Right ventricular myocardial activation delay in adult patients with right bundle branch block late after repair of Tetralogy of Fallot

D’Andrea, Antonello; Caso, Pio; Sarubbi, Berardo; D′Alto, Michele; Russo, M. G.; Scherillo, Marino; Cotrufo, Maurizio; Calabrò, Raffaele

doi:10.1016/s1525-2167(03)00053-2

Cited by 52 publications

(15 citation statements)

References 31 publications

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“…Many of the recent efforts to assess RV function have used tissue velocity (Doppler) signals to assess velocity at the tricuspid annulus 22,23 . Researchers have demonstrated the ability of DTI to characterize global and regional myocardial motion, or deformation, with high temporal resolution, but the angle dependency of Doppler, high noise-to-signal ratio and interobserver variability is an unavoidable limitation 21,28 .…”

Section: Discussionmentioning

confidence: 99%

Right ventricular mechanics in hypertrophic cardiomyopathy using feature tracking

Badran

Soliman

Hassan

et al. 2013

Global Cardiology Science and Practice

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Objectives: Right ventricular (RV) mechanics in hypertrophic cardiomyopathy (HCM) are poorly understood. We investigate global and regional deformation of the RV in HCM and its relationship to LV phenotype, using 2D strain vector velocity imaging (VVI). Methods: 100 HCM patients (42% females, 41 ± 19 years) and 30 control patients were studied using VVI. Longitudinal peak systolic strain (ϵsys), strain rate (SR), time to peak (ϵ) (TTP), displacement of RV free wall (RVFW) and septal wall were analyzed. Similar parameters were quantified in LV septal, lateral, anterior and inferior segments. Intra-V-delay was defined as SD of TTP. Inter-V-delay was estimated from TTP difference between the most delayed LV segment & RVFW. Results: ϵsys and SR of both RV & LV, showed loss of base to apex gradient and significant decline in HCM (p < 0.001). Deformation variables estimated from RVFW were strongly correlated with each other (r = 0.93, p < 0.0001). Both were directly related to LV ϵsys, SRsys, SRe, ejection fraction (EF)%, RVFW displacement (P < 0.001) and inversely related to age, positive family history (p < 0.004, 0.005), RV wall thickness, maximum wall thickness (MWT), intra-V-delay, LA volume (P < 0.0001), LVOT gradient (p < 0.02, 0.005) respectively. ROC curves were constructed to explore the cut-off point that discriminates RV dysfunction. Global and RVFW ϵsys: − 19.5% shows 77, 70% sensitivity & 97% specificity, SRsys: − 1.3s− 1 shows 82, 70% sensitivity & 30% specificity. Multivariate analyses revealed that RVFW displacement (β = − 0.9, p < 0.0001) and global LV SRsys (β = 5.9, p < 0.0001) are independent predictors of global RV deformation. Conclusions: Impairment of RV deformation is evident in HCM using feature tracking. It is independently influenced by LV mechanics and correlated to the severity of LV phenotype. RVFW deformation analysis and global RV assessment are comparable.

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Section: Discussionmentioning

confidence: 99%

Right ventricular mechanics in hypertrophic cardiomyopathy using feature tracking

Badran

Soliman

Hassan

et al. 2013

Global Cardiology Science and Practice

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“…The purpose of the current study was to, first, provide a detailed physiological characterization of this model, including a documentation of the effects of RV-LV interaction using tissue-Doppler imaging (TDI). TDI has emerged as a leading technique for the assessment of ventricular dyssynchrony using data obtained from myocardial motion (17,57). TDI-derived strain has been shown to be an excellent index of regional myocardial function because it is less influenced by overall cardiac motion (24,25,61).…”

