Shlomo Rogel

Transtelephone adjustment of antiarrhythmic therapy in ambulatory patients.

The electrocardiograms of 80 ambulatory patients receiving antiarrhythmic therapy were supervised with the help of a transtelephone monitoring system. The patients used a pocket-size modulator and reported several times daily to the receiving center integrated into the intensive cardiac care unit. The surveillance lasted for 5-28 days during which various drugs in varying dosages were administered to suppress or prevent dysrhythmias. In 94% of the patients, a satisfactory therapeutic achievement was obtained. The transtelephone system provides easy diagnosis, immediate pattern recognition, direct and frequent contact with the ambulatory patient and long periods of follow-up. During this time, the proper antiarrhythmic agent can successfully be defined, its effective dose can safely be determined and unnecessary hospitalization can thus be prevented.

Miniature Force Transducer for Myocardial Stimulation and Local Tension Measurements

The commercially available transducers for direct measurement of myocardial tension are either large in size or lack the ability of isometric measurement. Moreover, none of them enables measurement of local isometric tension just around the site of electrical stimulation of the heart. A miniature strain gauge transducer was developed in our laboratories and is herewith described. It weighs 150 mg, and consists of two arms with adjustable distance between 1-5 mm. It is applied to the heart by 2 needles which may serve also as stimulating or sensing electrodes. A full bridge made of constantan foil strain gauges ensures low drift. The device enables in vivo measurement of isometric tension of a myocardial segment of the site where the tension is being measured and permits simultaneous recording of the electrogram. Attachment of the gauge to the ventricular wall by means of needles makes simple the transfer of the transducer from one measuring point to another. The performance of the miniature force transducer was compared to that of a standard Walton-Brodie strain gauge arch demonstrating marked similarity of response at low heart rates. At high frequencies however differences in mechanical response of the heart were obtained by the two force transducers.

Force--velocity relation in cardiac muscle--analysis in the time domain. Application to the determination of quantitative and time dependent mechanisms.

Abstract This paper questions the convention that force-velocity relation in cardiac muscle determines the fundamental character of contraction. It is proposed that force-velocity relation is the consequence of force and velocity behaviour as functions of time. To demonstrate this, a simplified model was constructed. The model assumes each active site to be a load-dependent force-generator. It is proposed that the rate of appearance of calcium in the myofilament area is a preset function of time and determines that the contraction variables — tension, shortening and velocity of shortening — are also preset functions of time. Hence, force-velocity, length-velocity and other inter-relations between these contraction variables are simply obtained by plotting the appropriate variables one vs the other. The models ascending protion of isometric tension and the force-velocity relation plotted due to variations in initial muscle length, heart rate and cardio-active agents, are in good agreement with the curves produced by real cardiac muscle. The models length-velocity relation depends on instantaneous length, regardless of initial muscle length and time, as observed in real muscle. According to the model, V max and d p d t max depend on calcium and preload to the same extent as P 0 , suggesting a clue to the interpretation of similar real muscle response. Analysis of the contractile variables in the time-domain rather than in the force-velocity plane enables the determination of practical parameters of cardiac performance. The model predicts two independent clinical indices: (1) t- d p d t , the time interval from the onset of contraction to d p d t max for the estimation of the ‘time-dependent factors’ of contraction, and (2) A p , the product of t- d p d t and d p d t max for the estimation of the ‘quantitative factors’ of contraction. Experimental data support this prediction.

In vivo myocardial excitability studied by simultaneous electrocardiogram and electrogram

Summary In open-chest dogs with complete A-V block unipolar ventricular stimulation was applied at various current levels and at different time intervals in the relative refractory period. The silver-silver chloride electrode, used for stimulation, was also used for recording of electrograms. In other experiments an EG needle electrode was utilized; thereby stimulation and recording were carried out at different but very close sites. It was found that progressively increased current levels from zero to a few milliamperes cause distinct and well defined local electrical responses, the magnitude of which is related to the current level. The local response is not detectable in a simultaneously recorded conventional electrocardiogram until a certain magnitude is obtained, at which stage a generalized response of the heart is inscribed in both recording methods. A local response preceding the QRS complex is clearly seen in the electrogram prior to the generalized response. It is assumed that in the in vivo beating heart, current levels insufficient to stimulate the whole heart may evoke a local and detectable electrical response of a number of adjacent myocardial fibers. The lack of propagation of local responses of different magnitude may be explained by the various degrees of refractoriness offered by the ventricular and Purkinje fibers. The data presented in this study are in accordance with and offer a reasonable explanation for previously described marked variations in the threshold of excitability of the in situ heart.

