Time-normalized correlation of ventricular activation and the vectorcardiogram

Boineau, John P.; Spach, Madison S.; Ayers, Charles R.

doi:10.1016/0002-8703(67)90310-9

Cited by 24 publications

(3 citation statements)

References 37 publications

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“…The reason could be the polymorphic anatomical substratum of septal and posterobasal zones compared with the more homogeneous and concentric architecture of the ventricu lar free wall leading to a regular endoepicardial activation [26]. In our study, we used an original noninvasive meth od to verify this hypothesis in humans: the SVECG-QRS, which produces a good representation of the successive ventricular depolarization phases [4,5],…”

Section: Discussionmentioning

confidence: 90%

“…The results of two studies suggested that quini dine has a heterogeneous ventricular conduction effect, i.e. a more pronounced negative conduction effect at the onset and the end of the QRS complex, unrelated to the bundle branch block [2,3], In order to verify this hypothe sis, we performed a randomized placebo-controlled trial using the spatial velocity electrocardiogram of the QRS complex (SVECG-QRS) which allows a good representa tion of the successive ventricular depolarization phases [4,5], Before its introduction and application by Hellerstein and Hamlin [4], this method had only been used in healthy subjects and as a diagnostic tool in various cardiac diseases [6][7][8][9][10][11][12][13][14][15], This study involves the first application of SVECG-QRS for assessing the electropharmacodynamic effect of antiarrhythmic drugs.…”

Section: Introductionmentioning

confidence: 99%

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Heterogeneous Effect of Quinidine on the Ventricular Depolarization Process Assessed by the Spatial Velocity Electrocardiogram of the QRS Complex

et al. 1996

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The negative conduction effect of quinidine on each of the successive phases of the ventricular depolarization was investigated using an original noninvasive method: the spatial velocity electrocardiogram of the QRS complex (SVECG-QRS). We performed a randomized placebo-controlled trial in 10 healthy subjects with a single oral dose of quinidine (330 mg) or placebo. Electrocardiographic acquisition and processing (220 recordings for the complete trial) were performed using the Lyon vectorcardiographic program. For each SVECG-QRS curve, the position of seven specific points from A (onset of QRS) to G (end of QRS) were determined precisely. The six successive time intervals between these points (AB-FG) and five velocity values (B-F) were then calculated. The QRS complex was longer under quinidine than placebo (102.4 ± 1.6 vs. 100.3 ± 1.5 ms). The difference was at the periphery of statistical significance (p = 0.05), and this lack of statistical difference may be mainly due to the low serum levels of quinidine obtained at the peak of the concentration (1.46 ± 0.4 mg/l). All six QRS time intervals were longer under quinidine, but only the BC interval was significantly different (9.3 ± 1.1 vs. 18.8 ± 1.1 ms; p < 0.05) suggesting a more pronounced negative conduction effect at the onset of ventricular depolarization. No significant modifications were observed for the velocity values. We conclude that (1) the negative conduction effect of quinidine is heterogeneous, but a further study with a higher dose of quinidine (concentration-dependent effect) is required to confirm this hypothesis and (2) the spatial velocity electrocardiogram of the QRS complex allows a detailed analysis of the ventricular conduction phases. The results of the measurement were found to be reproducible. This noninvasive tool could be used in clinical practice to assess effects of antiarrhythmic drugs on successive ventricular depolarization phases.

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Heterogeneous Effect of Quinidine on the Ventricular Depolarization Process Assessed by the Spatial Velocity Electrocardiogram of the QRS Complex

et al. 1996

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“…In the center is a schematic presentation of the area of delay viewed in the frontal and left sagittal projections. In the control state, the loop moves counterclockwise in all three planes; such movement is characteristic of canine vectorcardiograms recorded by the McFee system (31,34). The frontal plane loop showed no marked axis change after left anterior divisional block; however, the terminal forces were shifted superiorly and delayed.…”

Section: Controlmentioning

confidence: 95%

Activation Studies following Experimental Hemiblock in the Dog

Gallagher

Ticzon

Wallace

et al. 1974

Circulation Research

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Electrocardiograms (ECG), McFee vectorcardiograms (VCG), and ventricular activation data were collected from 25 anesthetized dogs before, immediately after, and 4 weeks after surgically induced discrete left anterior divisional block. Left anterior divisional block resulted in minor ECG changes: small S waves developed in leads II, HI, and aVF and the QRS complex was prolonged 5-15 msec (mean 9 ± 2.7 [SD] msec). Prominent VCG changes also occurred: maximal and terminal forces were shifted posteriorly, superiorly, and slightly leftward, the duration of the loop was increased 5-15 msec (mean 9.8 ± 2.8 msec), and the terminal portions of the loop were slurred. Epicardial surface mapping revealed a consistent area of 5-20-msec delay (mean 12 ± 5.1 msec) confined to the lateralbasal surface of the left ventricle. Transmural activation studies in this area invariably revealed 6-20-msec (mean 12.8 ± 4.8 msec) delays in Purkinje and 3-25-msec (mean 12.4 ± 5.6 msec) delays in endocardial activation. The wave front propagated across the wall with normal velocity. Q waves developed due to a "window effect" in the area of delay. Combining division of the septal fibers with left anterior divisional block resulted in surface delays of greater magnitude with marked axis shifts toward the left. Despite the extensive interconnections of the left ventricular conduction system, discrete proximal left anterior divisional block resulted in a significant alteration in the sequence of ventricular activation, confirming the fascicular nature of the left ventricular conduction system. The septal division appears to be an integral part of this system. The methodology described in this paper can be used to readily differentiate between epicardial delay due to conduction delay and that due to intramural myocardi'al delay. KEY WORDS epicardial mapping left anterior hemiblock vectors myocardial conduction delayPurkinje activation myocardial infarction• Experimental injury to subdivisions of the left bundle branch was first reported in 1910 (1). Subsequent studies over the ensuing 60 years have gradually led to the concept of two functionally distinct subdivisions of the left bundle, i.e., the anterior and posterior divisions (2-24). More recently, in vitro studies by Myerburg et al. (25,26) have suggested that widespread interconnections between the anterior and posterior Purkinje networks of the left ventricle make it unlikely that isolated lesions in proximal subdivisions of the left bundle branch would result in significant changes in ventricular activation. Furthermore, histological examinations of the human conduction system in patients who exhibited electrocardiographic evi- This investigation was supported in part by U. S. Public Health Service Grants HL 05736 and HL 08845 from the National Heart and Lung Institute.Dr. Wallace is the recipient of Research Career Development Award HL 19949 from the National Heart and Lung Institute.This study was presented in part at the 46th Annual Scientific Session of the American Heart Asso...

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Right Bundle-Branch Block and the Velocity of the Electrocardiogram

Gamboa¹

1967

Arch Intern Med

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Time-normalized correlation of ventricular activation and the vectorcardiogram

Cited by 24 publications

References 37 publications

Heterogeneous Effect of Quinidine on the Ventricular Depolarization Process Assessed by the Spatial Velocity Electrocardiogram of the QRS Complex

Heterogeneous Effect of Quinidine on the Ventricular Depolarization Process Assessed by the Spatial Velocity Electrocardiogram of the QRS Complex

Activation Studies following Experimental Hemiblock in the Dog

Right Bundle-Branch Block and the Velocity of the Electrocardiogram

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