tract

The right ventricular outflow tract (RVOT) has been demonstrated as an important focus in idiopathic ventricular arrhythmias. However, the role of the gap junction in this region in arrhythmic events has not been fully investigated. The purpose of this study was to evaluate the expression and distribution of the gap junction protein connexin 43 (Cx43) in the myocardium of the RVOT area of normal adult rabbits. Tissue samples were obtained from 6 regions of normal rabbit heart, i.e. the left ventricle (LV) free wall, the LV papillary muscle, the RVOT free wall, and the RVOT septum which was subdivided into the RV side, the central layer, and the LV side. Immunohistochemical analysis was performed to investigate the characteristics of Cx43 distribution in the RVOT area. In the LV free wall and papillary muscle, Cx43 was abundantly, homogeneously, and approximately equally expressed in end-to-end- and side-to-side intercellular connections. In the free wall of the RVOT, Cx43 expression was poor compared to both these LV regions and side-to-side cell connections were predominant. Cx43 was as richly and homogeneously distributed in the central layer and LV side of the RVOT septum as in the two LV regions. However, in the RV side of the RVOT septum, its distribution was scant and an unstained area was noted. The heterogeneous expression of Cx43 in the RVOT area may serve as substrate for idiopathic ventricular arrhythmia.     

Tailoring cardiac resynchronisation therapy to non-left bundle branch block: Successful cardiac resynchronisation for right bundle branch block with left posterior fascicular block without implantation of a left ventricular lead

Despite advances, cardiac resynchronisation therapy (CRT) remains fundamentally orientated to the dyssynchrony of left bundle branch block (LBBB), in which septo-lateral electrical and mechanical delays predominate. For non-LBBB patients response rates to conventional CRT are lower and mortality and rehospitalisation rates are not reduced. Despite this, alternative approaches which tailor CRT to the differing dyssynchrony patterns of non-LBBB have yet to be developed. In the specific non-LBBB subgroup of right bundle branch block (RBBB) with left posterior fascicular block (LPFB), ventricular conduction via the left anterior fascicle results in a unique early lateral, and late septal depolarisation, or lateral to septal left ventricular (LV) delay, an electrical sequence which is followed mechanically. This latero-septal delay is somewhat the reverse of LBBB and was overcome by fusing right ventricular (RV) septal pacing with intrinsic conduction via the left anterior fascicle, achieving successful resynchronisation without implantation of a left ventricular lead. A stable fusion pattern was achieved via the ‘Negative AV Hysteresis with Search’ algorithm (Abbott, St Paul, Minnesota). Improvement in all standard CRT response indices was achieved at 3 months: QRS duration was reduced from 153 to 106 ms, ejection fraction increased from 14 to 32%, and LV end-systolic and end-diastolic diameters reduced by 19% and 12.5% respectively. NYHA class improved from III-IV to class II. Cardiac resynchronisation for RBBB with LPFB can be successfully achieved with a standard pacemaker or defibrillator without left ventricular lead implantation by fusing RV septal-only pacing with intrinsic conduction.     

A 2D FE model of the heart demonstrates the role of the pericardium in ventricular deformation

During pulmonary artery constriction (PAC), an experimental model of acute right ventricular (RV) pressure overload, the interventricular septum flattens and inverts. Finite element (FE) analysis has shown that the septum is subject to axial compression and bending when so deformed. This study examines the effects of acute PAC on the left ventricular (LV) free wall and the role the pericardium may play in these effects. In eight open-chest anesthetized dogs, LV, RV, aortic, and pericardial pressures were recorded under control conditions and with PAC. Model dimensions were derived from two-dimensional echocardiography minor-axis images of the heart. At control (pericardium closed), FE analysis showed that the septum was concave to the LV; stresses in the LV, RV, and septum were low; and the pericardium was subject to circumferential tension. With PAC, RV end-diastolic pressure exceeded LV pressure and the septum inverted. Compressive stresses developed circumferentially in the septum out to the RV insertion points, forming an arch-like pattern. Sharp bending occurred near the insertion points, accompanied by flattening of the LV free wall. With the pericardium open, the deformations and stresses were different. The RV became much larger, especially with PAC. With PAC, the arch-like circumferential stresses still developed in the septum, but their magnitudes were reduced, compared with the pericardium-closed case. There was no free wall inversion and flattening was less. From these FE results, the pericardium has a significant influence on the structural behavior of the septum and the LV and RV free walls. Furthermore, the deformation of the heart is dependent on whether the pericardium is open or closed.     

