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PubMed1994

Does septal position affect right ventricular function during left ventricular assist in an experimental porcine model?

Right ventricular (RV) failure has been a major problem with patients supported by left ventricular (LV) assist devices (LVADs). To assess the importance of interventricular septal (IVS) position as a mechanism of RV failure, 7 Yorkshire pigs underwent implantation of a Thoratec LVAD. RV function was assessed before and during LVAD operation under differing conditions: (1) with an LV intraventricular latex balloon inflated or deflated to alter IVS position and (2) with and without pulmonary artery (PA) constriction to assess the effect of changes in afterload. RV stroke work, RV dP/dt, and RV end-diastolic length did not change significantly with LVAD operation or with changing afterload conditions. Septal shift was documented as a change in LV shape index (LVSI) calculated using echocardiography. LVSI decreased by 11% when the LVAD was turned on, indicating leftward shifting of the IVS (P = .01). During LVAD support and increased RV afterload, the LVSI decreased by 14.8% (P = .02). RV cardiac output decreased somewhat during LVAD support. However, RV output was worst when the septal position was normalized using the inflated intraventricular balloon during increased RV afterload (P = .05). Unloading by the LVAD of the left ventricle results in a leftward shift of the interventricular septum, which does not appear to adversely affect RV function. However, during conditions of increased RV afterload, septal shifting may be beneficial to RV function.

Animals↗
PubMed2005

Pretreatment with pinacidil promotes arrhythmias in an isolated tissue model of cardiac ischemia and reperfusion.

It is not clear whether activation of ATP-sensitive potassium channels (K(ATP)) with pinacidil in advance of ischemia and reperfusion promotes or suppresses arrhythmias. This study determines the effects of pinacidil pretreatment on arrhythmias and the changes in cellular electrophysiological parameters in segments of guinea pig right ventricular free walls exposed to simulated ischemia and reperfusion. Microelectrode recordings were made from endo- and epicardium during endocardial pacing. Preparations were superfused with Tyrode's solution and then exposed for 5 min to either 100 muM pinacidil or its solvent. After a 5-min washout, preparations were exposed to 15 min of ischemic conditions (hypoxia, hypercapnia, hyperkalemia, acidosis, lactate accumulation, and glucose-free) followed by reperfusion with Tyrode's solution. Pinacidil pretreatment increased ischemia-induced abbreviation of endo- and epicardial action potential durations and effective refractory periods. Pinacidil had no effect on endocardial conduction times but greatly prolonged transmural conduction during ischemia and early reperfusion, and it increased the incidence of transmural conduction block. Pinacidil pretreatment caused a significant increase in the incidence of arrhythmias in ischemia and reperfusion. Reperfusion arrhythmias in control preparations had electrophysiological characteristics of activity initiated by afterpotentials; however, arrhythmias with these characteristics were absent in pinacidil-pretreated preparations, and all reperfusion arrhythmias exhibited characteristics of reentry. The increased incidence of re-entrant arrhythmias is likely explained by pinacidil-induced reduction in effective refractory periods in combination with prolonged transmural conduction times. Thus, pinacidil pretreatment enhanced the effects of ischemia and reperfusion on action potential duration, effective refractory period, and transmural conduction, and it promoted re-entrant arrhythmias.

Animals↗
PubMed1996

Assessment of right ventricle function and pulmonary artery circulation by cine-MRI in patients with AIDS.

