Right Ventricular Dyssynchrony Research Articles

The Incremental Value of Right Ventricular Indices for Predicting Response to Cardiac Resynchronization Therapy

Right ventricular (RV) dysfunction in chronic heart failure (HF) is associated with poor prognosis. Cardiac resynchronization therapy (CRT) is an established method of improving prognosis in HF. However, the majority of known indices predictive of response to CRT are based on left ventricular (LV) assessment. The authors hypothesized that baseline RV function and tissue Doppler-derived dyssynchrony may have incremental value over LV dyssynchrony measures for predicting CRT response. In this retrospective study, echocardiographic examinations were performed in 90 patients before pacemaker implantation and up to 18 months afterward. CRT results were evaluated using clinical criteria (death, hospitalization for decompensation, change in New York Heart Association class ≥1, and 10% decreases in both peak ventilatory oxygen uptake and 6-min walking distance) and reverse remodeling (>15% reduction in LV end-systolic volume). Baseline RV dyssynchrony during isovolumic contraction of 26 msec facilitated the segregation of responders from nonresponders with 85% sensitivity and 100% specificity, as well as synchrony in peak deformation of 54 msec, with 89% sensitivity and 67% specificity. The minor axis of the RV inflow tract predicted reverse remodeling after CRT with sensitivity of 73% and specificity of 58% with a cutoff value of 35 mm. According to the clinical criteria, LV indices (end-diastolic and end-systolic volumes) and interventricular delay gave an overall R(2) value of 0.20 (86.2% correctly classified patients; area under the curve, 0.80). The addition of RV dyssynchrony parameters (measured in peak strain and isovolumic contraction peak velocities) significantly increased the power of the model (R(2) = 0.86; 100% of patients correctly classified; area under the curve, 1; P for change in R(2) < .0001). The value of baseline RV function analysis is incremental to LV indices for the prediction of clinical response to CRT but not reverse remodeling. RV synchronous longitudinal deformation and RV dyssynchronous isovolumic velocity are independent predictors of clinical response to CRT.

Exercise induces biventricular mechanical dyssynchrony in children with repaired tetralogy of Fallot

ObjectiveThe mechanisms underlying adverse electro-mechanical interaction after tetralogy of Fallot (TOF) repair remain unclear. This study investigated biventricular dyssynchrony in children with TOF and its relationship to exercise, QRS duration...

Biventricular stimulation improves right and left ventricular function after tetralogy of Fallot repair: Acute animal and clinical studies

Optimal treatment of right ventricular (RV) dysfunction observed in patients after tetralogy of Fallot (TOF) repair is unclear. Studies of biventricular (BiV) stimulation in patients with congenital heart disease have been retrospective or have included patients with heterogeneous disorders. The purpose of this study was to determine the effects on cardiac function of stimulating at various cardiac sites in an animal model of RV dysfunction and dyssynchrony and in eight symptomatic adults with repaired TOF. Pulmonary stenosis and regurgitation as well as RV scars were induced in 15 piglets to mimic repaired TOF. The hemodynamic effects of various configurations of RV and BiV stimulation were compared with sinus rhythm (SR) 4 months after surgery. In eight adults with repaired TOF, RV and left ventricular (LV) dP/dt(max) were measured invasively during SR, apical RV stimulation, and BiV stimulation. At 4 months, RV dilation, dysfunction, and dyssynchrony were present in all piglets. RV stimulation caused a decrease in LV function but no change in RV function. In contrast, BiV stimulation significantly improved LV and RV function (P < .05). Echocardiography and epicardial electrical mapping showed activation consistent with right bundle branch block during SR and marked resynchronization during BiV stimulation. In patients with repaired TOF, BiV stimulation increased significantly RV and LV dP/dt(max) (P < .05). In this swine model of RV dysfunction and in adults with repaired TOF, BiV stimulation significantly improved RV and LV function by alleviating electromechanical dyssynchrony.

The Effects of Pulmonary Arterial Hypertension on Left Ventricular Systolic and Diastolic Synchrony

