Study of the sequence of ventricular activation and the QRS complex of the normal human heart using direct epicardial leads

Barbato, E; Pileggi, F; Debes, Antonio Carlos; Fujioka, Terutaka; Magalhães, Mário S.; Tranchesi, J; Juan, Edgard San; Décourt, Luiz V.

doi:10.1016/0002-8703(58)90102-9

Cited by 33 publications

(2 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on the results of this study, we hypothesize that conduction delay, one of the defining features of ARVD/C, plays an important role in the disease process. The epicardial RV perivalvular area and LV posterolateral wall are late activated regions in the normal heart during sinus rhythm . In ARVD/C, this activation delay is aggravated, since desmosomal mutations have been shown to give rise to conduction delay through gap junction remodeling and sodium channel dysfunction .…”

Section: Discussionmentioning

confidence: 99%

“…The epicardial RV perivalvular area and LV posterolateral wall are late activated regions in the normal heart during sinus rhythm. 22,23 In ARVD/C, this activation delay is aggravated, since desmosomal mutations have been shown to give rise to conduction delay through gap junction remodeling and sodium channel dysfunction. 24,25 It is notable that involvement of the RVOT, which also is a physiologically late activated region, was only observed in moderate and advanced ARVD/C.…”

Section: Insights Into Etiopathophysiology Of Arvd/cmentioning

confidence: 99%

See 1 more Smart Citation

Mutation‐Positive Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: The Triangle of Dysplasia Displaced

Riele

James

Philips

et al. 2013

Cardiovasc electrophysiol

170

105

View full text Add to dashboard Cite

Introduction The traditional description of the Triangle of Dysplasia in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) predates genetic testing and excludes biventricular phenotypes. Methods and Results We analyzed Cardiac Magnetic Resonance (CMR) studies of 74 mutation-positive ARVD/C patients for regional abnormalities on a 5-segment RV and 17-segment LV model. The location of electroanatomic endo- and epicardial scar and site of successful VT ablation was recorded in 11 ARVD/C subjects. Among 54/74 (73%) subjects with abnormal CMR, the RV was abnormal in almost all (96%), and 52% had biventricular involvement. Isolated LV abnormalities were uncommon (4%). Dyskinetic basal inferior wall (94%) was the most prevalent RV abnormality, followed by basal anterior wall (87%) dyskinesis. Subepicardial fat infiltration in the posterolateral LV (80%) was the most frequent LV abnormality. Similar to CMR data, voltage maps revealed scar (<0.5 mV) in the RV basal inferior wall (100%), followed by the RV basal anterior wall (64%) and LV posterolateral wall (45%). All 16 RV VTs originated from the basal inferior wall (50%) or basal anterior wall (50%). Of 3 LV VTs, 2 localized to the posterolateral wall. In both modalities, RV apical involvement never occurred in isolation. Conclusion Mutation-positive ARVD/C exhibits a previously unrecognized characteristic pattern of disease involving the basal inferior and anterior RV, and the posterolateral LV. The RV apex is only involved in advanced ARVD/C, typically as a part of global RV involvement. These results displace the RV apex from the Triangle of Dysplasia, and provide insights into the pathophysiology of ARVD/C.

show abstract

Section: Discussionmentioning

confidence: 99%