OBJECTIVE: To evaluate right ventricle (RV) anatomy and performance and its relationships with pulmonary circulation in AIDS patients. DESIGN: We conducted a prospective blinded study by using cine-MRI, a well-accepted method to assess RV and pulmonary circulation. SETTING: A university hospital. PARTICIPANTS: Ten healthy volunteers and 13 asymptomatic AIDS patients. MEASUREMENTS: RV end-diastolic and end-systolic volumes, RV ejection fraction (RVEF), pulmonary artery (PA) diameter, main pulmonary artery distensibility (MPAD), RV free wall diastolic thickness (RVWT), and RV mass were measured. The RVWT/left ventricular wall thickness index was calculated. RESULTS: AIDS patients had significantly increased RV end-diastolic and end-systolic volumes and decreased RVEF (50 +/- 10 vs 59 +/- 6; p < 0.03). Four AIDS patients had RV wall motion abnormalities; 5 (38%) had an RVEF under 45%. RVWT, the RVWT/left ventricular wall thickness index, and PA diameter were significantly increased in AIDS patients. RV mass was increased in 54% of AIDS patients. MPAD was significantly lower in AIDS patients (18.8 +/- 15 vs 26 +/- 4; p < 0.01). A significant relationship was found between RV mass and MPAD (r = 0.76; p = 0.02). CONCLUSIONS: RV function is frequently impaired in AIDS patients. Anatomic and functional abnormalities found in RV and PA parameters suggest a systolic overload on RV. Pulmonary circulation abnormalities may influence RV structure and function in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Prevalence and electrocardiographic characteristics of idiopathic ventricular arrhythmia originating in the free wall of the right ventricular outflow tract.

BACKGROUND: The prevalence and ECG characteristics of idiopathic ventricular arrhythmia originating in the free wall of the right ventricular outflow tract (RVOT) require further clarification, which was the aim of the present study of 110 patients with idiopathic ventricular tachycardia (n=34) or premature ventricular contraction (n=76; OT-VT/PVC) who underwent successful catheter ablation at the RVOT. METHODS AND RESULTS: Ten OT-VT/PVCs (9%) were ablated successfully at the free wall (FW-VT/PVC); the remaining 100 (91%) were ablated at the RVOT septum (Sep-VT/PVC). R wave amplitudes in the inferior leads were significantly smaller in FW-VT/PVC than in Sep-VT/PVC (p<0.01). An RR' pattern in the inferior leads was observed significantly more often in FW-VT/PVC than in Sep-VT/PVC (p<0.001). QS-wave amplitude in each of leads V(1) to V(3) was significantly deeper in FW-VT/PVC than in Sep-VT/PVC (p<0.001). ECG criteria requiring an RR' pattern in all inferior leads as well as an S-wave amplitude of at least 3.0 mV in lead V(2) differentiated FW-VT/PVC from Sep-VT/PVC with high sensitivity, specificity, and predictive accuracy. CONCLUSIONS: Although FW-VT/PVC has a relatively low prevalence, it has several distinctive ECG characteristics and detailed ECG analysis can differentiate it from Sep-VT/PVC.

Adult↗
PubMed2003

Genetic basis for chamber-specific ventricular phenotypes in the rat infarct model.

BACKGROUND: We, and others, have previously reported a strong correlation between increased inter-ventricular dispersion of repolarization and the occurrence of fatal arrhythmia in animal models of CHF. The existence of this and other such distinct electrophysiologic phenotypes in right (RV) vs. left ventricles (LV) could be explained by chamber-specific patterns of gene expression. METHODS: We employed microarray gene profiling of 13824 sequence-verified, nonredundant rodent cDNAs to compare myocardial gene expression in RV vs. LV of rats with surgically induced myocardial infarction (MI: n=3) and in sham-operated animals (Sham: n=3). RESULTS: Significant LV infarction (32+/-4% LV) and severe CHF were observed in all MI animals at 4 weeks. In Sham animals, 937 genes exhibited significant differential expression in RV vs. LV myocardium. In MI animals, 1158 genes exhibited significant differential expression in RV vs. LV. Of those genes exhibiting significant differential expression, only 241 were common to both Sham and MI animals. Differentially expressed genes included those involved in signal transduction, cell growth and maintenance, and apoptosis. Genes with potential roles in altered dispersion of repolarization included voltage-dependent Ca(2+) channel gamma subunit (MI 8-fold increasing) and K(+) inwardly rectifying channel subfamily J, member 10 (MI 6-fold decreasing). Gap junction membrane channel protein alpha 4 (MI 6-fold decreasing) and cardiac troponin I (MI 8-fold decreasing) were also significantly differentially expressed. Inter-ventricular comparisons revealed significantly greater alterations in gene expression vs. intra-ventricular comparisons. CONCLUSIONS: Microarray gene profiling has revealed candidate genes, some of them novel, which may account for chamber-specific ventricular electrophysiologic phenotypes, both in physiologic as well as in arrhythmogenic states such as CHF.