Purpose: Pulmonary arterial hypertension (PAH) is known to alter right ventricular (RV) function and mechanics, resulting in RV dyssynchrony. However, the effects of PAH on left ventricular (LV) mechanics are less well known. We therefore queried our tissue Doppler imaging (TDI) database to identify patients with chronic PAH who had normal QRS duration and normal LV ejection fraction to examine the effect of PAH on LV systolic and diastolic synchronicity. Methods: The mid LV septum and lateral wall were sampled, as seen in Figure 1A, to obtain a TDI velocity signal. Systolic synchronicity was determined by the time interval between peak TDI systolic velocities (Ss) while diastolic synchronicity was defined as the time interval between peak TDI early (E) wave diastolic signals in 2 groups of patients. Figure 1B is a sample TDI velocity signal from a normal patient (Group I) and Figure 1C is a sample from a patient with PAH (Group II). Group I consisted of 18 patients (57 ± 16 years) with chronic PAH (PA systolic pressure of 78 ± 20 mmHg) and Group II included 18 healthy volunteers (47 ± 14 years; p = NS and PA systolic pressure of 21 ± 4 mmHg; p<0.001). Results: There was no difference between Group I and II regarding LV ejection fraction (79 ± 12% vs 65 ± 5%) or QRS duration (89 ± 14 ms vs. 90 ± 7 ms). However, Group I patients had significantly longer temporal delay between their septal and LV lateral wall systolic TDI signals (41 ± 36 ms vs. 8 ± 12ms; p<0.001) as well as their early diastolic E wave TDI signals (45 ± 56ms vs. 11 ± 9ms; p<0.01) than Group II as seen in Figure 1D and 1E. Conclusions: Systolic as well as early diastolic dyssynchrony is present in PAH patients despite having normal LV ejection fraction and a narrow QRS duration. It appears that geometric alterations in RV anatomy, due to pressure overload, rather than a electromechanical coupling delay in these patients not only impair LV systolic mechanics but also early LV relaxation. Further studies are now needed to determine the temporal evolution of these alterations and their relation to clinical outcomes.

Prevalence and Pathophysiologic Attributes of Ventricular Dyssynchrony in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

This study sought to investigate the prevalence and mechanisms underlying right ventricular (RV) dyssynchrony in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) using tissue Doppler echocardiography (TDE). An ARVD/C is characterized by fibrofatty replacement of RV myocardium and RV dilation. These pathologic changes may result in electromechanical dyssynchrony. Echocardiography, both conventional and TDE, was performed in 52 ARVD/C patients fulfilling Task Force criteria and 25 control subjects. The RV end-diastolic and -systolic areas, right ventricular fractional area change (RVFAC), and left ventricular (LV) volumes and function were assessed. Mechanical synchrony was assessed by measuring differences in time-to-peak systolic velocity (T(SV)) between the RV free wall, ventricular septum, and LV lateral wall. An RV dyssynchrony was defined as the difference in T(SV) between the RV free wall and the ventricular septum, >2 SD above the mean value for control subjects. The mean difference in RV T(SV) was higher in ARVD/C compared with control subjects (55 +/- 34 ms vs. 26 +/- 15 ms, p < 0.001). Significant RV dyssynchrony was not noted in any of the control subjects. Based on a cutoff value of 56 ms, significant RV dyssynchrony was present in 26 ARVD/C patients (50%). Patients with RV dyssynchrony had a larger RV end-diastolic area (22 +/- 5 cm(2) vs. 19 +/- 4 cm(2), p = 0.02), and lower RVFAC (29 +/- 8% vs. 34 +/- 8%, p = 0.03) compared with ARVD/C patients without RV dyssynchrony. No differences in QRS duration, LV volumes, or function were present between the 2 groups. An RV dyssynchrony may occur in up to 50% of ARVD/C patients, and is associated with RV remodeling. This finding may have therapeutic and prognostic implications in ARVD/C.

Abstract 5779: Quantification of Right Ventricular Dyssynchrony in Acute Pulmonary Embolism and Right Ventricular Pressure Overload Using Speckle-Tracking Strain Imaging

Acute right ventricular (RV) pressure overload can alter RV systolic synchronicity associated with RV expansion and wall motion abnormalities in patinets with acute pulmonary thrombo-embolism (APTE). Twenty patients with massive or sub-massive APTE (mean age 57 ± 18 years, estimated peak systolic pulmonary pressure 51 ± 16mmHg) had echocardiography with speckle-tracking strain imaging on admission. RV dyssynchrony was defined as the time difference from earliest to latest peak strain among 6-sites (basal septum, mid septum, apical septum, apical free wall, mid free wall, basal free wall) form apical 4-chamber view using speckle-tracking longitudinal strain imaging. All intervals were corrected for heart rate (corrected interval = measured interval/(RR interval) 1/2 ). Twenty normal subjects (Control: mean age 58 ± 10 years) were also assessed RV function and synchronicity for comparison. APTE had significantly low RV fractional area change (29 ± 10%* vs. 50 ± 7%), low global RV strain (−13 ± 4%* vs. −25 ± 3%), and large RV dyssynchorny (220 ± 103msec* vs. 78 ± 39msec) compared with Control (*p&lt;0.05 vs. Control). After hemodynamic recovery from acute RV pressure overload by primary thrombolysis and/or anticoagulation therapy, both global RV strain and dyssynchrony were improved (−18 ± 4%† and 130 ± 53msec†, †p&lt;0.05 vs. APTE on admission, respectively). Acute RV pressure overload induced reversible RV systolic dyssynchrony associated with RV systolic dysfunction in patients with APTE.