Quantification of the relative contribution of the different right ventricular wall motion components to right ventricular ejection fraction: the ReVISION method

Three major mechanisms contribute to right ventricular (RV) pump function: (i) shortening of the longitudinal axis with traction of the tricuspid annulus towards the apex; (ii) inward movement of the RV free wall; (iii) bulging of the interventricular septum into the RV and stretching the free wall over the septum. The relative contribution of the aforementioned mechanisms to RV pump function may change in different pathological conditions.Our aim was to develop a custom method to separately assess the extent of longitudinal, radial and anteroposterior displacement of the RV walls and to quantify their relative contribution to global RV ejection fraction using 3D data sets obtained by echocardiography.Accordingly, we decomposed the movement of the exported RV beutel wall in a vertex based manner. The volumes of the beutels accounting for the RV wall motion in only one direction (either longitudinal, radial, or anteroposterior) were calculated at each time frame using the signed tetrahedron method. Then, the relative contribution of the RV wall motion along the three different directions to global RV ejection fraction was calculated either as the ratio of the given direction’s ejection fraction to global ejection fraction and as the frame-by-frame RV volume change (?V/?t) along the three motion directions.The ReVISION (Right VentrIcular Separate wall motIon quantificatiON) method may contribute to a better understanding of the pathophysiology of RV mechanical adaptations to different loading conditions and diseases.     

Differential effects of left ventricular pacing sites in an acute canine model of contraction dyssynchrony

The goal of the present study was to assess the effects of left ventricular (LV) pacing sites (apex vs. free wall) on radial synchrony and global LV performance in a canine model of contraction dyssynchrony. Ultrasound tissue Doppler imaging and hemodynamic (LV pressure-volume) data were collected in seven anesthetized, opened-chest dogs. Right atrial (RA) pacing served as the control, and contraction dyssynchrony was created by simultaneous RA and right ventricular (RV) pacing to induce a left bundle-branch block-like contraction pattern. Cardiac resynchronization therapy (CRT) was implemented by adding simultaneous LV pacing to the RV pacing mode at either the LV apex (CRTa) or free wall (CRTf). A new index of synchrony was developed via pair-wise cross-correlation analysis of tissue Doppler radial strain from six midmyocardial cross-sectional regions, with a value of 15 indicating perfect synchrony. Compared with RA pacing, RV pacing significantly decreased radial synchrony (11.1 +/- 0.8 vs. 4.8 +/- 1.2, P < 0.01) and global LV performance (cardiac output: 2.0 +/- 0.3 vs. 1.4 +/- 0.1 l/min and stroke work: 137 +/- 22 vs. 60 +/- 14 mJ, P < 0.05). Although both CRTa and CRTf significantly improved radial synchrony, only CRTa markedly improved global function (cardiac output: 2.1 +/- 0.2 l/min and stroke work: 113 +/- 13 mJ, P < 0.01 vs. RV pacing). Furthermore, CRTa decreased LV end-systolic volume compared with RV pacing without any change in LV end-systolic pressure, indicating an augmented global LV contractile state. Thus, LV apical pacing appears to be a superior pacing site in the context of CRT. The dissociation between changes in synchrony and global LV performance with CRTf suggests that regional analysis from a single plane may not be sufficient to adequately characterize contraction synchrony.     

RV functional imaging: 3-D echo-derived dynamic geometry and flow field simulations

We describe a novel functional imaging approach for quantitative analysis of right ventricular (RV) blood flow patterns in specific experimental animals (or humans) using real-time, three-dimensional (3-D) echocardiography (RT3D). The method is independent of the digital imaging modality used. It comprises three parts. First, a semiautomated segmentation aided by intraluminal contrast medium locates the RV endocardial surface. Second, a geometric scheme for dynamic RV chamber reconstruction applies a time interpolation procedure to the RT3D data to quantify wall geometry and motion at 400 Hz. A volumetric prism method validated the dynamic geometric reconstruction against simultaneous sonomicrometric canine measurements. Finally, the RV endocardial border motion information is used for mesh generation on a computational fluid dynamics solver to simulate development of the early RV diastolic inflow field. Boundary conditions (tessellated endocardial surface nodal velocities) for the solver are directly derived from the endocardial geometry and motion information. The new functional imaging approach may yield important kinematic information on the distribution of instantaneous velocities in the RV diastolic flow field of specific normal or diseased hearts.     

