(Radiographics. 2002;22:639-648.)
© RSNA, 2002
Diagnosis of Arrhythmogenic Right Ventricular Dysplasia: A Review1
Hein W. M. Kayser, MD,
Ernst E. van der Wall, MD,
Mohan U. Sivananthan, MD,
Sven Plein, MD,
Timothy N. Bloomer, MD and
Albert de Roos, MD
1 From the Departments of Radiology (H.W.M.K., E.E.v.d.W., A.d.R.) and Cardiology (E.E.v.d.W.), Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands; Interuniversity Cardiology Institute of the Netherlands, Utrecht (H.W.M.K., A.d.R.); and Cardiac MRI Unit, General Infirmary at Leeds, England (M.U.S., S.P., T.N.B.). Received May 11, 2001; revision requested July 5 and received January 21, 2002; accepted January 21. Address correspondence to A.d.R. (e-mail: a.de_roos@lumc.nl).
 |
Abstract
|
|---|
Arrhythmogenic right ventricular dysplasia (ARVD) is a myocardial disorder of primarily the right ventricle, with unknown cause and prevalence and with a frequent familial occurrence. The typical clinical manifestation consists of ventricular arrhythmias with a left bundle branch block (LBBB) pattern that occur predominantly in young adults. ARVD may result in sudden death. Other manifestations are electrocardiographic repolarization and depolarization changes, structural abnormalities that range from subtle wall aneurysms within the so-called "triangle of dysplasia" to biventricular regional or global dysfunction, and localized or widespread fibrofatty infiltration of the right ventricular myocardium. The diagnosis of ARVD is based on the presence of major and minor criteria encompassing genetic, electrocardiographic, pathophysiologic, and histopathologic factors. The imaging modalities used to evaluate right ventricular abnormalities include conventional angiography, echocardiography, radionuclide angiography, ultrafast computed tomography, and magnetic resonance (MR) imaging. Among these techniques, MR imaging allows the clearest visualization of the heart. Because MR imaging depicts both functional and structural abnormalities, positive MR imaging findings should be used as important additional criteria in the clinical diagnosis of ARVD. MR imaging appears to be the optimal technique for detection and follow-up of clinically suspected ARVD.
© RSNA, 2002
Index Terms: Heart, arrhythmia, 523.6999 • Heart, cardiomyopathy, 523.1935 • Heart, MR, 523.12141
|
LEARNING OBJECTIVES FOR TEST 5
|
|---|
After reading this article and taking the test, the reader will be able to:
- Describe the clinical manifestations and pathologic characteristics of ARVD.
- Discuss an optimized MR imaging protocol for patients with possible ARVD.
- List the criteria leading to the clinical diagnosis of ARVD.
|
Introduction
|
|---|
Arrhythmogenic right ventricular dysplasia (ARVD) is a form of cardiomyopathy that is characterized clinically by ventricular arrhythmias with left bundle branch block (LBBB) that may lead to cardiac arrest and morphologically by fatty or fibrofatty infiltration of the right ventricular myocardium (1–5). Although incidence and prevalence of ARVD are unknown, ARVD is recognized as a major cause of sudden death in young adolescents, and in one series it accounted for 20% of sudden deaths in all individuals younger than 35 years and 22% of sudden deaths in young athletes (6). Therefore, an early and accurate diagnosis followed by appropriate therapy for this condition is increasingly important for it may prevent lethal arrhythmias.
The most important diagnostic modalities for the detection of ARVD include conventional angiography, echocardiography, radionuclide angiography, ultrafast computed tomography (CT), and magnetic resonance (MR) imaging. In this article, we address the causes of ARVD; its pathologic and clinical characteristics, its diagnosis, prognosis, and therapy; and the imaging evaluation of ARVD, with special emphasis on MR imaging.
