Sixty-five consecutive autopsied cases of ventricular aneurysm are reviewed. The incidence of aneurysm following myocardial infarction is similar to that reported in other series. Myocardial infarction preceded the formation of an aneurysm of the ventricle in the vast majority of patients, and a new myocardial infarction was the cause of death of about 50 per cent of them. The survival rate of patients with ventricular aneurysm is not significantly different from the long-term survival of all patients with myocardial infarction found in the same institution. Complications of ventricular aneurysm such as chronic congestive heart failure and rupture of the aneurysm were infrequent causes of death, and systemic embolic phenomena were not observed as a cause of death. In only four patients was the diagnosis made ante mortem. The lack of characteristic clinical, radiologic, and electrocardiographic findings is discussed. It is suggested that the hemodynamic significance of ventricular aneurysms is not ordinarily great, in view of the unaffected statistical prognosis in its presence. The recommended indications for surgery of ventricular aneurysms, based on this retrospective study, are presented.
Artificial pacing of patients with Stokes-Adams disease provided an opportunity to study experimentally the ways of operation of concealed antegrade or retrograde conduction, or both, in the AV junction. With a catheter electrode in the right atrium the classical experiment of Lewis and Master was repeated, revealing, during a 2:1 ventricular response to an atrial tachycardia, the delaying effect of seemingly blocked atrial impulses on subsequent AV conduction. Shifting the position of a single premature atrial impulse within a constant driving cycle of the atria produced graded effects of "blocked" atrial impulses on AV junctional refractoriness, permitting an estimation of the duration of the "phase of concealed AV conduction." Interpolation of such premature atrial impulses into successive driving cycles resulted in "repetitive concealed conduction." In an artificially produced atrial parasystole there was observed "concealed discharge" of a subsidiary (escaping) AV junctional pacemaker by an apparently nonconducted atrial impulse. With a catheter electrode in the right ventricle in a case of advanced AV block, concealed retrograde conduction of pacer stimuli disturbed the rhythmicity of a spontaneous AV junctional pacemaker. In a case of advanced AV block with preserved retrograde conduction (unidirectional block), evidence of penetration of the upper AV junction by the "blocked" antegrade impulse was found. With electrodes implanted in the left ventricle in a case of advanced AV block, concealed retrograde conduction of the artificial pacemaker stimuli enhanced antegrade conduction by transiently changing an area of unidirectional block to one of supernormal conduction. Thus, all known manifestations of concealed atrioventricular and ventriculo-atrial conduction, occurring spontaneously in clinical records or induced in animal experiments, were artificially reproduced in the human heart.
The heart rate can be controlled by an electrical pacemaker when its frequency of stimulation is greater than that inherent in the heart. 1 " 3 However, no method has been described, to our knowledge, by which a rapidly beating heart may be slowed by means of repetitive electrical impulses applied to the heart. The commercial pacemakers available for clinical application generate d-c electrical impulses with a duration of about 3 msec. Although the voltage and frequency of the impulses can be changed within certain limits, the duration of the impulses is kept constant. 2 " 4 While studying the control of heart rate in dogs by means of an intracardiac electrical pacemaker, we found that the frequency of effective ventricular contractions, namely those that produced an arterial pulse or at least a clearly visible ventricular pulse, could be reduced by almost 50% by increasing appropriately the duration of the electrical impulse of the artificial pacemaker. It was soon determined that this effect was due to proper spacing between the make and break of the repetitive impulses. Electrotonus was not involved in the change of ventricular rate. This decrease of the frequency of effective ventricular contractions could be reproduced with pairs of impulses, each 3 msec in duration, when the two impulses of the pair were properly spaced. A decrease in ventricular frequency could also be induced when the interval between break and make of successive long impulses fell in an appropriate range; in which case it was the break that became the first and the make the second stimulus-just the reverse of the usual sequence when long impulses were used.This finding was subjected to repeated tests in dogs with sinus rhythm and in several animals with experimentally produced arrhythmias. It was studied also in one patient with Stokes-Adams attacks due to intermittent A-V block, who had an intracardiac electrode catheter introduced to pace the heart. Our observations and a discussion of the mechanisms by which this reduction of heart rate is produced are the subjects of this communication. I. Ventricular Stimulation MethodsThirteen dogs, weighing 18 to 23 kg and anesthetized with pentobarbital (20 to 25 mg/kg iv), were used for these experiments. Unipolar right atrial intracavitary electrocardiograms (RA ECG), right atrial (RA), and right (RV) and left ventricular (LV) pressures were recorded simultaneously by catheters. The catheters in the right atrium and ventricle were introduced via the jugular vein; the one in the left ventricle was introduced via a femoral artery. A thoracotomy was performed after the catheters were in place and intermittent positive pressure breathing was maintained throughout the entire procedure. A pericardiotomy was then done and a pair of platinum electrodes was hooked into the free wall of the right ventricle for stimulation by the artificial pacemaker. In some dogs the left atrium (LA) was cannulated after the chest had been opened and left atrial pressure was also recorded.Electrocardiograms and pressures...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.