Electroanatomic mapping of arrhythmogenic right ventricular dysplasia

Boulos, Munther; Lashevsky, Ilan; Reisner, Shimon A.; Gepstein, Lior

doi:10.1016/s0735-1097(01)01625-4

Cited by 82 publications

(74 citation statements)

References 22 publications

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“…In ARVD, however, the process is patchy and may cause inhomogeneous scarring in anatomically disparate areas. Regardless, previous data have shown that it is still possible to identify well-demarcated borders around these abnormal regions, 12 and our present study corroborates this finding.…”

Section: Verma Et Al Substrate-based Ablation Of Vt In Arvd 3213supporting

confidence: 91%

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Short- and Long-Term Success of Substrate-Based Mapping and Ablation of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

et al. 2005

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Background-Multiple morphologies, hemodynamic instability, or noninducibility may limit ventricular tachycardia (VT) ablation in patients with arrhythmogenic right ventricular dysplasia (ARVD). Substrate-based mapping and ablation may overcome these limitations. We report the results and success of substrate-based VT ablation in ARVD. Methods and Results-Twenty-two patients with ARVD were studied. Traditional mapping for VT was limited because of multiple/changing VT morphologies (nϭ14), nonsustained VT (nϭ10), or hemodynamic intolerance (nϭ5). Sinus rhythm CARTO mapping was performed to define areas of "scar" (Ͻ0.5 mV) and "abnormal" myocardium (0.5 to 1.5 mV). Ablation was performed in "abnormal" regions, targeting sites with good pace maps compared with the induced VT(s). Linear lesions were created in these areas to (1) connect the scar/abnormal region to a valve continuity or other scar or (2) encircle the scar/abnormal region. Eighteen patients had implanted cardioverter defibrillators, 15 had implanted cardioverter defibrillator therapies, and 7 had sustained VT (6 with syncope). VTs (3Ϯ2 per patient) were induced (cycle length, 339Ϯ94 ms), and scar was identified in all patients. Scar areas were related to the tricuspid annulus, proximal right ventricular outflow tract, and anterior/inferior-apical walls. Lesions connected abnormal regions to the annulus (nϭ12) or other scars (nϭ4) and/or encircled abnormal regions (nϭ13). Per patient, a mean of 38Ϯ22 radiofrequency lesions was applied. Short-term success was achieved in 18 patients (82%). VT recurred in 23%, 27%, and 47% of patients after 1, 2, and 3 years' follow-up, respectively. Conclusions-Substrate-based ablation of VT in ARVD can achieve a good short-term success rate. However, recurrences become increasingly common during long-term follow-up. (Circulation. 2005;111:3209-3216.)

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Section: Verma Et Al Substrate-based Ablation Of Vt In Arvd 3213supporting

confidence: 91%

“…1,11 Furthermore, the use of electroanatomic voltage mapping has been previously validated to correlate with areas of scar and fatty infiltration detected by magnetic resonance imaging in ARVD patients. 12 Therefore, our definition of the substrate seems to be consistent with prior published data.…”

Section: Substrate In Arvdsupporting

confidence: 88%

Short- and Long-Term Success of Substrate-Based Mapping and Ablation of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

et al. 2005

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“…111 Genetic testing in high-probability cases has a diagnostic yield of 40% to 50%; thus, a positive test is useful, but a negative test is not. The genes underlying ARVC are characterized by considerable natural variability, making a variant of unknown significance a common outcome of genetic testing, further emphasizing the need for careful phenotyping.…”

Section: Modi and Krahnmentioning

confidence: 99%

Sudden Cardiac Arrest Without Overt Heart Disease

Modi

Krahn

2011

Circulation

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“…14 Three-dimensional electroanatomic voltage mapping has been recently demonstrated to accurately identify the presence, location, and extent of the pathological substrate of ARVC/D by detection of low-voltage regions that reflect RV fibrofatty myocardial atrophy. 18 The present study was designed to test whether characterization of the RV wall by electroanatomic voltage mapping increases the accuracy for diagnosing ARVC/D in a consecutive series of patients fulfilling noninvasive Task Force criteria.…”

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confidence: 99%

Three-Dimensional Electroanatomic Voltage Mapping Increases Accuracy of Diagnosing Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia

et al. 2005

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Background— Three-dimensional electroanatomic voltage mapping offers the potential to identify low-voltage areas that correspond to regions of right ventricular (RV) myocardial loss and fibrofatty replacement in patients with arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). Methods and Results— Thirty-one consecutive patients (22 men and 9 women; mean age, 30.8±7 years) who fulfilled the criteria of the Task Force of the European Society of Cardiology and International Society and Federation of Cardiology (ESC/ISFC) for ARVC/D diagnosis after noninvasive clinical evaluation underwent further invasive study including RV electroanatomic voltage mapping and endomyocardial biopsy (EMB) to validate the diagnosis. Multiple RV endocardial, bipolar electrograms (175±23) were sampled during sinus rhythm. Twenty patients (group A; 65%) had an abnormal RV electroanatomic voltage mapping showing ≥1 area (mean 2.25±0.7) with low-voltage values (bipolar electrogram amplitude <0.5 mV), surrounded by a border zone (0.5 to 1.5 mV) that transitioned into normal myocardium (>1.5 mV). Low-voltage electrograms appeared fractionated with significantly prolonged duration and delayed activation. In 11 patients (group B; 35%), electroanatomic voltage mapping was normal, with preserved electrogram voltage (4.4±0.7 mV) and duration (37.2±0.9 ms) throughout the RV. Low-voltage areas in patients from group A corresponded to echocardiographic/angiographic RV wall motion abnormalities and were significantly associated with myocyte loss and fibrofatty replacement at EMB ( P <0.0001) and familial ARVC/D ( P <0.0001). Patients from group B had sporadic disease and histopathological evidence of inflammatory cardiomyopathy ( P <0.0001). During the time interval from onset of symptoms to the invasive study, 11 patients (55%) with electroanatomic low-voltage regions received an implantable cardioverter/defibrillator because of life-threatening ventricular arrhythmias, whereas all but 1 patient with a normal voltage map remained stable on antiarrhythmic drug therapy ( P =0.02). Conclusions— Three-dimensional electroanatomic voltage mapping enhanced accuracy for diagnosing ARVC/D (1) by demonstrating low-voltage areas that were associated with fibrofatty myocardial replacement and (2) by identifying a subset of patients who fulfilled ESC/ISFC Task Force diagnostic criteria but showed a preserved electrogram voltage, an inflammatory cardiomyopathy mimicking ARVC/D, and a better arrhythmic outcome.

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Electroanatomic mapping of arrhythmogenic right ventricular dysplasia

Cited by 82 publications

References 22 publications

Short- and Long-Term Success of Substrate-Based Mapping and Ablation of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

Short- and Long-Term Success of Substrate-Based Mapping and Ablation of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

Sudden Cardiac Arrest Without Overt Heart Disease

Three-Dimensional Electroanatomic Voltage Mapping Increases Accuracy of Diagnosing Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia

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