|
Etiology
|
|---|
ARVD must be considered as a part of the group of idiopathic cardiomyopathies, based on its nature of progressive heart muscle disease with unclear pathogenesis and etiology. The male-to-female ratio is 2.7:1.0. Basso et al (1) addressed the etiology and pathogenesis and proposed four hypotheses as possible explanations. The first hypothesis concerns apoptosis, that is, programmed cell death, which leads to progressive myocardial muscle loss followed by fibrofatty replacement and enhances the electrical vulnerability of the right ventricle, which in turn can cause potentially life-threatening arrhythmias (7). According to the disontogenic theory, ARVD should be regarded as a congenital heart disease in which abnormal development of the right ventricle may lead to dysplasia. In the degenerative theory, a metabolic disorder may affect the right ventricle and result in progressive replacement of myocardial cells by fat and fibrous tissue. In the inflammatory theory, the fibrofatty replacement is viewed as a healing process in the context of myocarditis (8).
Several reports suggest that there is a familial occurrence of ARVD of about 30%–50% (2,9–12), with mainly autosomal dominant inheritance, various penetrance, and polymorphic phenotypic expression. Several genetic disorders responsible for ARVD have been identified on chromosome 14 and recently on chromosome 3 (9,11,12). The diagnosis of ARVD may have important consequences for direct relatives, because they have an increased chance of having the disease, with an increased risk of sudden death.
Gene mapping may open new avenues for cloning the defective gene, identifying the encoded protein, and potentially instituting gene therapy. Four loci have been mapped, but none of the genes have been identified yet, and the findings of polymorphism in ARVD currently preclude gene therapy (5,9,11).
|
Pathologic Features
|
|---|
Two morphologic variants of ARVD have been reported: fatty and fibrofatty (6,13). The fatty form is characterized by almost complete replacement of the myocardium without thinning of the ventricular wall, and it occurs exclusively in the right ventricle. The fibrofatty variant is associated with significant thinning of the right ventricular wall, and the left ventricular myocardial wall may also be involved. Other anatomic malformations of the right ventricle associated with ARVD consist of mild to severe global dilatation of the ventricle, ventricular aneurysms, and segmental hypokinesia. The sites of involvement of anatomic abnormalities are found in the so-called triangle of dysplasia, namely, the right ventricular subtricuspid areas, the apex, and the infundibulum (14).
|
Clinical Characteristics and Diagnosis
|
|---|
The clinical manifestations of ARVD may vary widely, but the disorder is classically characterized by ventricular tachycardia with LBBB, originating from the right ventricle. ARVD probably represents a spectrum of different abnormalities, rather than a single identity, which ranges from an asymptomatic form consisting of ventricular ectopic beats to biventricular heart failure with or without arrhythmias and sudden death in young patients and athletes (5,15). Furthermore, ARVD is a disease that may have a temporal progression, and the disease may manifest differently according to the time of patient presentation.
The electrocardiogram in patients with ARVD usually shows a regular sinus rhythm, with a QRS duration of greater than 110 msec in lead V1, an epsilon wave just beyond the QRS complex in lead V1, and an inversion of T waves in precordial leads V1–V3 (16). Figure 1 shows an electrocardiogram with an epsilon wave in lead V2 and inverted T waves in leads V1–V3.
View larger version (131K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1. Electrocardiogram shows a regular sinus rhythm with an epsilon wave in lead V2 and an inversion of T waves in precordial leads V1-V3, which is a major criterion for the diagnosis of ARVD.
|
|
According to the 1994 Task Force Report on ARVD by McKenna et al (16), the diagnosis of ARVD is based on the presence of structural, histologic, electrocardiographic, arrhythmic, and genetic factors (Table). Detection of functional and structural alterations is performed with echocardiography, conventional angiography, MR imaging, or radionuclide angiography. To fulfill the appropriate criteria for ARVD, patients must have either two major criteria, one major and two minor criteria, or four minor criteria.
