Journal of cardiovascular electrophysiology · 2000
Augmentation of QRS wave amplitudes in the precordial leads during narrow QRS tachycardia.
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Wakimoto H, Izumida N, Asano Y, Hiraoka M, Kawara T, Hiejima K, Hirao T K, Suzuki F
Аннотация
INTRODUCTION: QRS morphology during narrow QRS supraventricular tachycardia in patients without ventricular preexcitation generally is considered the same as that seen during sinus rhythm. This study presents a new ECG observation that the QRS amplitude increased significantly in leads V2 through V5 during tachycardia.
METHODS AND RESULTS: Using the same ECG machine and the same electrode patches applied to the same electrode positions, 12-lead ECGs during sinus rhythm and narrow QRS tachycardia were analyzed comparatively in 23 patients without ventricular preexcitation. Precordial QRS amplitudes were measured as the vertical distance from the peak of the R to the nadir of the S wave. The amplitudes also were measured during atrial rapid pacing and extrastimulation. Furthermore, ventricular excitation during sinus rhythm and tachycardia was studied using body surface mapping. Body surface distributions of QRS potentials and ventricular activation time (VAT) were displayed as maps. Gross area of QRS (AQRS, equivalent to the QRS amplitude) was compared during sinus rhythm versus tachycardia. During tachycardia, QRS amplitude significantly increased in leads V2 through V5, without any noticeable change in the transitional zone or QRS wave duration. Increase of QRS amplitude also was noted during atrial rapid pacing and extrastimulation. Gross AQRS values during tachycardia significantly increased in the left parasternal area, whereas QRS isopotential and VAT isochronal maps were similar during sinus rhythm and tachycardia, suggesting a minimal role of conduction delay in the increase of QRS amplitude.
CONCLUSION: QRS wave amplitude significantly increased in leads V2 through V5 during narrow QRS tachycardia compared with QRS waves in sinus rhythm. Increase of QRS amplitude seemed unlikely due to a conduction delay within the ventricular myocardium.
METHODS AND RESULTS: Using the same ECG machine and the same electrode patches applied to the same electrode positions, 12-lead ECGs during sinus rhythm and narrow QRS tachycardia were analyzed comparatively in 23 patients without ventricular preexcitation. Precordial QRS amplitudes were measured as the vertical distance from the peak of the R to the nadir of the S wave. The amplitudes also were measured during atrial rapid pacing and extrastimulation. Furthermore, ventricular excitation during sinus rhythm and tachycardia was studied using body surface mapping. Body surface distributions of QRS potentials and ventricular activation time (VAT) were displayed as maps. Gross area of QRS (AQRS, equivalent to the QRS amplitude) was compared during sinus rhythm versus tachycardia. During tachycardia, QRS amplitude significantly increased in leads V2 through V5, without any noticeable change in the transitional zone or QRS wave duration. Increase of QRS amplitude also was noted during atrial rapid pacing and extrastimulation. Gross AQRS values during tachycardia significantly increased in the left parasternal area, whereas QRS isopotential and VAT isochronal maps were similar during sinus rhythm and tachycardia, suggesting a minimal role of conduction delay in the increase of QRS amplitude.
CONCLUSION: QRS wave amplitude significantly increased in leads V2 through V5 during narrow QRS tachycardia compared with QRS waves in sinus rhythm. Increase of QRS amplitude seemed unlikely due to a conduction delay within the ventricular myocardium.