Animals↗
PubMed2003

Total right ventricular exclusion improves left ventricular function in patients with end-stage congestive right ventricular failure.

BACKGROUND: We developed a total right ventricular (RV) exclusion procedure for the treatment of isolated congestive RV failure. The objective of the present study was to elucidate the effects of a complete removal of RV volume overload (RVVO) on the surgically created single left ventricle (LV). METHODS AND RESULTS: Three adults (2 arrhythmogenic RV dysplasia, 1 Ebstein) and 5 children (all Ebstein) in NYHA class IV underwent the procedure. The RV free wall was resected from the heart, and the tricuspid orifice was closed. Pulmonary blood supply was obtained by a cavopulmonary connection in 6 patients and a systemic-pulmonary shunt in 2. The LV function was evaluated by 2-dimensional echocardiography 1 month after the surgery. All patients are alive. The paradoxical movement of the interventricular septum and geometry of the LV expressed by its eccentricity (2.1 to 1.2, P<0.01) were normalized after the operation in all 8 patients. LV end-diastolic volumes (59% to 109% of normal value, P<0.01), indexed maximal left atrial area (6.5 to 10.5 cm2/m2, P<0.01), LV ejection fraction (27% to 62%, P<0.01), and cardiac index (2.1 to 3.3 L/min/m2, P<0.05) all significantly increased. CONCLUSIONS: Removal of the RVVO by means of the total RV exclusion procedure provides effective volume loading, restores a cylindrical shape, and improves contractile function of the LV, thus leading to increased systemic output.

Adult↗
PubMed2001

Left ventricular dysfunction after long-term right ventricular apical pacing in the young.

OBJECTIVES: The goal of this study was to assess long-term global left ventricular (LV) function in patients paced from the right ventricular (RV) apex at a young age. BACKGROUND: Ventricular contraction asynchrony with short-term RV apical pacing has been associated with reduced LV pump function and relaxation. The long-term effect of RV apical pacing on global LV function in the young remains unknown. METHODS: Twenty-four patients with normal segmental anatomy paced from the RV apex (follow-up 1 to 19 years) underwent noninvasive assessment of global LV function with automated border detection echocardiography-derived fractional area of change (FAC), coupled with the Doppler index of myocardial performance (MPI). Data were analyzed from 24 RV-paced patients (mean follow-up 9.5 years, age 19 years, body surface area [BSA] 1.6 m2, QRS duration 140 ms) and compared with 33 age- and BSA-matched control subjects (age 16.4 years, BSA 1.6 m2). Multiple linear regression analysis was performed to identify patient variables that can affect these indexes of LV function. RESULTS: Assessment of LV function (median follow-up 10 years) in 24 paced patients demonstrated impaired area- and Doppler flow-derived indexes of LV systolic and diastolic function, compared with those indexes of control subjects (FAC: 52% vs. 60%, p < 0.01; MPI: 0.46 vs. 0.34, p < 0.01). Paced QRS interval and age were found to significantly influence global LV contraction in these patients (R2 = 0.4, p < 0.05). CONCLUSIONS: In the presence of impaired LV function with long-term RV apical pacing, alternative sites of ventricular pacing that simulate normal biventricular electrical activation should be explored to preserve function in pediatric patients in need of long-term pacing.

Adolescent↗
PubMed2006

Enhanced ubiquitination of cytoskeletal proteins in pressure overloaded myocardium is accompanied by changes in specific E3 ligases.