The standard of reference for the diagnosis of ARVD is based on histologic demonstration of transmural fibrofatty replacement of right ventricular myocardium at either autopsy or surgery. However, myocardial biopsy lacks sufficient sensitivity owing to the segmental nature of the lesions and because the biopsy samples are obtained mostly from the septum whereas the typical pathologic changes of ARVD occur in the right ventricular free wall, where fat is growing from the epicardial region of the myocardium to the endocardial region (13,17). Even when the biopsy specimen is obtained from the right ventricular free wall, the sensitivity is 67% and the specificity is 92% for the diagnosis of ARVD, based on the criteria of greater than 3% fat and less than 40% fibrous tissue replacing the myocardial muscle (18). Also, recent studies demonstrated that significant fatty infiltration of the right ventricle occurs in more than 50% of normal hearts in elderly people. A degree of intramyocardial fat in the anterior apex of the right ventricle existed in 15% of control subjects (19,20). Thus, demonstration of some fat in the right ventricular myocardium may not be specific enough to help in establishing the diagnosis of ARVD (1,21–24). Therefore, in most cases, use of endomyocardial biopsy to confirm the diagnosis is not recommended, especially since the right ventricular wall is very thin and biopsy of this region risks perforation and cardiac tamponade.
Differential diagnosis of ARVD consists of idiopathic dilated cardiomyopathy and the Uhl anomaly, which is characterized by a paper-thin right ventricle due to almost complete absence of myocardial muscle fibers (14,25). Uhl anomaly can be distinguished from ARVD because the former has no gender predilection or familial occurrence. The differentiation of ARVD from idiopathic dilated cardiomyopathy may be difficult, but the patient with the latter, generalized cardiomyopathy usually has a progressive decline in left ventricular function, whereas the patient with ARVD will develop primarily right ventricular failure.
|
Prognosis and Therapy
|
|---|
Although the prognosis of ARVD is considerably better than that of sustained ventricular tachycardia with left ventricular heart disease, ARVD is a progressive disease and will probably lead to right ventricular failure in the long term unless sudden cardiac death occurs beforehand. The death rate for patients with ARVD has been estimated at 2.5% per year (22). The disease certainly cannot be considered as a benign condition in patients with symptoms of syncope, episodes of recurrent ventricular tachycardia, and anatomic or functional abnormalities of the right ventricle (26). Fortunately, patients with recurrences of ventricular tachycardia have a favorable outcome when they are treated medically.
The four therapeutic options in patients with ARVD include antiarrhythmic agents, catheter ablation, implantable cardioverter defibrillators, and surgery (27). Pharmacologic treatment is the first choice, with the antiarrhythmic agents being sotalol, verapamil, beta-receptor blocking agents, amiodarone, and flecainide. Catheter ablation is an alternative in patients who are refractory to drug treatment and who have localized disease. In addition, catheter ablation has been shown to improve the effectiveness of pharmacologic treatment: 70% of patients may respond to antiarrhythmic agents to which they were unresponsive prior to ablation therapy (28). Implantation of cardioverter defibrillators is indicated in patients who are intolerant of antiarrhythmic therapy and who are at serious risk for sudden death. Surgery should be considered only as a very last resort, and treatment consists initially of ventriculotomy, followed by total disconnection of the right ventricular free wall. In case of progressive or intractable right ventricular failure, cardiac transplantation may be the ultimate option for treating patients with ARVD. Currently, drug treatment, ablation, and cardioverter defibrillator therapy are the most suitable therapeutic approaches in patients with ARVD.
|
Imaging Evaluation of ARVD
|
|---|
Imaging techniques for diagnosing morphofunctional abnormalities consistent with ARVD include conventional angiography, echocardiography, radionuclide angiography, ultrafast CT, and MR imaging. Right ventricular angiography has usually been regarded as the standard of reference for the diagnosis of ARVD, especially for discerning abnormalities such as akinetic or dyskinetic bulging in infundibular, apical, and subtricuspid regions (Fig 2). Echocardiography is a noninvasive, widely available technique that can be used for diagnosing anatomic abnormalities other than ARVD (13). However, the traditionally used imaging modalities have been shown to be relatively insensitive and nonspecific in the detection of structural or functional abnormalities of the right ventricular myocardium (23,26,29). Also, all these imaging modalities are limited by a lack of spatial resolution in diagnosing the typical fatty and fibrofatty changes of the right ventricular myocardium.