Stereo photogrammetric studies on the dynamic geometry of the canine left ventricular epicardium

Length-time relationships of segments of the left ventricular epicardium were determined in eight anesthetized thoracotomized canine subjects. The instantaneous three-dimensional positions of four epicardial sites on both the anterior wall and lateral free wall were measured using a system (Analytic Stop Motion Stereo Photogrammetry) developed in these laboratories. Segmental shortening was found to be maximum at approximately right angles to the Left Anterior Descending Coronary Artery (LAD) in all regions studied, with the greatest extent of shortening in the mid base-apex region. Shortening of segments approximately parallel to the LAD was negligible near the septum and greatest on the lateral free wall. These findings support an asymmetric anisotropic model of normal ventricular systole in which all points on the lateral free wall move towards one another while simultaneously pivoting about a point near the apex, moving toward a relatively fixed septum.     

Catheter Ablation of Idiopathic Premature Ventricular Contractions and Ventricular Tachycardias Originating from Right Ventricular Septum

Background

Idiopathic premature ventricular contractions (PVCs) and ventricular tachycardias (IVTs) originating from the subtricuspid septum and near the His bundle have been reported. However, little is known about the prevalence, distribution, electrocardiographic characteristics and the efficacy of radiofrequency catheter ablation (RFCA) for the ventricular arrhythmias arising from the right ventricular (RV) septum. This study aimed to investigate electrocardiographic characteristics and effects of RFCA for patients with symptomatic PVCs/IVTs, originating from the different portions of the RV septum.

Methodology/Principal Findings

Characteristics of body surface electrocardiogram and electrophysiologic recordings were analyzed in 29 patients with symptomatic PVCs/IVTs originating from the RV septum. Among 581 patients with PVCs/IVTs, the incidence of ventricular arrhythmias originating from the RV septum was 5%. Twenty (69%) had PVCs/IVTs from the septal portion of the tricuspid valvular RV region (3 from superoseptum, 15 from midseptum, 2 from inferoseptum), and 9 (31%) from the septal portion of the basal RV (1 from superoseptum, 4 from midseptum, 4 from inferoseptum). There were different characteristics of ECG of PVCs/VT originating from the different portions of the RV septum. Twenty-seven of 29 patients with PVCs/IVTs arising from the RV septum were successfully ablated (93.1% acute success).

Conclusions/Significance

ECG characteristics of PVCs/VTs originating from the different portions of the RV septum are different, and can help regionalize the origin of these arrhythmias. The septal portion of the tricuspid valvular RV region was the preferential site of origin. RFCA was effective and safe for the PVCs/IVTs arising from the RV septum.     

RV instantaneous intraventricular diastolic pressure and velocity distributions in normal and volume overload awake dog disease models

Intraventricular diastolic right ventricular (RV) flow field dynamics were studied by functional imaging using three-dimensional (3D) real-time echocardiography with sonomicrometry and computational fluid dynamics in seven awake dogs at control with normal wall motion (NWM) and RV volume overload with diastolic paradoxical septal motion. Burgeoning flow cross section between inflow anulus and chamber walls induces a convective pressure rise, which represents a "convective deceleration load" (CDL). High spatiotemporal resolution dynamic pressure and velocity distributions of the intraventricular RV flow field revealed time-dependent, subtle interactions between intraventricular local acceleration and convective pressure gradients. During the E-wave upstroke, the total pressure gradient along intraventricular flow is the algebraic sum of a pressure decrease contributed by local acceleration and a pressure rise contributed by a convective deceleration that partially counterbalances the local acceleration gradient. This underlies the smallness of early diastolic intraventricular gradients. At peak volumetric inflow, local acceleration vanishes and the total adverse intraventricular gradient is convective. During the E-wave downstroke, the strongly adverse gradient embodies the streamwise pressure augmentations from both local and convective decelerations. It induces flow separation and large-scale vortical motions, stronger in NWM. Their dynamic corollaries on intraventricular pressure and velocity distributions were ascertained. In the NWM pattern, the strong ring-like vortex surrounding the central core encroaches on the area available for flow toward the apex. This results in higher linear velocities later in the downstroke of the E wave than at peak inflow rate. The augmentation of CDL by ventriculoannular disproportion may contribute to E wave and E-to-A ratio depression with chamber dilatation.