Patterns of Atrioventricular Conduction in the Human Heart

Wit, Andrew L.; Weiss, Melvin B.; Berkowitz, Walter D.; Rosen, Kenneth M.; Steiner, Charles; Damato, Anthony N.

doi:10.1161/01.res.27.3.345

Cited by 309 publications

(45 citation statements)

References 16 publications

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“…Analogous to human subjects (9,(13)(14)(15), assessment of catecholaminergic effects on cardiac conduction was performed following intravenous infusion of isoproterenol. In mice that were noninducible during the baseline EP study, an isoproterenol infusion (1-10 ng/g per min) was started.…”

Section: Methodsmentioning

confidence: 99%

Electrophysiological abnormalities and arrhythmias in alpha MHC mutant familial hypertrophic cardiomyopathy mice.

Berul

Christe²,

Aronovitz³

et al. 1997

J. Clin. Invest.

101

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A new mouse cardiac electrophysiology method was used to study mice harboring an ␣ -myosin heavy chain Arg403Gln missense mutation ( ␣ -MHC 403/ ϩ ), which results in histological and hemodynamic abnormalities characteristic of familial hypertrophic cardiomyopathy (FHC) and sudden death of uncertain etiology during exercise. Wild-type animals had completely normal cardiac electrophysiology. In contrast, FHC mice demonstrated ( a ) electrocardiographic abnormalities including prolonged repolarization intervals and rightward axis; ( b ) electrophysiological abnormalities including heterogeneous ventricular conduction properties and prolonged sinus node recovery time; and ( c ) inducible ventricular ectopy. These data identify distinct electrophysiologic abnormalities in FHC mice with a specific ␣ -myosin mutation, and also validate a novel method to explore in vivo the relationship between specific genotypes and their electrophysiologic phenotypes. ( J. Clin. Invest. 1997. 99: 570-576.)

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Section: Methodsmentioning

confidence: 99%

Electrophysiological abnormalities and arrhythmias in alpha MHC mutant familial hypertrophic cardiomyopathy mice.

Berul

Christe²,

Aronovitz³

et al. 1997

J. Clin. Invest.

101

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“…During these studies, patients were isolated and all equipment was grounded at equipotential. The following protocol for electrical stimulation was performed: (1) incremental atrial pacing to achieve the antegrade AV nodal Wenckebach cycle; (2) antegrade refractory periods using atrial basic drive of eight beats (A1A,), followed by premature atrial stimulation (A2); (3) (table I) The control CL that produced VA block was 364.6 ± 87.9 msec before PA. After PA, VA conduction was abolished in five of 13 cases (patients 2, 6, 7, 11 HV-50 fig. 3).…”

Section: Methodsmentioning

confidence: 99%

Procainamide and retrograde atrioventricular nodal conduction in man.

Shenasa¹,

Gilbert²,

Schmidt³

et al. 1982

Circulation

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SUMMARY Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 ± 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset ages 53-82 years (mean + SD 66.2 ± 9.9 years), were studied because of recurrent ventricular arrhythmias, dizziness or syncope. Eight patients had arteriosclerotic heart disease and five had no clinically detectable heart disease. Ten had normal intraventricular conduction and three had right bundle branch block. Four patients had ventricular premature complexes and one patient had an old inferior myocardial infarction.Patients gave informed, signed consent for the study.Right-heart catheterization was performed in a nonsedated, postabsorptive state. With the patients under local anesthesia, quadripolar electrode catheters were percutaneously introduced through the femoral and antecubital veins and positioned under fluoroscopic guidance across the tricuspid valve near the AV junction to permit recording of the His bundle potential. The catheters were also advanced to the high right atrium and the right ventricle to permit recordings and electrical stimulation as previously described.3The intracardiac electrograms (filtered at 30-500Hz) and three sufrace lead ECGs (usually leads I, II, and V,) and a time line were simultaneously displayed on a multichannel oscilloscope (Electronics for Medicine VR-12) and recorded on a magnetic tape (Honeywell model 96). Recordings were reproduced on photographic paper at 100 or 150 mm/sec. Electrical stimulation was performed using a digital stimulator (DTU; Bloom Associated, Ltd.). During these studies, patients were isolated and all equipment was grounded at equipotential. The following protocol for electrical stimulation was performed:(1) incremental atrial pacing to achieve the antegrade AV nodal Wenckebach cycle; (2) antegrade refractory periods using atrial basic drive of eight beats (A1A,), followed by premature atrial stimulation (A2); (3) incremental ventricular pacing to achieve ventriculoatrial (VA) block; and (4)