Ubiquitin conjugation of proteins is critical for cell homeostasis and contributes to both cell survival and death. Here we studied ubiquitination of proteins in pressure overloaded (PO) myocardium in the context of cardiomyocyte survival. Analysis using a feline right ventricular pressure overload (RVPO) model revealed a robust and transient increase in ubiquitination of proteins present in the Triton X-100-insoluble fraction in 24 to 48 h PO myocardium, and confocal micrographs indicate this increase in ubiquitination occurs subsarcolemmaly near the intercalated disc area of cardiomyocytes. The ubiquitination was accompanied by changes in E3 ligases including Cbl, E6AP, Mdm2 and cIAP in the same period of PO, although atrophy-related E3 ligases, MuRF1 and MuRF3 were unaltered. Furthermore, Cbl displayed a substantial increase in both levels of expression and tyrosine phosphorylation in 48 h PO myocardium. Confocal studies revealed enrichment of Cbl at the intercalated discs of 48 h PO cardiomyocytes, as evidenced by its colocalization with N-cadherin. Although apoptosis was observed in 48 h PO myocardium by TUNEL staining, cardiomyocytes showing ubiquitin staining were not positive for TUNEL staining. Furthermore, 48 h PO resulted in the phosphorylation of inhibitor of nuclear factor kappa B (IkappaB), suggesting its ubiquitin-mediated degradation and the nuclear localization of NFkappaB for the expression of specific cell survival factors such as cIAPs. Together these data indicate that increased levels of E3 ligases that regulate cell homeostasis and promote cell survival could ubiquitinate multiple cytoskeletal protein targets and that these events that occur during the early phase of PO may contribute to both cardiomyocyte survival and hypertrophy.

Animals↗
PubMed2005

Acute changes of biventricular gene expression in volume and right ventricular pressure overload.

OBJECTIVE: We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-alpha), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca2+-handling proteins (SERCA2a, phospholamban and calsequestrin). METHODS: Male Wistar rats (n=45) instrumented with pressure tip micromanometers in right (RV) and left ventricular (LV) cavities were assigned to one of three protocols: i) Acute RV pressure overload induced by pulmonary trunk banding in order to double RV peak systolic pressure, during 120 or 360 min; ii) acute volume overload induced by dextran40 infusion (5 ml/h), during 120 or 360 min; iii) Sham. RV and LV samples were collected for mRNA quantification. RESULTS: BNP upregulation was restricted to the overloaded ventricles. TNF-alpha, IL-6, ppET-1, SERCA2a and phospholamban gene activation was higher in volume than in pressure overload. IGF-1 overexpression was similar in both types of overload, but was limited to the RV. TNF-alpha and CSQ mRNA levels were increased in the non-overloaded LV after pulmonary trunk banding. No significant changes were detected in ACE or iNOS expression. RV end-diastolic pressures positively correlated with local expression of BNP, TNF-alpha, IL-6, IGF-1, ppET-1 and SERCA2a, while RV peak systolic pressures correlated only with local expression of IL-6, IGF-1 and ppET-1. CONCLUSIONS: Acute cardiac overload alters myocardial gene expression profile, distinctly in volume and pressure overload. These changes correlate more closely with diastolic than with systolic load. Nonetheless, gene activation is also present in the non-overloaded LV of selectively RV overloaded hearts.

Acute Disease↗
PubMed1998

Real-time three-dimensional echocardiography for determining right ventricular stroke volume in an animal model of chronic right ventricular volume overload.

BACKGROUND: The lack of a suitable noninvasive method for assessing right ventricular (RV) volume and function has been a major deficiency of two-dimensional (2D) echocardiography. The aim of our animal study was to test a new real-time three-dimensional (3D) echo imaging system for evaluating RV stroke volumes. METHODS AND RESULTS: Three to 6 months before hemodynamic and 3D ultrasonic study, the pulmonary valve was excised from 6 sheep (31 to 59 kg) to induce RV volume overload. At the subsequent session, a total of 14 different steady-state hemodynamic conditions were studied. Electromagnetic (EM) flow probes were used for obtaining aortic and pulmonic flows. A unique phased-array volumetric 3D imaging system developed at the Duke University Center for Emerging Cardiovascular Technology was used for ultrasonic imaging. Real-time volumetric images of the RV were digitally stored, and RV stroke volumes were determined by use of parallel slices of the 3D RV data set and subtraction of end-systolic cavity volumes from end-diastolic cavity volumes. Multiple regression analyses showed a good correlation and agreement between the EM-obtained RV stroke volumes (range, 16 to 42 mL/beat) and those obtained by the new real-time 3D method (r=0.80; mean difference, -2.7+/-6.4 mL/beat). CONCLUSIONS: The real-time 3D system provided good estimation of strictly quantified reference RV stroke volumes, suggesting an important application of this new 3D method.