Ventricular Rhythms in Acute Myocardial Infarction

Ectopic ventricular activity in acute myocardial infarction is considered to be benign if it is slow and regular (accelerated idioventricular rhythm), but ominous when rapid (ventricular tachycardia). However, it has been observed in an increasing number of reports that these two types may coexist in the same patient, altering thereby the clinical significance of both. In the present study electrocardiograms were analyzed of 55 patients hospitalized for acute myocardial infarction, in whom idioventricular rhythm occurred. It was found that three major types of ventricular rhythms could be identified: a regular-stable rhythm, an irregularunstable one, and a third variant which was a combination of these two types. The stable ventricular rhythm was self limited and harmless. The unstable and combined types which were characterized by random coupling times and varying interbeat intervals, were frequently associated with re-entrant beats and fast ventricular rates and therefore a potentially ominous prognosis. It is suggested that the Ca++ dependent slow diastolic depolarization may be the mechanism responsible for the unstable ventricular rhythm, and the reasons for this assumption are discussed. A therapeutic approach based on the above considerations is described.

Evaluation of time-dependent and quantitative properties of contraction from left ventricular pressure

SummarySeveral mechanical indices predicted from a model of cardiac muscle contraction are tested. In thein-vivo canine heart, dp/dtmax and t-dp/dt, the time, interval from onset of contraction to dp/dtmax, were measured. The product of these parameters Ap=t-dp/dt×dp/dtmax was calculated. t-dp/dt was shortened when heart rate was elevated and remained constant when ventricular end diastolic volume was changed. Ap increased with augmentation of ventricular end diastolic volume. To achieve constant muscle length when heart rate is changed, analogous tension measurements (assigned as dT/dtmax, t-dT/dt and AT) of prestretched Walton Brodie strain-gauge arch had been taken instead of pressure measurements. In the experiments in which Tmax, maximal isometric tension, was not changed for various heart rates, AT was also unchanged. These results are consistent with the predictions that t-dp/dt and Ap can be used as two independent mechanical indices: 1) t-dp/dt for the evaluation of the “time-dependent properties” of contraction and 2) Ap, for the evaluation of the “quantitative properties” of contraction. The advantages of applying these two mechanical indices for use in the intact ejecting heart, instead of the well-established parameters Vmax and Po are emphasized.ZusammenfassungIn der vorliegenden Studie werden verschiedene mechanische Indizes getestet, die auf der Grundlage eines Modells der Herzmuskelkontraktion entwickelt wurden. Beim Hundeherzen in vivo wurden dP/dtmax und t-dp/dt, das Zeitintervall vom Beginn der Kontraktion bis zur maximalen Druckanstiegesgeschwindigkeit, gemessen und das Produkt aus diesen Parametern Ap=t-dp/dt×dp/dtmax berechnet. t-dp/dt nahm mit steigender Herzfrequenz ab, war jedoch unabhängig von Veränderungen des enddiastolischen Ventrikelvolumens Dagegen stieg Ap mit Zunahme eine konstante Muskellänge zu erreichen, wurden mit Hilfe eines Dehnungsmeßstreifens anstelle der Druckmessungen analoge Spannungsmessungen (dT/dtmax, t-dT/dt und AT) durchgeführt. Wurde die maximale isometrische Spannung bei unterschiedlichen Herzfrequenzen nicht verändert, so war auch At konstant. Diese Ergebnisse sprechen dafür, daß t-dp/dt und Ap als zwei unabhängige mechanische Indizes verwendet werden können: 1. t-dp/dt für die Bewertung der „zeitabhängigen Eigenschaften” der Kontraktion und 2. Ap für die Bewertung der „quantitativen Eigenschaften” der Kontraktion. Die Vorteile einer Anwendung dieser beiden mechanischen Indizes für den Gebrauch beim intakten Herzen anstelle der weit verbreiteten Parameter Vmax und Po werden betont.

