ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY Changes in cardiac metabolism in myocardial failure and after alcohol ingestion are discussed. The main effect of alcohol ingestion is loss of cardiac contractility. Since heart muscle does not contain alcohol dehydrogenase, its toxicity is probably the result of a direct toxic effect of ethanol and acetaldehyde on the myocardial cell, possibly involving various membrane systems. Alcohol inhibits mitochondrial respiration and the activity of enzymes in the tricarboxylic acid cycle, and it interferes with both mitochondrial calcium uptake and binding. Ethanol profoundly affects myocardial lipid metabolism. Acetaldehyde diminishes myocardial protein synthesis and inhibits Ca+ +-activated myofibrillar ATPase. In myocardial failure, a series of possibilities may be responsible for the loss of contractility. Excitation-contraction coupling could be disturbed at the level of the sarcolemma, at the sarcoplasmic reticulum, at the mitochondria, and between calcium and the regulatory proteins. Deficiencies in Ca++ delivery systems of excitation-contraction coupling on the myosin ATPase activity could be responsible for the diminution in cardiac contractility. Mitochondrial function may also be involved, since mitochondria from failing human hearts are defective with respect to respiratory control and calcium accumulation. Under certain conditions, the relationship of mitochondria to calcium sequestration is very important in influencing contractility. The involvement of contractile and regulatory proteins in myocardial failure cannot be excluded.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY We performed intracardiac electrophysiologic studies in 33 patients with recurrent ventricular tachycardia. Nineteen patients underwent one, 10 patients two, and four patients three serial electrophysiologic studies. Ventricular tachycardia was successfully induced in 83% of the patients, and pacing methods were successful in terminating tachycardia in 71% of the studies, although pacing-induced acceleration of ventricular tachycardia occurred at least once in 36% of the studies. Seventeen of the 33 patients (52%) required a total of 24 external direct current cardioversions during study.In 21 patients a variety of antiarrhythmic drugs were given I.V. and attempts at ventricular tachycardia induction were repeated to assess prophylactic effects of the drugs. An acutely effective drug or combination of drugs was found in 15 of the patients (71%). Fourteen of the 15 were placed on chronic oral therapy with the effective agent and were followed for an average period of 8.1 months (range one to 33 months). In all 14 patients we could document complete (13 patients) or partial (one patient) long-term prophylaxis against ventricular tachycardia.We conclude that drug efficacy trials in patients with recurrent ventricular tachycardia using intracardiac pacing techniques is a rapid and accurate method of selecting effective long-term antiarrhythmic therapy.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY Twenty patients with recurrent sustained ventricular tachycardia (VT) underwent serial electrophysiological studies (EPS) 1) to determine the predictive value of the EPS in the selection of antiarrhythmic therapy, and 2) to establish the therapeutic efficacy of available antiarrhythmic agents. In each patient VT could be reproducibly initiated by programmed stimulation. After control EPS, the effects of several drugs (lidocaine, procainamide, quinidine, disopyramide and diphenylhydantoin) on the ability to initiate VT were assessed. An oral regimen was chosen on the basis of acute EPS and its effectiveness was evaluated by repeat EPS in 24-72 hours. Blood levels achieved acutely were used as guidelines to chronic therapy.In 14 patients the initiation of VT was prevented by the acute administration of one or more agents. In 13 of these patients, a chronic oral regimen based on these results prevented recurrence of VT with a three- to 27- month follow-up. In the remaining patient, oral therapy could not achieve blood levels of procainamide shown to be effective intravenously, and VT recurred. In six patients no single drug or drug combination was effective during acute EPS, and VT recurred in all while on therapy with the agent shown to make initiation of VT most difficult. Procainamide prevented VT in nine patients; quinidine in three patients; lidocaine in three patients; diphenylhydantoin in two patients; and disopyramide in one patient. The mean duration of EPS studies was 4.5 days.This study suggests that serial EPS provides rapid identification of successful antiarrhythmic therapy and can predict in which patients conventional therapy would be ineffective, thereby identifying patients requiring more aggressive modes of therapy.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY Fixed coupled ventricular premature depolarizations (VPDs) are usually considered reentrant; recent experimental models have demonstrated that parasystolic rhythms may also appear in fixed coupled patterns. To analyze the mechanisms of fixed coupled VPDs, 60 exercise tests were chosen to evaluate the response of VPD coupling intervals to changes in cycle length of the dominant supraventricular rhythm. Selection criteria included the presence of frequent, unifocal VPDs that were fixed coupled (variation < 80 msec) at any one cycle length, with the persistence of VPDs at several different cycle lengths. Three patterns of response of coupling intervals to changes in cycle length were noted: 1) 32 patients with a direct linear relation (r > 0.9) of coupling intervals to cycle length; 2) 16 patients with coupling intervals fixed, independent of cycle length; and 3) 12 patients with no consistent relation over a wide range of cycle lengths. Two patients in group 2 and four in group 3 fulfilled criteria for parasystole with interectopic intervals that remained constant at different cycle lengths. These results suggest that VPDs in group I are reentrant, while some patients with group 2 or 3 responses have evidence for parasystolic rhythms. We conclude that 1) fixed coupling of VPDs is not diagnostic of reentry, and 2) changes in cycle length induced with exercise may be useful in the analysis of mechanisms of VPDs.