MR imaging allows a three-dimensional evaluation of ventricular anatomy and volumes, and, in view of its excellent spatial resolution and unlimited field of view, MR imaging is an excellent tool for visualizing the right ventricle. It is therefore well suited for comprehensive assessment of the right ventricle and the characteristic changes seen in ARVD (5,13,23,24,30–32).
MR Imaging Assessment
ARVD is being diagnosed with increasing frequency, mostly because MR imaging allows improved recognition of myocardial fatty and fibrofatty replacement (13). Several studies have reported on the use of MR imaging to detect the characteristic high signal intensity of fat in the right ventricular myocardium on T1-weighted images (1,6,21,25,31,33). However, as mentioned before, recent studies demonstrated that significant fatty infiltration of the right ventricle occurs in more than 50% of normal hearts in elderly people (19,20). Mehta et al (34) found signs of fatty replacement in only 22% of 27 patients with ventricular tachycardia with LBBB (as diagnosed with endomyocardial biopsy). Menghetti et al (21) reported a sensitivity and specificity of 67% and 100%, respectively, with use of spin-echo MR imaging, whereas Aufferman et al (31) reported a sensitivity of only 22%. Basso et al (1), however, found that among nine patients with the pathologic diagnosis of ARVD (based on gross or histologic evidence of regional or diffuse transmural fatty or fibrofatty replacement), MR imaging revealed abnormal high signal intensity in all cases (1). Although these findings indicate that the presence of some fat in the right ventricular myocardium may not be specific enough for the diagnosis of ARVD, the presence of transmural fatty replacement or diffuse thinning of the right ventricular myocardium as demonstrated with MR imaging should be considered in the entire clinical context to be a major criterion for the diagnosis of ARVD.
Several studies examined the value of using MR imaging in patients for whom the first manifestation of right ventricular disease was right ventricular outflow tract tachycardia (23,30,33,35–39). Globits et al (33) and Carlson et al (35) showed that right ventricular outflow tract tachycardia was associated with local structural and wall motion abnormalities of the right ventricular outflow tract and that the structural abnormalities observed with MR imaging were often not detected with echocardiography. Proclemer et al (39) investigated 19 patients who had frequent ventricular extrasystoles (>100/hour) with LBBB pattern (minor criterion). In all 19 patients, results from two-dimensional echocardiography were normal; however, MR imaging showed significantly greater dimensions of the right ventricular outflow tract compared with those seen in the control group of 10 volunteers. The similarity of these findings with those previously obtained in patients with right ventricular tachycardia suggests a similar underlying mechanism of the right ventricular outflow tract arrhythmias.
MR imaging can also be used to assess both systolic and diastolic function in great detail. Several studies have addressed the presence of right ventricular diastolic dysfunction as an early marker of disease, even when systolic function is still preserved (31,40). In a previous study, we showed that diastolic function of the right ventricle was significantly altered in 15 patients with nonischemic tachyarrhythmias of right ventricular origin, even though systolic function was normal (36). Of the 15 patients in that study, five (33%) had a clinical diagnosis of ARVD, indicating that ARVD may be associated with diastolic function abnormalities preceding systolic function abnormalities. Therefore, we suggest that diastolic dysfunction might be considered as an additional feature or criterion of ARVD.
The typical criteria that can be demonstrated with MR imaging are (a) fatty infiltration of the right ventricular myocardium with high signal intensity on T1-weighted images (Fig 3) (major criterion); (b) fibrofatty replacement, which leads to diffuse thinning of the right ventricular myo-cardium (Fig 4) (major criterion); (c) aneurysms of the right ventricle and right ventricular outflow tract (Figs 5, 6) (major criterion); (d) dilatation of the right ventricle and right ventricular outflow tract (when severe, major criterion; when mild, minor criterion) (Figs 7, 8); (e) regional contraction abnormalities (minor criterion); and (f) global systolic dysfunction (major criterion) and global diastolic dysfunction (minor criterion).
