Biomedical subjects
Publications and source records attributed to C R Wyndham.
Classic and concealed entrainment was demonstrated in a patient with spontaneous typical atrial flutter and pacing-induced atypical atrial flutter. The form of entrainment manifested depended on the site of pacing and the direction of tachycardia as determined by endocardial mapping.
To determine whether a regional approach to surgery for ventricular tachycardia would improve on the results of previously reported methods of endocardial resection, an analysis was performed of our surgical experience over a 5 year period. Of 46 consecutive patients operated on for recurrent sustained ventricular tachycardia or ventricular fibrillation, 39 patients with ischemic heart disease underwent subendocardial resection and/or cryoablation. The mean age of the patients was 61 +/- 8 (SD) years, the mean left ventricular ejection fraction was 32 +/- 11%, and the mean number of ineffective antiarrhythmic drugs was 3.8 +/- 1.2 per patient. In 35 of 39 patients in whom mapping data were obtainable, 56 (86%) tachycardias had earliest sites of activation in the left ventricle and nine (14%) had earliest sites in the right ventricle. Ten patients had 14 tachycardias (21%) mapped to areas outside visible dense scar. Of these 35 patients, 10 underwent localized subendocardial resection and 25 underwent a regional procedure in which all areas activated before the surface QRS during ventricular tachycardia were excised and/or cryoablated. In the operative survivors of electrophysiologically guided surgery, three of eight (38%) patients with the localized and one of 24 (4%) patients who underwent the regional procedure had recurrence of ventricular tachycardia during a follow-up period of 1 to 59 (mean 22 +/- 17) months (p = .04). The favorable outcome of regional surgery was not influenced by the presence of multiple morphologies in 54%, disparate sites of origin in 29%, or inferior wall foci in 46% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The use of cryothermy in addition to other newer surgical techniques has improved the outcome for patients undergoing operation for ventricular tachycardia. However, the depth to which the cryothermic lesions penetrate the myocardium may be a limiting factor in some situations. In an attempt to overcome this problem, we applied cryothermia from both sides using a new biventricular approach in five patients with documented interventricular septal foci. The advantages, disadvantages, and possible indications for the use of this approach are discussed, as are methods for avoiding potential complications.
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Between 1981 and 1985, ninety patients were treated surgically for cardiac arrhythmias and have been followed for a mean interval of 21 months (range, one to 49 months). Follow-up is 100% complete. Fifty accessory pathways were divided in 35 patients (25 male and ten female; mean age, 35.2 years; range, 10 to 72 years), with no deaths. Five females, aged 10 to 35 years, were treated for focal atrial tachycardia, three for an atrial focus alone, and two with other arrhythmia procedures; four were cured and one was improved. Two patients (one man and one woman, both aged 33 years) had ablation of the atrioventricular node. Forty-one patients (32 male and nine female; average age, 56.9 years; range, 15 to 74 years) had ablation of ventricular tachycardia. Kent bundle division and focal atrial tachycardia ablation were also performed in two of these patients. More than 80% of patients had coronary disease. Mean preoperative ejection fraction was 33.9% with a range of 14% to 65%. Aneurysmectomy, endocardial resection, cryoablation, and coronary artery bypass were the procedures used. The perioperative mortality rate was 9.8% but there were no deaths in the last 23 patients. Ventricular tachycardia was abolished in all but three survivors in whom medical treatment is now effective. The automatic implantable defibrillator was implanted in 11 patients, with no surgical deaths. These results confirm the feasibility of relieving a variety of serious arrhythmias by surgical intervention.
The effect of bradycardia on dispersion of ventricular refractoriness was evaluated. Refractory periods were measured at 3 right ventricular sites in 16 patients with severe bradycardia (average heart rate 39 +/- 5 beats/min) and were compared with those measured in 11 control subjects, (average heart rate 72 +/- 12 beats/min). Patients with bradycardia had significantly longer effective (377 +/- 36 ms) and functional (421 +/- 39 ms) refractory periods (ERP and FRP) than control subjects (ERP 296 +/- 25 ms, FRP 346 +/- 18 ms) (p less than 0.001). However, dispersion of refractoriness was similar in the 2 groups. Dispersion of ERP was 43 +/- 38 ms and FRP was 48 +/- 35 ms in patients with bradycardia. In control subjects dispersion of ERP was 37 +/- 12 ms, and FRP was 36 +/- 20 ms. Pacing of 120 beats/min significantly decreased ERP and FRP in both groups. Pacing shortened dispersion significantly in control subjects. In patients with bradycardia, pacing failed to significantly decrease dispersion. Compared with control subjects with normal heart rates, patients with bradycardia have longer absolute refractory periods but do not have significantly increased dispersion of refractoriness. Single and double, twice threshold ventricular extrastimuli (S2 and S3) failed to induce ventricular tachycardia in any patient during bradycardia. Bradycardia alone does not appear to be a factor in the induction of ventricular tachyarrhythmias.