Animals↗
PubMed2000

Right ventricular injury in young swine: effects of catecholamines on right ventricular function and pulmonary vascular mechanics.

Acute right ventricular (RV) injury is commonly encountered in infants and children after cardiac surgery. Empiric medical therapy for these patients results from a paucity of data on which to base medical management and the absence of animal models that allow rigorous laboratory testing. Specifically, exogenous catecholamines have unclear effects on the injured right ventricle and pulmonary vasculature in the young. Ten anesthetized piglets (9-12 kg) were instrumented with epicardial transducers, micromanometers, and a pulmonary artery flow probe. RV injury was induced with a cryoablation probe. Dopamine at 10 microg/kg/min, dobutamine at 10 microg/kg/min, and epinephrine (EP) at 0.1 microg/kg/min were infused in a random order. RV contractility was evaluated using preload recruitable stroke work. Diastolic function was described by the end-diastolic pressure-volume relation, peak negative derivative of the pressure waveform, and peak filling rate. In addition to routine hemodynamic measurements, Fourier transformation of the pressure and flow waveforms allowed calculation of input resistance, characteristic impedance, RV total hydraulic power, and transpulmonary vascular efficiency. Cryoablation led to a stable reproducible injury, decreased preload recruitable stroke work, and impaired diastolic function as measured by all three indices. Infusion of each catecholamine improved preload recruitable stroke work and peak negative derivative of the pressure waveform. Dobutamine and EP both decreased indices of pulmonary vascular impedance, whereas EP was the only inotrope that significantly improved transpulmonary vascular efficiency. Although all three inotropes improved systolic and diastolic RV function, only EP decreased input resistance, decreased pulmonary vascular resistance, and increased transpulmonary vascular efficiency.

Animals↗
PubMed2006

Compression induced by RV pressure overload decreases regional coronary blood flow in anesthetized dogs.

Pulmonary artery constriction (PAC), a model of right ventricular (RV) pressure overload, flattens or inverts the septum and may flatten the left ventricular (LV) free wall. Finite element (FE) analysis predicts that such deformations may cause substantial compression. This study tests the hypothesis that deformation-induced myocardial compressive stress impedes coronary blood flow (CBF). Colored microspheres ( approximately 2 x 10(6)) were injected into the left atrium of 13 open-chest, anesthetized dogs under control conditions and during PAC, which decreased the end-diastolic transseptal pressure gradient (LV - RV) from 1.6 +/- 1.3 to -3.4 +/- 1.7 mmHg. Septal and LV deformation was assessed with the use of two-dimensional echocardiography, and by FE analysis, the hydrostatic component of stress was assessed. Postmortem, a 2.5-cm wide, LV equatorial ring was divided into 16 endocardial and epicardial samples. PAC decreased CBF in the FE-predicted compression zones, areas with the greatest compression having the greatest reductions in CBF. During PAC, compression reached a maximum of 25.3 +/- 1.8 mmHg on the (LV) endocardial sides of the RV insertion points, areas that saw CBF decrease from 1.05 +/- 0.08 to 0.68 +/- 0.05 ml.min(-1).g(-1) (P < 0.001), more than 30%. CBF decreased (from 1.08 +/- 0.07 to 0.81 +/- 0.07 ml.min(-1).g(-1); P < 0.001) on the RV side of the midseptum, an area with as much as 16.0 +/- 1.0 mmHg of compression. Overall, average compressions of 10 mmHg decreased CBF by approximately 30%. We conclude that acute RV pressure overload deforms the septum and LV and induces compressive stresses that reduce CBF substantially. This may help explain why some patients with pulmonary hypertension and no critical coronary disease have chest discomfort indistinguishable from angina pectoris.

Anesthesia↗
PubMed2006

Ventricular remodeling during long-term right ventricular pacing following His bundle ablation.