View larger version (179K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3a. Axial T1-weighted black blood spin-echo images show extensive transmural fatty replacement of the right ventricular myocardium (RV) (arrow in a) and the right ventricular outflow tract (RVOT) (arrow in b), which is a major criterion for the diagnosis of ARVD.
|
|
View larger version (181K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3b. Axial T1-weighted black blood spin-echo images show extensive transmural fatty replacement of the right ventricular myocardium (RV) (arrow in a) and the right ventricular outflow tract (RVOT) (arrow in b), which is a major criterion for the diagnosis of ARVD.
|
|
View larger version (89K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4a. Axial T1-weighted black blood spin-echo images show diffuse thinning and fatty replacement of the right ventricular myocardium (RV) (arrow in a) and the right ventricular outflow tract (RVOT) (arrow in b), which is a major criterion for the diagnosis of ARVD.
|
|
View larger version (87K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4b. Axial T1-weighted black blood spin-echo images show diffuse thinning and fatty replacement of the right ventricular myocardium (RV) (arrow in a) and the right ventricular outflow tract (RVOT) (arrow in b), which is a major criterion for the diagnosis of ARVD.
|
|
In summary, MR imaging is useful for evaluating not only fatty replacement of the right ventricular myocardium but also global and regional functional abnormalities of the right ventricle and right ventricular outflow tract. The demonstration of right ventricular abnormalities should be considered in the entire clinical context.
MR Imaging Protocol
In our institution, we use the following optimized MR imaging protocol, which we suggest for the evaluation of patients with clinically suspected ARVD. For all examinations, we use a phased-array cardiac synergy coil with five elements.
For the evaluation of right ventricular anatomy, we use a multisection inversion-recovery ("black blood") segmented turbo spin-echo pulse sequence to obtain images with section thicknesses of 4 mm or less in transverse and sagittal planes. "Black blood" in MR images can be achieved by using a nonselective 180° pulse to invert all spins. This inversion pulse is directly followed by a selective 180° pulse, which resets the signal of the section under investigation. This technique causes the blood with inverted signal to flow into the selected section. After a delay (inversion time), the blood signal is nulled (inversion time depends on heart rate) and the imaging pulse sequence (eg, a fast spin echo during patient breath hold) is started (41,42).
For the evaluation of right ventricular global and regional systolic function, we use a multisection, multiphase, balanced fast-field-echo pulse sequence (43) to obtain images with section thicknesses of 8–9 mm in the transverse plane. Balanced fast-field-echo pulse sequences belong to the group of "steady state free precession" sequences and are characterized by the application of time-balanced gradients for all gradient directions: section selection, frequency readout, and phase encoding. Together with the alternating phase of the excitation pulse, this technique ensures that both signals (free induction decay and echo) are obtained. The sequence produces a very high signal for tissues with a high T2:T1 ratio, independent of the repetition time. The balanced gradients contribute to a low sensitivity for flow disturbances. Because the field homogeneity is very important, balanced fast field echo requires the use of shimming before each study.
For the evaluation of right ventricular diastolic function, MR velocity mapping is performed to measure flow across the tricuspid valve, as previously described (44). The number of time frames used to sample the cardiac cycle is set to 30, resulting in a temporal resolution of less than 30 msec per cardiac frame. Peak velocity is set at 100 cm/sec to avoid aliasing. Flow measurements are performed in double oblique planes, identified from a coronal spin-echo image and a transverse gradient-echo image. End-diastolic and end-systolic positions of the tricuspid valve are determined, and the imaging plane is selected between these positions perpendicular to transtricuspid flow direction.
