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Electrophysiological studies with prenalterol in 19 patients (6 women, 13 men, 5 with sinus node disease, 4 with AV node disease, 7 with double node disease, 2 with conduction disturbance below His bundle, 1 normal) showed that sinus node function (heart rate, sinus node recovery time) is uniformly improved by this beta-stimulator. Also AV conduction is significantly and uniformly improved (shortening of AH interval and of the functional refractory period of AV conduction). There is no or little influence on intra-atrial conduction and on conduction below the His bundle. However, spontaneous depolarisation in His-Purkinje fibers--as tested in patients with complete AV block and ventricular demand pacemaker--is increased through beta-stimulation with prenalterol as reflected by shorter escape intervals and higher frequency escape rhythm. Prenalterol may be of clinical use in patients with cardiomyopathies who developed bradycardia under digitalisation or patients with severe bradyarrhythmia either with or without digitalis. It might also be useful in rare emergency situations, when complete pacemaker failure develops.

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Electrophysiologic studies were performed in a 41 year old man for analysis of paroxysmal tachycardias appearing in various electrocardiographic patterns of supraventricular and ventricular bigeminy, junctional and ventricular tachycardia and atrial fibrillation, among others. All these arrhythmias were due to dual atrioventricular (A-V) nodal pathways with simultaneous dual fast and slow conduction of single atrial beats at a normal basic sinus rate. Moderate changes in sinus rate and in fast or slow pathway conduction times, or both, changed the position of the slowly conducted beats between the neighboring two fast conducted beats and resulted in various electrocardiographic manifestations of the conduction disturbance. Different blocks, such as second degree type 1, 2:1, 3:1 and possibly also type II, in one of the two pathways and occasionally aberrant conduction induced even more unusual tracings. After intravenous injection of 25 mg of ajmaline, unexpected lengthening and shortening of the A-H interval occurred, suggesting variable shifts between fast and slow pathway conduction. The incidence of dual A-V nodal pathways is discussed; it was documented in 17 (4.2 percent) of 405 patients studied. A theoretical model of A-V nodal conduction is proposed to explain its normal properties and abnormal patterns.

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Standstill and inexcitability (quiescence) of the high right atrium could be demonstrated in a patient with sinus node dysfunction and bradycardia--tachycardia syndrome. The onset of P wave in surface electrocardiogram did not represent the beginning of atrial excitation but followed 130 msec the high right atrial and 50 msec the low right atrial deflection, leading thereby to a short PR interval which gave misinformation on the atrioventricular conduction. A pacemaker implant with right ventricular stimulation freed the patient of his previous complaints. 4 wk after the implantation the demand unit was inhibited for 5 h by external stimulation. Continuous ECG monitoring, esophageal ECG recording and fluoroscopic study could not reveal any atrial activity. The conditions for atrial pacemaker implantation are discussed.

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A change in the voltage and character of the His bundle deflection following premature atrial stimuli was observed and analysed in 5 of 95 patients having intracardiac conduction studies because of AV conduction disturbances. Of these 5 patients, 3 had spontaneous block within the His bundle, 2 of them showing block in other segments of the conduction system. With increasing prematurity of programmed atrial stimuli, there was a progressive decrease in the voltage of the His deflection, followed by a split His deflection, and finally disappearance of the His deflection. The voltage of the His deflection was also reduced in sinus beats following spontaneous His bundle premature beats. Similarly, during atrial stimulation at increasing rates, the His deflection decreased in voltage, split, and finally disappeared, but when Wenckebach periods appeared the His deflection reappeared in the first paced beat after the dropped beat. The preceding H-H interval was the only electrophysiological variable consistently related to the changes in the His deflection. These changes in His deflection can be explained electrophysiologically as the result of a conduction disturbance within the His bundle. The clinical significance of the phenomenon is discussed. The occurrence of this phenomenon during a conduction study makes it difficult or even impossible to localise the AV block precisely.

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Effects of hemodynamic parameters of heart rate were studied in 19 patients with low cardiac output syndrome following open heart surgery for mitral and/or aortic valve replacement in the first five postoperative days. The central venous pressure (CVP), left atrial mean pressure (LAMP), and arterial blood pressures were determined at spontaneous heart rate (SHR), and during graded atrial (12 pts.) or ventricular (7 pts.) pacing each day. An "optimal pacing rate" (OPR), characterized by the most advantageous arterial pressures at the possible lowest levels of CVP and LAMP, and by the suppression of preexisting arrhythmias, if any, was established daily for maintaining each patient on that rate. The SHR was 69 +/- 9 and the OPR was 102 +/- 9 on the first postoperative day. For the fifth postoperative day the SHR was 68 +/- 10 and the OPR decreased to 90 +/- 9. Pacing with the OPR significantly increased cardiac performance. E.g. the hemodynamic improvement on the first postoperative day induced by pacing was comparable to the spontaneous improvement seen during the first five postoperative days. The hemodynamic effect of atrial pacing on circulation was more definitive than that of ventricular pacing. Since OPR may be significantly higher than SHR and varies from day to day, we suggest that, in cases where pacing is applied to improve cardiac performance, it be determined for each patient individually each postoperative day.

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The diagnostical use of pacemaker after cardiac surgery is presented. Temporary pacemaker electrodes have been inserted during surgery into the wall of atrial and ventricular myocardium. With the aid of these electrodes, an analysator wire of 6 volts, and a Medtronic 5840 type pacemaker electrophysiological studies have been performed. The diastolic and supernormal stimulation threshold, the duration of atrial and ventricular relative refractory period were measured, the clinical significance of latency was analysed. It has been found that decrease of stimulation threshold, shortening of relative refractory period, and appearance of latency phenomenon promote arrhythmias. By investigating the conduction capacity of atrioventricular conduction system, latent conduction disturbances could be revealed, and a significant difference could be demonstrated between the atrioventricular conduction of WPW syndrome and that of other kinds of PR interval shortening. In addition the optimal heart rate requirement (optimal pacing rate) following heart surgery was defined. These parameters present more precise information on the electrophysiological condition of the heart than does the generally used ECG monitoring. When these parameters are repeatedly determined, the significance of patient's arrhythmias can be evaluated more safely and accurately; in a number of cases, even in the absence of any rhythm disturbances, impending arrhythmias can be predicted. "Pacemaker monitoring" of the postoperative heart patients, therefore, affords greater possibility for preventing the development of major cardiac arrhythmias.

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Cholinesterase and succinyldehydrogenase activity of surgically removed left atrial auricles from patients in atrial fibrillation and in sinus rhythm have been compared, using histochemical methods. Higher cholinesterase and lower succinyldehydrogenase activity has been found in atrial fibrillation than in sinus rhythm. The pulmonary capillary mean pressure of patients with atrial fibrillation and sinus rhythm have been also compared. There was no significant difference between the two groups. On the basis of the reported examinations, it is not possible to decide whether the changes in enzyme activities are the cause or the result of atrial fibrillation.

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