Do Patients with Right Ventricular Outflow Tract Ventricular Arrhythmias Have a Normal Right Ventricular Wall Motion?

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Abstract

Background/Aim: Patients with ventricular ectopy from the right ventricular (RV) outflow tract (RVOT) are often referred for RV angiography to exclude disorders such as arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). This is usually based on a qualitative assessment of the wall motion. We present a method to quantify the wall motion and to apply this method to compare patients with RVOT ectopy to normal subjects. Methods: RV angiograms were analyzed from 19 normal subjects and 11 subjects with RVOT ventricular arrhythmias (RVOT arrhythmia subjects) who had no other clinical or other evidence for ARVC/D. By a newly developed computer-based method, RV contours were first traced from multiple frames spanning the entire cardiac cycle. The fractional change in area between contours was then calculated as a serial function of time and location to determine both total contour area change and timing of contour movement. Contour area strain, defined as the differential change in area between nearby regions, was also computed. Results: The contour area change was greatest in the tricuspid valve region and least in the RVOT and midanterior regions. The onset of contraction was earliest in the RVOT region and latest in the apical, inferior, inferoapical, and subtricuspid valve regions. The contour strain was largest in superior tricuspid valve and inferior wall and near zero within the lateral tricuspid valve region. There were significant pairwise differences in contraction area, timing, and strain in the various regions. There were no significant differences between normal subjects and RVOT arrhythmia subjects. Conclusions: The RV wall motion is nonuniform in contour area change, strain, and timing of motion. Patients with RVOT ventricular ectopy demonstrate wall motion parameters similar to those of normal subjects. This technique should be applicable in analyzing RV wall motion in patients suspected of having ARVC/D.

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Most cited references 8

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Magnetic resonance imaging in right ventricular dysplasia.

R Bussani, Ricardo Palma, F Camerini … (1992)

Fifteen patients with right ventricular dysplasia were investigated by T1-weighted spin- and gradient-echo pulse sequences, using a protocol that enabled both a subjective analysis of myocardial signal intensity and a quantitative/qualitative analysis of right and left ventricular function. In 8 patients, 3 investigators independently recognized abnormally hyperintense areas in the anatomic sites usually affected by the disease. In 7 of these patients, these areas showed an overlap with a-dyskinetic areas imaged by both magnetic resonance imaging (MRI) and echocardiography. In 1 patient who underwent a cardiac transplant, MRI of the explanted heart showed an excellent correlation between the distribution of the lesions and the in vivo/in vitro features. The data were compared with those from an equivalent sample of patients affected by dilated cardiomyopathy. In the latter patients, no focal hyperintensities were attributed to any anatomic sites in the right ventricule, and no focal a-dyskinetic foci were observed. Furthermore, the 2 groups of patients were significantly different in regard to dimensional and functional quantitative parameters. The results suggest that MRI is useful in integrating echocardiographic data and can be helpful in diagnosing this disease in late stages.

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Radiology of the right ventricle.

Lawrence Boxt (1999)

RV changes may be generalized into dilatation and hypertrophy. Increased preload results in ventricular dilatation. Increased afterload causes hypertrophy. Change in the shape of the RV resulting from increased afterload and myocardial hypertrophy induces tricuspid regurgitation, which superimposes changes of chamber dilatation onto those of hypertrophy. Sustained ventricular dilatation and hypertrophy frequently progresses to RV failure. In these cases, RV systolic function decreases in association with elevation of RV and right atrial diastolic pressure. Changes in the wall thickness and shape of the RV are variable, and depend upon the severity of the volume or pressure load presented, as well as its duration and rate of progression. Because the RV is an anterior cardiac structure, it occupies little of any heart border. Therefore, the sensitivity of plain film examination to RV disease is limited. Inferential diagnosis of RV disease can often be made based upon identification of other radiographic changes, notably the state of the pulmonary circulation, and the position of the heart in the chest. Conventional contrast right ventriculography may be used to assess the size and position of the RV, as well as associated acquired and congenital lesions that result in RV dysfunction. Due to the unusual shape of the RV cavity, however, and the unpredictable manner in which it dilates, accurate quantitative analysis by this technique is limited. Furthermore, the common association between RV disease and pulmonary hypertension limits the applicability of this imaging technique for evaluating patients with RV disease. Multiplanar MR imaging allows direct demonstration of changes in RV size and wall morphology. Furthermore, application of Simpson's rule to tomographic slices acquired at ventricular diastole and systole allows direct, accurate, and reproducible quantitative analysis of ventricular volume and myocardial mass, allowing radiographic assessment in patients for diagnosis, as well as longitudinally during medical management or after surgical treatment for congenital and acquired diseases that result in RV dysfunction.

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MR Imaging of Arrhythmogenic Right Ventricular Cardiomyopathy: Morphologic Findings and Interobserver Reliability

David A. Bluemke, Elizabeth Krupinski, Theron Ovitt … (2003)

Background: Magnetic resonance (MR) imaging is frequently used to diagnose arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D). However, the reliability of various MR imaging features for diagnosing ARVC/D is unknown. The purpose of this study was to determine which morphologic MR imaging features have the greatest interobserver reliability for diagnosing ARVC/D. Methods: Forty-five sets of films of cardiac MR images were sent to 8 radiologists and 5 cardiologists with experience in this field. There were 7 cases of definite ARVC/D as defined by the Task Force criteria. Six cases were controls. The remaining 32 cases had MR imaging because of clinical suspicion of ARVC/D. Readers evaluated the images for the presence of (a) right ventricle (RV) enlargement, (b) RV abnormal morphology, (c) left ventricle enlargement, (d) presence of high T 1 signal (fat) in the myocardium, and (e) location of high T 1 signal (fat) on a Likert scale with formatted responses. Results: Readers indicated that the Task Force ARVC/D cases had significantly more (χ 2 = 119.93, d.f. = 10, p 2 = 33.98, d.f. = 1, p 2 = 78.4, d.f. = 1, p 2 = 0.9, d.f. = 2, p > 0.05). Conclusions: Reviewers found that the size and shape of abnormalities in the RV are key MR imaging discriminates of ARVD. Subsequent protocol development and multicenter trials need to address these parameters. Essential steps in improving accuracy and reducing variability include a standardized acquisition protocol and standardized analysis with dynamic cine review of regional RV function and quantification of RV and left ventricle volumes.

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Author and article information

Journal

Journal ID (publisher-id): CRD

Journal ID (nlm-ta): Cardiology

Journal ID (doi): 10.1159/issn.0008-6312

Title: Cardiology

Publisher: S. Karger AG

ISSN (Print): 0008-6312

ISSN (Electronic): 1421-9751

Publication date Subscription-year: 2005

Publication date (Print): August 2005

Publication date (Electronic): 19 August 2005

Volume: 104

Issue: 1

Pages: 10-15

Affiliations

^aSection of Cardiology, Sarver Heart Center, and ^bDepartment of Radiology, University of Arizona, Tucson, Ariz., USA; ^cDepartment of Cardiology and Angiology, University Hospital, Münster, Germany

Article

Publisher ID: 86047 Other ID: Cardiology 2005;104:10–15

DOI: 10.1159/000086047

PubMed ID: 15942177

SO-VID: f2bb70f9-167f-421b-ac89-cf825899537e

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