|
Summary
|
|---|
ARVD is part of the group of cardiomyopathies, characterized pathologically by fibrofatty replacement of the right ventricular myocardium and clinically by right ventricular arrhythmias of the LBBB pattern. Pathogenesis, prevalence, and etiology are yet not fully known. The diagnosis of ARVD is based on the presence of structural, histologic, electrocardiographic, and genetic factors. Therapeutic options include antiarrhythmic medication, catheter ablation, implantable cardioverter defibrillation, and surgery. Angiography and echocardiography lack sensitivity and specificity in the diagnosis of ARVD. MR imaging allows a three-dimensional evaluation of especially the right ventricle and provides the most important anatomic, functional, and morphologic criteria for diagnosis of ARVD within one single study. Although demonstration of morphofunctional abnormalities of the right ventricle, especially fat in the right ventricular myocardium, shows high specificity but low sensitivity, MR imaging appears to be the optimal imaging technique for detection and follow-up of clinically suspected ARVD. Positive MR imaging findings, based on the criteria of McKenna et al (16), should be used as important additional criteria in the clinical diagnosis of ARVD, although negative MR imaging findings do not rule out ARVD.
|
Footnotes
|
|---|
Abbreviations: ARVD = arrhythmogenic right ventricular dysplasia,
LBBB = left bundle branch block
See also the commentary by Boxt
following this article.
|
References
|
|---|
-
Basso C, Thiene G, Corrado D, Angelini A, Nava A, Valente M. Arrhythmogenic right ventricular cardiomyopathy: dysplasia, dystrophy, or myocarditis?. Circulation 1996; 94:983-991.[Medline]
-
Corrado D, Fontaine G, Marcus FI, et al. Arrhythmogenic right ventricular dysplasia/cardiomyopathy: need for an international registry. Circulation 2000; 101:E101-E106.
-
Metzger J, de Chillou C, Cheriex E, Rodriguez LM, Smeets JL, Wellens HJ. Value of the 12-lead electrocardiogram in arrhythmogenic right ventricular dysplasia, and absence of correlation with electrocardiographic findings. Am J Cardiol 1993; 72:964-967.[CrossRef][Medline]
-
Pinamonti B, Sinagra G, Camerini F. Clinical relevance of right ventricular dysplasia/cardiomyopathy (editorial). Heart 2000; 83:9-11.[Free Full Text]
-
van der Wall EE, Kayser HW, Bootsma MM, de Roos A, Schalij MJ. Arrhythmogenic right ventricular dysplasia: MRI findings. Herz 2000; 4:356-364.
-
Thiene G, Nava A, Corrado D, Rossi L, Pennelli N. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med 1988; 318:129-133.[Abstract]
-
James T. Normal and abnormal consequences of apoptosis in the human heart: from postnatal morphogenesis to paroxysmal arrhythmias. Circulation 1994; 90:556-573.[Medline]
-
Hofmann R, Trappe HJ, Klein H, Kemnitz J. Chronic (or healed) myocarditis mimicking arrhythmogenic right ventricular dysplasia. Eur Heart J 1993; 14:717-720.[Abstract/Free Full Text]
-
Ahmad F, Li D, Karibe A, et al. Localization of a gene responsible for arrhythmogenic right ventricular dysplasia to chromosome 3p23. Circulation 1998; 98:2791-2795.[Medline]
-
Nava A, Thiene G, Canciani B, et al. Familial occurrence of right ventricular dysplasia: a study involving nine families. J Am Coll Cardiol 1988; 12:1222-1228.[Abstract]
-
Rampazzo A, Nava A, Danieli GA, et al. The gene for arrhythmogenic right ventricular cardiomyopathy maps to chromosome 14q23-q24. Hum Mol Genet 1994; 3:959-962.[Abstract/Free Full Text]
-
Rampazzo A, Nava A, Erne P, et al. A new locus for arrhythmogenic right ventricular cardiomyopathy (ARVD2) maps to chromosome 1q42-q43. Hum Mol Genet 1995; 4:2151-2154.[Abstract/Free Full Text]
-
Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy: diagnosis, prognosis, and treatment. Heart 2000; 83:588-595.[Free Full Text]
-
Fontaine G, Fontaliran F, Frank R. Arrhythmogenic right ventricular cardiomyopathies: clinical forms and main differential diagnoses (editorial). Circulation 1998; 97:1532-1535.[Free Full Text]
-
Pinamonti B, Pagnan L, Bussani R, Ricci C, Silvestri F, Camerini F. Right ventricular dysplasia with biventricular involvement. Circulation 1998; 98:1943-1945.[Medline]
-
McKenna WJ, Thiene G, Nava A, et al. Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Br Heart J 1994; 71:215-218.[Free Full Text]
-
Wiesfeld AC, Crijns HJ, van Dijk RB, et al. Potential role of endomyocardial biopsy in the clinical characterization of patients with idiopathic ventricular fibrillation: arrhythmogenic right ventricular dysplasia—an undervalued cause. Am Heart J 1994; 127:1421-1424.[CrossRef][Medline]
-
Strain J. Adipose dysplasia of the right ventricle: is endomyocardial biopsy useful?. Eur Heart J 1989; 10(suppl D):84-88.