To investigate ventricular remodeling during long-term right ventricular (RV) pacing after His bundle ablation (HBA) in patients with atrial arrhythmias, a retrospective analysis was performed on echocardiographic data from 45 patients (mean age 57 +/- 11 years) with atrial arrhythmias who underwent HBA and pacemaker implantation (HBA-PI) to control ventricular rate. Echocardiography was performed 1 year before HBA-PI, and up to 7 +/- 2 years of follow-up was conducted. An inverse linear relation was found between the relative increase of left ventricular (LV) end-diastolic diameter (EDD) during long-term RV pacing and LVEDD before HBA-PI (r = -0.61, p<0.001). Patients were divided into 2 groups: those with LVEDDs smaller than the mean LVEDD of 50 mm (group I, 46 +/- 2 mm, n = 28) and those with LVEDDs >50 mm (group II, 56 +/- 4 mm, n = 17). Before HBA-PI, patients in group I had significantly smaller LV weights (167 +/- 44 vs 238 +/- 56 g) and LV end-systolic diameters (30 +/- 2 vs 42 +/- 7 mm) and higher LV ejection fractions (64 +/- 5% vs 49+/- 12%) than those in group II. In group I, long-term RV pacing increased LVEDD, LV end-systolic diameter, LV weight, and left atrial diameter; increased mitral regurgitation; and decreased the LV ejection fraction and LV fractional shortening. No significant changes were observed during long-term RV pacing in group II. In conclusion, long-term RV pacing after HBA adversely affects LV structure and function in patients with initially normal LV dimensions and function.

Arrhythmias, Cardiac↗
PubMed2005

Arrhythmogenic right ventricular dysplasia: a United States experience.

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is an inherited cardiomyopathy characterized by right ventricular dysfunction and ventricular arrhythmias. The purpose of our study was to describe the presentation, clinical features, survival, and natural history of ARVD in a large cohort of patients from the United States. METHODS AND RESULTS: The patient population included 100 ARVD patients (51 male; median age at presentation, 26 [interquartile range {IQR}, 18 to 38; range, 2 to 70] years). A familial pattern was observed in 32 patients. The most common presenting symptoms were palpitations, syncope, and sudden cardiac death (SCD) in 27%, 26%, and 23% of patients, respectively. Among those who were diagnosed while living (n=69), the median time between first presentation and diagnosis was 1 (range, 0 to 37) year. During a median follow-up of 6 (IQR, 2 to 13; range, 0 to 37) years, implantable cardioverter/defibrillators (ICD) were implanted in 47 patients, 29 of whom received an appropriate ICD discharge, including 3 patients who received the ICD for primary prevention. At follow-up, 66 patients were alive, of whom 44 had an ICD in place, 5 developed signs of heart failure, 2 had a heart transplant, and 18 were on drug therapy. Thirty-four patients died either at presentation (n=23: 21 SCD, 2 noncardiac deaths) or during follow-up (n=11: 10 SCD, 1 of biventricular heart failure), of whom only 3 were diagnosed while living and 1 had an ICD implanted. On Kaplan-Meier analysis, the median survival in the entire population was 60 years. CONCLUSIONS: ARVD patients present between the second and fifth decades of life either with symptoms of palpitations and syncope associated with ventricular tachycardia or with SCD. Diagnosis is often delayed. Once diagnosed and treated with an ICD, mortality is low. There is a wide variation in presentation and course of ARVD patients, which can likely be explained by the genetic heterogeneity of the disease.

Adolescent↗
PubMed2001

Dynamics of intramural and transmural reentry during ventricular fibrillation in isolated swine ventricles.

The intramural dynamics of ventricular fibrillation (VF) remain poorly understood. Recent investigations have suggested that stable intramural reentry may underlie the mechanisms of VF. We performed optical mapping studies of VF in isolated swine right ventricles (RVs) and left ventricles (LVs). Nine RV walls were cut obliquely in their distal edge exposing the transmural surface. Six LV wedge preparations were also studied. Results showed that intramural reentry was present. In RV, 28 of 44 VF episodes showed reentry; 15% of the activation pathways were reentrant. Except for 4 episodes, reentry was transmural, involving subendocardial structures as the papillary muscle (PM) or trabeculae. In LV, reentry was observed in 27 of 27 VF episodes; 23% of the activations were part of reentrant pathways (P<0.05 compared with RV). All LV reentrant pathways were truly intramural (confined to the wall) and were frequently located at the PM insertion. In both ventricles, reentry was spatially and temporally unstable. Histological studies showed abrupt changes in fiber orientation at sites of reentry and wave splitting. Connexin 40 immunostaining demonstrated intramyocardial Purkinje fibers at sites of reentry in the PM root and around endocardial trabeculae. Our results confirm that reentry is frequent-but unstable-in the myocardial wall during VF. In RV, reentry is mostly transmural and requires participation of subendocardial structures. The LV has a greater incidence of reentry and is intramural. Anisotropic anatomic structures played key roles in the generation of wave splitting and in the maintenance of reentry.

