Fast Pacing Rates Research Articles

Recording from the body surface of arrhythmogenic ventricular activity during the S-T segment

Recent experimental reports have documented the delay of epicardial potentials beyond the QRS complex as a result of infarction, and the degree of delay was directly associated with the onset of ventricular arrhythmias. This study describes a method using high amplification, band pass filtering and signal averaging for recording from the body surface these delayed potentials presaging ventricular arrhythmias. This technique, has been used for recording low level cardiac potentials masked by noise. In 10 dogs control records of the electrocardiogram and surface averaged lead were obtained during sinus rhythm, atrial pacing and premature atrial beats. Subsequently, the left anterior descending coronary artery was ligated in each dog. Nine dogs survived the surgical procedure and underwent similar recordings 3 to 6 days after infarction. Electrocardiographic changes were consistent with a recent infarction. During the pacing protocol discrete multiphasic wave forms appeared during the S-T segment of the surface averaged lead, and concomitant changes in the terminal portions of the QRS complex were observed in seven dogs. In five of these dogs ventricular arrhythmias were observed at the faster pacing rates or after closely coupled premature atrial beats. The chest was then reopened and the pacing procedure repeated during recording of direct epicardial electrograms with a multicontact bipolar electrode. This electrogram validated the existence of potentials during the S-T segment in all but one dog and late activity that was not repeatable on a beat to beat basis in another. Thus, when late activity was confirmed with the epicardial electrogram, seven of eight dogs showed a corresponding change in the surface averaged lead. This technique may prove to be a sensitive indicator of abnormal electrical activity preceding ventricular arrhythmias.

Conduction disturbances of the bundlebranches produced by lesions in the nonbranching portion of His bundle

The present experiments were conducted on isolated dog hearts to demonstrate that conduction disturbances can be induced in the bundle branches by transection of about 50 per cent of the cross-sectional area of the His bundle on the right or left side. The His bundle, the posterior and anterior divisions of left bundle, and the right bundle were exposed by careful dissection, and microelectrode techniques were used to record action potentials from the three bundle branches. Pacing stimuli were applied to the nonbranching portion of His bundle proximal and then distal to the site of transection to study the effect of such lesions on impulse conduction to the bundle branches. It was demonstrated that conduction to the bundle branches was not affected by such lesions in the His bundle at pacing rates slower than 100 per minute; however, conduction disturbances were rate-dependent and manifested at faster pacing rates. In nine out of all 16 experiments, partial or complete block occurred in all three bundle branches regardless of the side of the lesion. In the remaining seven experiments, they were observed in the bundle branch on the same side as the lesion. It was assumed that conduction disturbances of the bilateral bundle branches resulted from decremental conduction in the uncut portion of His at the level of lesion, and those of the ipsilateral branch from the functional failure of transverse crossover connections between the longitudinal His bundle fibers. The results indicate that localized lesions in the nonbranching portion of His bundle can indeed produce the pattern of bundle branch block under certain conditions.

Phasic left ventricular blood velocity alternans in man

With use of the Doppler ultrasonic flowmeter catheter, phasic instantaneous left ventricular blood flow velocity was measured by radiotelemetry in 28 subjects during pacemaker-evoked pulsus alternans. Blood velocity alternation was more manifest at faster pacing rates. Four patients demonstrated diastolic blood velocity alternans at the mitral valve. Discordant right heart pressure and left ventricular blood velocity alternation was recorded in three subjects. In one such patient, rate-related shifts of concordant and discordant left ventricular blood velocity alternans occurred. Intermediate or variant forms of alternation, comprising weak and strong beats in a ratio of 2:1, were noted in two subjects. This study provides the first comprehensive description of left ventricular blood velocity alternans in man. The observed phenomena may be related to an altered inotropic state or to beat to beat variations in end-diastolic fiber length.

Effect of ventricular premature beats on idioventricular pacemaker activity

The effect of ventricular premature beats on idioventricular pacemaker activity was studied in open-chest dog hearts with a surgically induced block in the His bundle. While the ventricle was paced by basic stimuli at a given rate, the pacing was interrupted for about 2.5 seconds following every twelfth basic beat (V 1) in order to obtain the interval between V 1 and the first escape beat (V e) or the basic escape interval (V 1V e). Ventricular premature beats (V 2) were then introduced at various coupling intervals (V 1V 2) and the effect of these premature beats on the postextrasystolic escape interval (V 1V e) was observed. The plot of V 2V e against V 1V 2 intervals showed that the V 2V e interval was shortest at shorter V 1V 2 intervals, and it increased gradually with the increase in V 1V 2 intervals. The V 2V e intervals at shorter coupling intervals were much shorter than the basic escape interval (V 1V e), indicating enhanced automaticity after early premature beats. The V 2V e at longer coupling intervals were much longer than the basic escape intervals, indicating suppressed automaticity after late premature beats. The similar response to ventricular premature beats was noted during spontaneous idioventricular rhythm. The suppression was more pronounced at faster pacing rates and following two successive premature beats, probably due to the phenomenon of overdrive suppression. The same phenomena of altered automaticity after premature beats could be observed under the influence of ouabain, epinephrine, lidocaine, and propranolol, although these agents either decreased or increased the average escape intervals. The results may explain the clinically observed alteration of the idioventricular pacemaker rate following ventricular premature beats.

The haemodynamic effects of atrial pacing in patients with ischaemic heart disease.

Abstract. The haemodynamic effects of atrial pacing in 49 patients with ischaemic heart disease are described. The chief effect is a progressive reduction in stroke volume. Systemic pressure is unchanged but filling pressures first fall and then rise at the faster pacing rates. Cardiac output also falls at faster rates. It is concluded that atrial pacing has no deleterious effects in the range of rates that is used clinically to control bradycardia without atrio‐ventricular block, or to treat arrhythmias. It is preferable to ventricular pacing because it retains atrial transport.

HEART-BLOCK FOLLOWING ACUTE MYOCARDIAL INFARCTION: Treatment with Demand and Fixed-rate Pacemakers

The mortality was 45·5% in 55 patients treated with artificial pacing for atrio-ventricular conduction disturbance complicating acute myocardial infarction. The mortality in 18 patients who had fixed-rate pacemakers was 56%, compared with 38% in 37 patients with demand pacemakers—a difference that was not statistically significant. Demand pacing did not remove the risk of ventricular fibrillation, and fast pacing rates and suppressant drugs are still needed when ectopic competition occurs. The most important factor in the high mortality was myocardial failure, which caused 21 of the 25 deaths. Anterior infarction and syncopal attacks also carried a high mortality, and prevention of syncope by early electrode insertion appears to be beneficial.