-
Burke A, Farb A, Tashko G, Virmani R. Arrhythmogenic right ventricular cardiomyopathy and fatty replacement of the right ventricular myocardium: are they different diseases?. Circulation 1998; 97:1571-1580.[Abstract/Free Full Text]
-
Fontaliran F, Fontaine G, Fillette F, Aouate P, Chomette G, Grosgogeat Y. Nosologic frontiers of arrhythmogenic dysplasia: quantitative variations of normal adipose tissue of the right heart ventricle. Arch Mal Coeur Vaiss 1991; 84:33-38[French].
-
Menghetti L, Basso C, Nava A, Angelini A, Thiene G. Spin-echo nuclear magnetic resonance for tissue characterisation in arrhythmogenic right ventricular cardiomyopathy. Heart 1996; 76:467-470.[Abstract/Free Full Text]
-
Fontaine G, Fontaliran F, Hebert J, et al. Arrhythmogenic right ventricular dysplasia. Annu Rev Med 1999; 50:17-35.[CrossRef][Medline]
-
White RD, Trohman RG, Flamm SD, et al. Right ventricular arrhythmia in the absence of arrhythmogenic dysplasia: MR imaging of myocardial abnormalities. Radiology 1998; 207:743-751.[Abstract]
-
Blake LM, Scheinman MM, Higgins CB. MR features of arrhythmogenic right ventricular dysplasia. AJR Am J Roentgenol 1994; 162:809-812.[Abstract/Free Full Text]
-
Marcus FI, Fontaine G. Arrhythmogenic right ventricular dysplasia/cardiomyopathy: a review. Pacing Clin Electrophysiol 1995; 18:1298-1314.[Medline]
-
Marcus FI, Fontaine GH, Guirodon G, et al. Right ventricular dysplasia: a report of 24 adult cases. Circulation 1982; 65:384-398.[Medline]
-
Leclercq JF, Coumel P. Characteristics, prognosis and treatment of the ventricular arrhythmias of right ventricular dysplasia. Eur Heart J 1989; 10(suppl D):61-67.
-
Movsowitz C, Schwartzman D, Callans DJ, et al. Idiopathic right ventricular outflow tract tachycardia: narrowing the anatomic location for successful ablation. Am Heart J 1996; 131:930-936.[CrossRef][Medline]
-
Mehta D, Odawara H, Ward DE, McKenna WJ, Davies MJ, Camm AJ. Echocardiographic and histologic evaluation of the right ventricle in ventricular tachycardias of left bundle branch block morphology without overt cardiac abnormality. Am J Cardiol 1989; 3:939-944.
