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(Circulation. 2000;101:e176.)
© 2000 American Heart Association, Inc.

Circulation Electronic Pages

Right Bundle-Branch Block, ST-Segment Elevation, and Sudden Death

Bortolo Martini, MD

Department of Cardiology Ospedale Civile di Thiene, Thiene, Italy

Andrea Nava, MD; Domenico Corrado, MD; Gaetano Thiene, MD

Departments of Cardiology and Cardiovascular Pathology, University of Padua, Padua, Italy

	Introduction

 
To the Editor:

The review article of Alings and Wilde¹ on the syndrome of right bundle-branch block ST-segment elevation and sudden death, ignores many of the published data on this disease. It is not true that most of the published cases affected by the disease show no heart abnormalities.² Since the first detailed description of the syndrome in 1988–1989 by our group,^{3 4} a number of patients with similar ECG patterns (including some in the Brugada series) have been recognized as having structural heart disease, particularly of the conduction system and/or right ventricle, by both invasive and noninvasive techniques. Right ventricular abnormalities (at angiography, 2D echo, or MRI), a positive late potential study, a prolonged HV interval (indicative of an organic conduction disturbance), an abnormal right ventricular biopsy, and fibro-fatty replacement of the right ventricle have all been documented.^{1 5} From our data, it is evident that the right bundle-branch block pattern and ST-segment elevation (according to electrophysiological and necropsy data) are related to a diseased conduction sytem both at the septal and intramyocardial levels.⁵ The ST-segment elevation in the right precordial leads, especially when associated with minor forms of right bundle-branch block,³ has been explained in some cases by involvement of genetically isolated defective ion channels, which results in voltage gradient of repolarization between an abnormal epicardial action potential and a normal endocardial one.¹ This transmural dispersion of repolarization may either be acquired or enhanced in the setting of ischemia, inflammation, and degenerative heart disease.

In this regard, myocyte degeneration and . . . [Full Text of this Article]

Arthur Wilde, MD; Marco Alings, MD

Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam, Netherlands, Department of Cardiology, Heart Lung Institute, University Medical Centre Utrecht, Utrecht, Netherlands

This article has been cited by other articles:

				A.A.M. Wilde, C.A. Remme, R. Derksen, E.F.D. Wever, and R.N.W. Hauer Brugada syndrome Eur. Heart J., April 2, 2002; 23(8): 675 - 676. [Full Text] [PDF]