Animals↗
PubMed2003

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.

Animals↗
PubMed2007

Hemodynamic improvement is faster after percutaneous ASD closure than after surgery.

OBJECTIVES: Hemodynamic effects of surgical and percutaneous closure of atrial septal defect (ASD) were evaluated. BACKGROUND: ASD causes volume overload of right ventricle (RV) and is associated with distortion and dysfunction of left ventricle (LV). The amount and timing of hemodynamic changes after ASD closure are not well known. METHODS: The study group consisted of 7 children treated surgically and 17 treated in the catheterization laboratory. In the control group, there were 51 healthy children. RV size and LV end-diastolic and systolic dimensions, volumes, and function were examined by two- and three- dimensional echocardiography and serum concentrations of natriuretic peptides measured prior to ASD closure, and 1, 6, and 12 months thereafter. RESULTS: In all children with ASD, during the 1-year follow-up, the z score of RV end-diastolic diameter decreased from a median 5.00 SD to 2.25 SD (P < 0.001). Dilatation of RV did not resolve entirely during 1-year follow-up in either treatment group. End-diastolic LV diameter increased from -1.50 to -0.50 SD (P < 0.001). LV size increased slower in the surgical subgroup but reached control levels in both groups. Concentrations of natriuretic peptides increased during the first month after ASD closure and normalized thereafter in patients treated percutaneously but remained higher than in controls in patients treated surgically. CONCLUSIONS: During 1-year follow-up after ASD closure, RV size decreases but does not normalize in all patients. The size of the LV normalizes after ASD closure but the increase in LV size is slower in patients treated surgically. Serum levels of ANPN and proBNP are elevated prior to ASD closure but decrease thereafter to control levels in patients treated with the percutaneous technique but not in those treated surgically.

Adolescent↗
PubMed2003

Colour tissue Doppler echocardiographic evaluation of right ventricular function in patients with right ventricular infarction.

OBJECTIVE: This study was undertaken to determine right ventricular (RV) function as assessed by colour Doppler tissue imaging (DTI) in patients with RV infarction. METHODS: During the study period, 35 patients were evaluated: 14 patients had an inferior myocardial infarction (MI) with RV infarction and 21 patients had an inferior MI without RV involvement. Twenty age-matched healthy subjects served as controls. The diagnosis of RV infarction was defined by ST segment elevation >0.1 mV in lead V4R. Systolic and early and late diastolic velocities were acquired from the apical four-chamber view at the lateral tricuspid annulus, the septal side of the tricuspid annulus and the RV free mid-wall using colour DTI. RESULTS: Systolic and early diastolic velocities at the lateral tricuspid annulus were significantly reduced in patients with inferior MI with RV infarction compared with those in healthy individuals (7.8 +/- 1 vs. 11 +/- 2 cm/s, p < 0.002) and patients with inferior MI without RV infarction (7.8 +/- 1 vs. 10 +/- 1 cm/s, p < 0.002). The late diastolic lateral annular velocity did not differ between the groups. Systolic and early diastolic RV free wall velocities were also significantly decreased in patients with RV infarction compared with those in healthy individuals (7 +/- 1 vs. 8.7 +/- 1 cm/s, p < 0.01; 6.3 +/- 2 vs. 8.7 +/- 2 cm/s, p < 0.05, respectively) and patients with inferior MI without RV infarction (7 +/- 1 vs. 9 +/- 2 cm/s, p < 0.01; 6.3 +/- 2 vs. 8.3 +/- 2 cm/s, p < 0.05, respectively). CONCLUSION: The evaluation of tricuspid annular and RV free wall velocities using colour DTI provides a rapid and noninvasive tool for assessing RV function in patients with RV infarction.

Aged↗