Normal Range of Mechanical Variables in Pulmonary Hypertension: A Tissue Doppler Imaging Study

Tissue Doppler imaging (TDI) has been quite useful in determining the mechanical properties of right ventricular (RV) function in patients with pulmonary hypertension (PH). However, to what extent these mechanical properties are expected to identify RV dysfunction in PH patients is less clear. Our echocardiography database was queried for patients with PH of different etiologies (111 patients, age 55 +/- 14 years, mean pulmonary artery pressure 63 +/- 24 mmHg) who had undergone TDI analysis and compared to similarly collected data from a group of healthy individuals (35 patients, mean age 45 +/- 15 years, mean pulmonary artery pressure 27 +/- 5 mmHg). ROC analysis demonstrated that a mechanical delay between the RVFw and IS > 25 ms detects PH while a delay > 37 ms detects abnormal RV performance. Peak RV strain < -20% identifies PH greater than 40 mmHg and a reduced RV systolic function. However, on a stepwise multiple regression analysis model RV dyssynchrony was the most significant predictor of PH (r = 0.515; P = 0.0003) over peak longitudinal RV strain (r = 0.553; P = 0.02) and RVFAC (r =-0.603; P = 0.01). Peak longitudinal strain was the most significant predictor (r =-0.722; P < 0.0001) of an abnormal RVFAC over PH (r =-0.603; P = 0.004) and RV dyssynchrony (r =-0.471; P = 0.01). A normal range of RV mechanical variables in PH patients are provided that can be applied in the assessment of RV performance.

Right ventricular pump function after cardiac resynchronization therapy: A strain imaging study

Cardiac resynchronization therapy (CRT) produces an early improvement in left ventricular (LV) function in patients with congestive heart failure (CHF), but little is known about its effects on right ventricular (RV) function. To assess the early effects of CRT on RV function using myocardial strain analysis. Fifty CHF patients (New York Heart Association class III/IV, left ventricular ejection fraction [LVEF] less than 35%, QRS greater than 120 ms) were studied before and three months after CRT. RV chamber dimension was quantified using tricuspid annulus diameter and RV short- and long-axis dimensions. RV function was assessed by tricuspid annulus plane systolic excursion and velocity (V(s)) and lateral wall strain. RV mechanical dyssynchrony was calculated using the difference in time-to-peak strain between septal and lateral wall. After three months, LVEF had increased significantly (from 22+/-6 to 27+/-9%; P<0.01) and LV end-diastolic volumes had decreased significantly (from 232+/-73 to 219+/-78 ml; P<0.05) in patients with LV mechanical dyssynchrony at baseline (n=35). RV dimensions did not change significantly, but there was an early improvement in RV function as demonstrated by an increase in V(s) (from 5.3+/-2.4 to 6.4+/-1.8 cm s(-1), P=0.001) and RV lateral wall basal and mid strain (from 23+/-9 to 28+/-9%, P=0.009 and from 20+/-7 to 25+/-8%, P=0.01, respectively). The improvement in RV strain occurred in patients with septal RV lead position and correlated with the magnitude of RV dyssynchrony at baseline (r=0.74; P<0.05). After three months, CRT improved RV function significantly in CHF patients before any significant change in RV dimensions.

Presence of ventricular dyssynchrony and haemodynamic impact of right ventricular pacing in adults with repaired Tetralogy of Fallot and right bundle branch block

Late after surgical repair, adults with Tetralogy of Fallot (TOF) commonly present with right ventricular (RV) dysfunction and right bundle branch block (RBBB). We aimed at (i) investigating whether this prolonged RV conduction induced detrimental electromechanical dyssynchrony in both RV and left ventricle (LV) and (ii) determining the acute haemodynamic effects of pacing at different RV sites. A total of 42 adults with surgically repaired TOF and RBBB were investigated by echocardiography. Intra-RV dyssynchrony (IRVD) and intra-left ventricular dyssynchrony (ILVD) were compared with measurements performed in 30 healthy matched control subjects. An acute haemodynamic study was subsequently performed in a subgroup of 10 patients with New York Heart Association functional class II or class III and echocardiographic signs of RV dysfunction. Cardiac index was measured by a thermodilution technique during spontaneous rhythm (SR) and during atrio-synchronized RV pacing at four different sites (infundibulum, apex, septal, and lateral walls). Fifty-five per cent of the patients with repaired TOF demonstrated abnormal RV and/or LV dyssynchrony. We observed an increased IRVD (37 +/- 12 vs. 18 +/- 8 ms; P= 0.02) and ILVD (34 +/- 12 vs. 20 +/- 10 ms; P= 0.04) in TOF patients when compared with control subjects. We did not observe any significant acute improvement in the cardiac output during atrio-synchronized ventricular pacing vs. SR. Similarly, RV pacing did not induce any significant reduction in the QRS duration. Some TOF adults with RBBB exhibit biventricular electromechanical dyssynchrony. However, in symptomatic patients with RV dysfunction, atrio-synchronized RV pacing does not induce significant acute haemodynamic improvement.