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“…Refractory periods Surface electrocardiographic recordings in conjunction with intracardiac recordings and stimulation from various sites allows the determination of refractory periods of the various cardiac tissue in man (Wit, Weiss, Berkowitz, Rosen, Steiner & Damato, 1970; Caracta, Rusken & Lau, 1975). It should also be remembered that changing the atrial stimulation site can alter the functional properties of the AV node (Batsford, Akhtar, Caracta, Josephson, Seides & Damato, 1974), and that the antegrade and retrograde properties of the AV node and accessory pathways may differ (Akhtar, Damato, Batsford, Rusken & Ogunkelu, 1975).…”

Section: Intracardiac Recordings and Stimulationmentioning

confidence: 99%

The Electrocardiogram in the Assessment of the Effect of Drugs on Cardiac Arrhythmias

Reid¹

1980

Cardiovascular System

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upon Tyne NE7 7DNThe search for the ideal antiarrhythmic drug continues since none of the available agents offers optimum antiarrhythmic therapy. The continuing search coupled with the interest in the mechanisms of cardiac arrhythmias has led to the development of new techniques for the study of arrhythmias and antiarrhythmic drugs. In this article it is proposed to discuss the electrocardiographic methods used in the assessment of antiarrhythmic drugs. Firstly, to discuss the electrocardiogram in the assessment of the clinical electrophysiological properties of a drug and secondly, the electrocardiogram in the assessment of the value of the drug in the management of cardiac arrhythmias in man. Assessment of the electrophysiological effects of drugs Standard ECG intervalsThe standard electrocardiogram can give some information on the effects of a drug on automaticity and conduction velocity within the heart by analysis of the standard ECG intervals-P-P (or R-R), PR and QRS intervals (Table 1).The P-P interval reflects intrinsic sinus node function and the autonomic influences on the sinus node. Thus, any change in the P-P interval following drug administration can be a direct effect of that drug on sinus node function, or by its effect on the autonomic nervous system either directly or through reflex mechanisms. Thus, antiarrhythmic drugs such as quinidine and disopyramide can influence the P-P interval by their direct depressant effect on the sinus node, by their anticholinergic effects or by reflex autonomic changes as a result of a fall in systemic pressure.The P-R interval represents conduction through the atria, AV node and His purkinje tissue and changes in the PR interval following drug administration could reflect changes in any of these. However, because there is a difference in conduction velocity in the AV node and His purkinje system (it takes 100-120 ms for the impulse to cross the AV node and approximately 40 ms to traverse the His purkinje system), major changes in conduction in the His purkinje system have to occur before they are detected on the standard ECG run at conventional paper speeds of 25-50 mm/s. For example, a 10% change in AV nodal conduction may result in a change of 10-12 ms in PR interval, but a 10% change in His purkinje conduction will only be in the region of 4 ms. Thus, significant changes in His purkinje conduction can occur without being detected on the standard electrocardiogram.QRS duration reflects conduction through the ventricular myocardium and any change reflects changes in ventricular muscle conduction-e.g. procainamide prolongs QRS duration.Since the QT interval represents ventricular repolarization, analysis of the QT interval gives some information on the effect of the drug on ventricular repolarization time. Since repolarization time is dependent on heart rate it can be corrected for rate by formulas of Bazett (1920) or in children by that of Fraser, Froggatt & James (1964). Drugs that prolong ventricular repolarization such as amiodarone or quinidine will prolong...

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Patterns of Atrioventricular Conduction in the Human Heart

Cited by 309 publications

References 16 publications

Electrophysiological abnormalities and arrhythmias in alpha MHC mutant familial hypertrophic cardiomyopathy mice.

Electrophysiological abnormalities and arrhythmias in alpha MHC mutant familial hypertrophic cardiomyopathy mice.

Procainamide and retrograde atrioventricular nodal conduction in man.

The Electrocardiogram in the Assessment of the Effect of Drugs on Cardiac Arrhythmias

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