Quantitative analysis of myocardial force and contractile state in in vivo rate and rhythm disturbances

A working hypothesis is presented which is aimed to reach a quantitative analysis of the beat to beat changes in the contractile force and contractile state in various regular and irregular rates and rhythms in the beating canine heart. It is suggested that every electrical depolarization contributes a certain inotropic effect (IED) which is consumed during contractions (C), or if unused it is cumulated (CIED) to serve as the initial condition for the next beat. On the basis of a series of in vivo measurements of isometric myocardial tension in anesthetized dogs, with controlled rate and rhythm alterations, the interrelations between these factors were defined in a series of mathematical formulations. The conclusions thus reached indicate that: (1) the force of a beat is determined by the restitution of contractility which is time dependent; (2) the force developed at any steady rate or any irregular rhythm is different from the contractile state (FR) which is the potential force the myocardium would perform had a full recovery been provided; (3) FR rises with frequency as exponential function of the interbeat interval; (4) FR changes following extrasystoles as a function of their preceding interval irrespective of the basic heart rate; (5) the steady force of a beat following sudden rate change is reached in a rather constant number of beats (6–8) independent of the direction of change or the time required for that number of beats.

Myocardial conduction time and antiarrhythmic drugs.

Complete a-v block was induced in anesthetized mongrel dogs by direct electrocoagulation of the a-v node. The ventricles were paced by steady stimulation (S1) at a rate of 100/min. and by test stimuli (S2) with varying post S1 delay. Right ventricular myocardial tension was measured from the S2 stimulation site of a specially designed miniature strain gage and from a different site by a Walton-Brodie strain gage. A reproducible time lag between the two sites could be measured by comparing the differences in mechanical response to S2 stimuli. This time difference was called delta IT. delta IT varied markedly (from 10-60 msec) when measured at different sites but no linear relationship between delta IT and the inter-gage distance could be observed. Increasing the S2 current intensity induced shortening of delta IT from 37 +/- 13 msec (mean +/- S.D.) at the threshold current to 16 +/- 10 msec (mean +/- S.D.) with 10 mA. A strength-delta IT curve could be constructed and was found to be remarkably reproducible during the experiment. Quinidine and disopyramide induced upward displacement of the curve, lidocaine did not change it while verapamil lowered the delta IT values. We suggest that delta IT can be used as a reliable indicator of myocardial conduction rate. The possible reasoning for this suggestion has been discussed.

A new hazard in the use of an external demand pacemaker.

Ventricular pacing by a Medtronic model 5880A external demand pacemaker was shown to be inhibited as long as the metal coverplate of the pacemaker was touched with bare hands. The asystolic periods were induced by a previously undescribed malfunction of the pacemaker, inherent in its structure. This phenomenon occurred when both patient and physician were isolated from any main operated instrument. It could be demonstrated that pacer inhibition was induced by capacitive coupled 50 Hz fields from the environment, activating the sensing mechanism through the metal coverplate. The plastic covered Medtronic model 5840 pacemaker does not have such undesirable characteristics.

In vivo atrial excitability and anti-arrhythmic drugs

The threshold of excitability of the atrial muscle was studied in the in vivo beating canine heart. Unipolar cathodal and anodal strength-interval curves were constructed and found to be dissimilar in shape. It was found that at any interval within the relative refractory period of the atrium, as in the ventricle, there is a wide range of current levels delineated by an upper (TU) and lower (TL) limit of threshold which can stimulate the atrial myocardium. Within these limits the threshold varies spontaneously and can be reduced to TL level by a run of extrasystoles. Such TU and TL curves were repeatedly determined following administration of therapeutic doses of quinidine, procaine amide or lidocaine. It was observed that all three drugs prolonged the refractory period. The TU values increased following each of the drugs, and mostly after quinidine, while the TL curve was less affected by quinidine. It is suggested that the exit block thus produced is the principal mechanism whereby quinidine depresses atrial disrhythmias.