-
Markowitz SM, Litvak BL, Ramirez de Arellano EA, Markisz JA, Stein KM, Lerman BB. Adenosine-sensitive ventricular tachycardia: right ventricular abnormalities delineated by magnetic resonance imaging. Circulation 1997; 96:1192-1200.[Medline]
-
Auffermann W, Wichter T, Breithardt G, Joachimsen K, Peters PE. Arrhythmogenic right ventricular disease: MR imaging vs angiography. AJR Am J Roentgenol 1993; 161:549-555.[Abstract/Free Full Text]
-
Midiri M, Finazzo M, Brancato M, et al. Arrhythmogenic right ventricular dysplasia: MR features. Eur Radiol 1997; 7:307-312.[CrossRef][Medline]
-
Globits S, Kreiner G, Frank H, et al. Significance of morphological abnormalities detected by MRI in patients undergoing successful ablation of right ventricular outflow tract tachycardia. Circulation 1997; 96:2633-2640.[Medline]
-
Mehta D, Davies MJ, Ward DE, Camm AJ. Ventricular tachycardias of right ventricular origin: markers of subclinical right ventricular disease. Am Heart J 1994; 127:360-366.[CrossRef][Medline]
-
Carlson MD, White RD, Trohman RG, et al. Right ventricular outflow tract ventricular tachycardia: detection of previously unrecognized anatomic abnormalities using cine magnetic resonance imaging. J Am Coll Cardiol 1994; 24:720-727.[Abstract]
-
Kayser H, Schalij M, van der Wall E, Stoel B, de Roos A. Biventricular function in patients with nonischemic right ventricular tachyarrhythmias assessed with MR imaging. AJR Am J Roentgenol 1997; 159:995-999.
-
Kayser H, de Roos A, van der Wall E. Diagnosis of cardiac abnormalities in patients with nonischemic tachyarrhythmias: additional value of MR imaging. Int J Card Imaging 1998; 14:279-285.[CrossRef][Medline]
-
Midiri M, Finazzo M, Brancato M, et al. Arrhythmogenic right ventricular dysplasia: MR features. Eur Radiol 1997; 7:307-312.
-
Proclemer A, Basadonna PT, Slavich GA, Miani D, Fresco C, Fioretti PM. Cardiac magnetic resonance imaging findings in patients with right ventricular outflow tract premature contractions. Eur Heart J 1997; 18:2002-2010.[Abstract/Free Full Text]
-
Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988; 12:426-440.[Abstract]
-
Simonetti O, Kim R, Fieno D, et al. An improved MR imaging technique for the visualization of myocardial infarction. Radiology 2001; 218:215-223.[Abstract/Free Full Text]
-
Simonetti O, Finn J, White RD, Laub G, Henry D. "Black blood" T2-weighted inversion-recovery MR imaging of the heart. Radiology 1996; 199:49-57.[Abstract/Free Full Text]
-
Steenbeck J, Pruessmann K. Technical developments in cardiac MRI: 2000 update. Rays 2001; 26:15-34.[Medline]
-
Kayser H, Stoel B, van der Wall E, van der Geest R, de Roos A. MR velocity mapping of tricuspid flow: correction for through-plane motion. J Magn Reson Imaging 1997; 7:669-673.[Medline]
This article has been cited by other articles:
|
|
|
|
 
R. R. Edelman
Contrast-enhanced MR Imaging of the Heart: Overview of the Literature
Radiology,
September 1, 2004;
232(3):
653 - 668.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Castillo, H. Tandri, E. R. Rodriguez, K. Nasir, J. Rutberg, H. Calkins, J. A. C. Lima, and D. A. Bluemke
Arrhythmogenic Right Ventricular Dysplasia: Ex Vivo and in Vivo Fat Detection with Black-Blood MR Imaging
Radiology,
July 1, 2004;
232(1):
38 - 48.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Abbara, R. Q. Migrino, D. E. Sosnovik, J. A. Leichter, T. J. Brady, and G. Holmvang
Value of Fat Suppression in the MRI Evaluation of Suspected Arrhythmogenic Right Ventricular Dysplasia
Am. J. Roentgenol.,
March 1, 2004;
182(3):
587 - 591.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M.R.M Jongbloed, J.J Bax, A.E Borger van der Burg, E.E Van der Wall, and M.J Schalij
Radiofrequency catheter ablation of ventricular tachycardia guided by intracardiac echocardiography
Eur J Echocardiogr,
January 1, 2004;
5(1):
34 - 40.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. C. Gaerte, C. A. Meyer, H. T. Winer-Muram, R. D. Tarver, and D. J. Conces Jr
Fat-containing Lesions of the Chest
RadioGraphics,
October 1, 2002;
22(90001):
S61 - 78.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
LEARNING OBJECTIVES FOR TEST...