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confidence: 99%

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Urashima

Zhao²,

Wagner³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

114

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physiological characterization of RV remodeling in a murine model of pulmonary stenosis. Am J Physiol Heart Circ Physiol 295: H1351-H1368, 2008. First published June 27, 2008 doi:10.1152/ajpheart.91526.2007 dysfunction is a common long-term complication in patients after the repair of congenital heart disease. Previous investigators have examined the cellular and molecular mechanisms of left ventricular (LV) remodeling, but little is known about the stressed RV. Our purpose was to provide a detailed physiological characterization of a model of RV hypertrophy and failure, including RV-LV interaction, and to compare gene alterations between afterloaded RV versus LV. Pulmonary artery constriction was performed in 86 mice. Mice with mild and moderate pulmonary stenosis (PS) developed stable hypertrophy without decompensation. Mice with severe PS developed edema, decreased RV function, and high mortality. Tissue Doppler imaging demonstrated septal dyssynchrony and deleterious RV-LV interaction in the severe PS group. Microarray analysis showed 196 genes with increased expression and 1,114 with decreased expression. Several transcripts were differentially increased in the afterloaded RV but not in the afterloaded LV, including clusterin, neuroblastoma suppression of tumorigenicity 1, Dkk3, Sfrp2, formin binding protein, annexin A7, and lysyl oxidase. We have characterized a murine model of RV hypertrophy and failure, providing a platform for studying the physiological and molecular events of RV remodeling. Although the molecular responses of the RV and LV to afterload stress are mostly concordant, there are several key differences, which may represent targets for RV failure-specific therapy. gene expression; right ventricle; tetralogy of Fallot THE RIGHT VENTRICLE IS UNIQUELY at risk in patients with complex congenital heart disease involving right-sided obstructive lesions (e.g., tetralogy of Fallot, tetralogy/pulmonary atresia) and in patients with systemic right ventricles (1,40,46). Increased stress on the right ventricle in the form of increased hemodynamic loading (pressure and/or volume) may result in abnormalities in cardiac structure, function, metabolism, coronary perfusion, neurohormonal activation, and molecular signaling. These stresses lead to both adaptive and maladaptive structural and molecular remodeling of the right ventricle and deleterious effects on the left ventricle through ventricular-ventricular interaction and may limit long-term survival (3,7,29,42). For many of these patients, detrimental conditions for the right ventricle exist throughout life, even after successful repair or palliation. As surgical techniques for the primary repair of complex forms of congenital heart disease improve, long-term survival and quality of life will depend on our ability to preserve long-term right ventricular (RV) function. Decisions regarding the ideal time for surgical reintervention will need to be based on more quantitative rather than qualitative measures.Developing a better understanding of the molecu...

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“…Norozi et al [22] reported prolonged IVRT and increased myocardial performance index (MPI) of the RV, while Abd El Rahman et al [18] and Sachdev et al [19] reported a short or negative IVRT and paradoxically decreased MPI in the majority of the patients with repaired TOF. Uebing et al [11] and D'Andrea et al [23] found no significant difference in IVRT between patients with repaired TOF and normal control subjects. Our study showed that the so-called IVRT was short or absent in 13 of 16 patients with delayed onset of the TV flow and short in 8 of 15 patients without delayed onset of the TV flow.…”

Section: Discussionmentioning

confidence: 99%

Delayed onset of tricuspid valve flow in repaired tetralogy of Fallot: an additional mechanism of diastolic dysfunction and interventricular dyssynchrony

Sun

Alhabshan

Cheung

et al. 2011

Journal of Cardiovascular Magnetic Resonance

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BackgroundDiastolic dysfunction of the right ventricle (RV) is common after repair of tetralogy of Fallot. While restrictive physiology in late diastole has been well known, dysfunction in early diastole has not been described. The present study sought to assess the prevalence and mechanism of early diastolic dysfunction of the RV defined as delayed onset of the tricuspid valve (TV) flow after TOF repair.MethodsThe study population consisted of 31 children with repaired TOF (mean age ± SD, 12.3 ± 4.1 years) who underwent postoperative cardiovascular magnetic resonance (CMR). The CMR protocol included simultaneous phase-contrast velocity mapping of the atrioventricular valves, which enabled direct comparison of the timing and patterns of tricuspid (TV) and mitral (MV) valve flow. The TV flow was defined to have delayed onset when its onset was > 20 ms later than the onset of the MV flow. The TV and MV flow from 14 normal children was used for comparison. The CMR results were correlated with the findings on echocardiography and electrocardiography.ResultDelayed onset of the TV flow was observed in 16/31 patients and in none of the controls. The mean delay time was 64.81 ± 27.07 ms (8.7 ± 3.2% of R-R interval). The delay time correlated with the differences in duration of the TV and MV flow (55.94 ± 32.88 ms) (r = 0.90, p < 0.001). Delayed onset was associated with prolongation of the RV ejection time in 9 and delayed onset and cessation of the pulmonary arterial flow in 4. Delayed onset was not associated with timing changes in the pulmonary artery in 3. The patients with delayed onset showed reduced RV ejection fraction (p = 0.01). However, the two groups did not show significant differences in TV E/A ratio, ventricular end-diastolic volumes, left ventricular ejection fraction, pulmonary regurgitant fraction, heart rate, PR interval and QRS duration.ConclusionsEarly diastolic dysfunction with delayed onset of TV flow is common after TOF repair, and is associated with reduced RV ejection fraction. It is a further manifestation of interventricular dyssynchrony and represent an additional mechanism of ventricular diastolic dysfunction.

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Right ventricular myocardial activation delay in adult patients with right bundle branch block late after repair of Tetralogy of Fallot

Cited by 52 publications

References 31 publications

Right ventricular mechanics in hypertrophic cardiomyopathy using feature tracking

Right ventricular mechanics in hypertrophic cardiomyopathy using feature tracking

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Delayed onset of tricuspid valve flow in repaired tetralogy of Fallot: an additional mechanism of diastolic dysfunction and interventricular dyssynchrony

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