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY The effects of intravenous procainamide infusion of 10-14 mg/kg body weight (i.e., 750 mg) of procainamide (PA) on reentry within the His-Purkinje system (HPS) were studied in 13 patients using His bundle electrograms and ventricular extrastimulus method. PA abolished reentry in eight patients (group 1) and decreased the width of reentry zone in the remaining five (group 2). At comparable S,S2 intervals, the S2H, intervals after PA were longer than control in all patients. In group 1 patients, after PA, reentry did not occur even at S2WH intervals that were significantly longer than control critical S2H2 intervals. In two of eight patients in group 1, PA abolished reentry by converting unidirectional block into bidirectional block in the antegrade limb (right bundle) of the reentry circuit. In the remaining six patients reentry was abolished because of consistent retrograde block of 82 impulse at some point between the site of stimulation and the His bundle recording site. In group 2, reentry was initiated after PA at approximately the same S,S% intervals as in control, but required significantly longer S2H2 intervals; in these patients the zone of reentry was shortened due to increase in effective refractory period of the ventricular muscle. PA significantly increased the functional refractory period of HPS and the effective refractory period of ventricular muscle. The results of this study differ from the previously reported effects of lower concentrations of PA which facilitated reentry within the same circuit. We conclude that the effects of PA on reentry are dose-related and can both facilitate and suppress reentry, depending on critical changes in conduction and refractoriness of the HPS.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY The electrophysiologic changes associated with dysrhythmias induced by coronary occlusion and by subsequent reperfusion were characterized with six complimentary approaches in chloraloseanesthetized cats (n= 57) with proximal occlusion of the left anterior descending (LAD) coronary artery. Occlusion led to reproducible ventricular dysrhythmia which abated in 35 minutes. The electrophysiologic effects of reperfusion initiated at this time could be studied. Simultaneous bipolar electrograms (epi-, myo- and endocardial) from ischemic and normal zones were analyzed by computer. Before the onset of the dysrhythmia induced by occlusion, conduction was markedly slowed, with dV/dt decreasing to 34% ± 6% of control and conduction time (endo- to epicardial activation) prolonged to 328 ± 77% of control. However, these values returned toward normal with reperfusion, even though it also consistently induced dysrhythmia. The idioventricular escape rate (determined by intense vagal stimulation) was 62 ± 6 beats/min during the dysrhythmia induced by occlusion (equal to control), but increased during the reperfusion dysrhythmia to 188 ± 12 beats/min. The occlusion dysrhythmia was exacerbated, but the reperfusion dysrhythmia was suppressed by rapid atrial pacing. The refractory period progressively shortened after ocdusion and remained decreased during early reperfusion. Thus, increased conduction time through myocardial and epicardial regions, asynchronous depolarization and shortening of the refractory period accompanied dysrhythmia induced by occlusion.In contrast, the dysrhythmia induced by reperfusion was characterized by normal conduction time, through myocardial regions with continued significant epicardial delay, overdrive suppression, synchronous depolarization and a high idioventricular rate.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SUMMARY In studies to ascertain the basis of dynamic changes in the P wave, bipolar epicardial potentials were recorded from multiple atrial electrodes in dogs. One hundred to 120 activation times were displayed by a digital computer and used to construct atrial isotemporal activation sequence maps. Changes in heart rate or beat-to-beat cycle length were induced by vagal stimulation or infusion of autonomic mediating drugs. Changes in cycle length were associated with dynamic changes in the atrial activation sequence and surface P-wave. A conspicuous finding was that epicardial atrial depolarization began at three widely separated locations. These three points were consistently present in all animals and were generally located at the 12, 3, and 6 o'clock positions of the superior vena cava-right atrial junction. The dynamic changes in P waves and atrial activation sequence which accompanied the changes in cycle length were due to sudden shifts in the point of earliest activity between the three early sites. Asymmetric atrial depolarization with more rapid conduction along the crista terminalis, superior interatrial band, and pectinate muscles was present in all dogs. Although the anisotropic atrial geometry played an important role in the asymmetric conduction, the widely distributed onset of activity contributed significantly to the uneven spread. The multiple points of origin of the atrial wavefront might be explained by either a trifocal, distributed pacemaker or the epicardial exits of three specialized pathways conducting an impulse emanating from a single focus. These data explain the dynamic variation in P-wave morphology in normal hearts and also imply a relationship between the altered origin of atrial depolarization, atypical P waves, brady- or tachyarrhythmias, and heart rate control.

ISSN:0009-7322    

出版商:OVID    

年代:1978

数据来源: OVID