Mechanical Right Ventricular Dyssynchrony in Patients After Atrial Switch Operation for Transposition of the Great Arteries

Recent data suggest potential benefits of cardiac resynchronization therapy in the management of right ventricular (RV) dysfunction in congenital heart disease. The aim of this study was to determine the nature, prevalence, and functional implications of mechanical RV dyssynchrony in patients after Senning or Mustard procedures for transposition of the great arteries. Twenty-eight patients (mean age 21.1 +/- 3.5 years) at 19.9 +/- 3.2 years after atrial switch operations and 29 healthy controls were studied. The times from the onset of QRS to peak systolic strain (T epsilon) at the base of and the mid RV free wall, the ventricular septum (VS), and the left ventricular (LV) free wall were determined using tissue Doppler echocardiography. Intraventricular mechanical delay was defined as Delta T epsilon(RV-VS) and interventricular mechanical delay as Delta T epsilon(RV-LV). In patients, the magnitude of RV intra- and interventricular mechanical delay was correlated with cardiac magnetic resonance-derived RV volumes and ejection fractions (n = 26) and treadmill exercise testing parameters (n = 20). Compared with controls, patients had significantly longer Delta T epsilon(RV-VS) (48.1 +/- 50.9 vs 17.0 +/- 16.1 ms, p <0.001) and Delta T epsilon(RV-LV) (63.1 +/- 49.5 vs 19.0 +/- 12.9, p <0.001). Nine patients (32%) exhibited RV dyssynchrony (Delta T epsilon(RV-VS) >49 ms, control mean +/- 2SD), and 16 patients (57%) showed interventricular dyssynchrony (Delta T epsilon(RV-LV) >45 ms). In patients, RV intra- and interventricular mechanical delay was correlated negatively with the RV ejection fraction (both r = -0.42, p = 0.03) and percentage predicted maximum oxygen consumption (r = -0.50, p = 0.03, and r = -0.52, p = 0.02, respectively) and positively with minute ventilation/carbon dioxide production slope (r = 0.49, p = 0.03, and r = 0.56, p = 0.01, respectively). In conclusion, RV dyssynchrony is common in young adults after atrial switch operations and is associated with RV systolic dysfunction and impaired exercise performance.

Abnormal Right Ventricular Myocardial Strain Generation in Mild Pulmonary Hypertension

Although right ventricular (RV) dyssynchrony has been identified in patients with severe pulmonary hypertension due to significant RV enlargement and compromise in systolic function, a more clinically relevant question pertains to RV mechanical properties in patients with mild elevation in pulmonary artery systolic pressures (PASP). Several echocardiographic parameters and peak longitudinal strain were measured in 40 patients and divided into two groups of 20 patients based on their PASP. Group I included 20 individuals (mean age 48 +/- 16 years with a mean PASP of 27 +/- 5 mmHg) and Group II included 20 patients (mean age 63 +/- 14 years with a mean PASP of 49 +/- 7 mmHg.) All time intervals were adjusted for heart rate. RV fractional area change and tricuspid annular plane systolic excursion for Group I (62 +/- 12% and 2.74 +/- 0.56 cm) and Group II (49 +/- 14%; P < 0.02 and 2.09 +/- 0.40; P < 0.002) were both normal. However, Group II had lower peak longitudinal RV free wall (RVF) strain (-27.3 +/- 7.1 % vs. -31.9 +/- 8.7%, P < 0.04), longer time to peak RVF strain (448 +/- 57 ms vs. 411 +/- 43 ms; P < 0.03) and evidence of significant RV dyssynchrony (-83 +/- 55 ms vs. 1 +/- 17 ms, P < 0.00001) in contrast to Group I. In conclusion, mild elevations in PASP affect the mechanical properties of the RV and result in RV dyssynchrony despite absence of gross abnormalities in RV size or function.