Permanent pacemakers capable of triggered ventricular stimulation were implanted in 28 patients with a history of sustained ventricular tachycardia or fibrillation. Noninvasive programmed ventricular stimulation was performed on 125 occasions during follow-up periods ranging from 1 to 25 months and was used to assess the efficacy of antiarrhythmic drug therapy, drug or dosage changes and left ventricular endocardial resection. Drug or dosage changes based on noninvasive programmed ventricular stimulation were made in 19 of the 28 patients. In addition, 126 episodes of spontaneous sustained ventricular tachycardia were terminated noninvasively in nine patients. It is concluded that a permanent pacemaker capable of triggered ventricular stimulation is useful in patients with ventricular tachycardia or fibrillation that is difficult to control.
Transient entrainment by pacing has been demonstrated during various tachyarrhythmias, including ventricular tachycardia. A patient is described who had two morphologically distinct forms of sustained ventricular tachycardia induced by programmed stimulation. Entrainment of both configurations of ventricular tachycardia was demonstrated. Evidence for entrainment included the presence of different degrees of fusion between paced and ventricular tachycardia complexes at different pacing cycle lengths, and the observation that the last entrained beat was always unfused and identical in configuration to the ventricular tachycardia complexes. Termination of ventricular tachycardia only occurred at pacing cycle lengths at which there was loss of fusion. Catheter endocardial mapping suggested a septal origin of both configurations of ventricular tachycardia. Demonstration of entrainment was dependent on pacing site, being seen only during pacing in the ventricle opposite from that showing earliest activation during ventricular tachycardia. Thus, when attempting to entrain ventricular tachycardia, multiple pacing sites in both ventricles should be used.
Direct application of electrical current to the heart utilizing special equipment such as implantable defibrillators or specially designed catheters has been useful in patients with recurrent ventricular tachyarrhythmias. We describe a patient who developed intractable ventricular fibrillation (VF) during the course of electrophysiologic testing. VF continued for 50 minutes, during which time multiple transthoracic shocks of 360 joules failed to convert the arrhythmia. Intracardiac shocks were then delivered via a transvenous 6 French standard quadripolar pacing catheter positioned in the right ventricular apex by direct application of the defibrillator paddle to the catheter, with the patient lying on the posterior paddle. Energy of up to 300 joules failed to defibrillate the patient, but use of 360 joules delivered in this fashion defibrillated the patient twice. Despite the protracted time of cardiac arrest, the patient recovered without sequelae. We report this case to demonstrate that VF refractory to transthoracic defibrillation may be converted by intracardiac shocks using a temporary pacing catheter without special equipment.
This study examined the site of atrioventricular (AV) block in mitral valve prolapse (MVP). Sixty symptomatic patients with MVP underwent electrophysiologic study; 49 had documented arrhythmias and 28 had syncope. Eight patients had spontaneous second- or third-degree AV block and 10 had chronic bundle branch block. Electrophysiologic study revealed abnormal sinus node function in 8 patients, prolonged HV interval in 10, intra-Hisian delay in 9, and functional bundle branch block in 15. Dual AV nodal pathways were demonstrated in 24 patients. Comparison with 101 similarly symptomatic patients without MVP revealed a greater prevalence of dual AV nodal pathways in the MVP patients. Infranodal conduction abnormalities and dual AV nodal pathways are frequently revealed by electrophysiologic testing in symptomatic patients with MVP.
This study examined the frequency of atrioventricular (AV) dissociation and accelerated junctional rhythms in 59 patients receiving oral verapamil. Accelerated junctional rhythms and AV dissociation were frequent in patients with supraventricular tachyarrhythmias, particularly AV nodal reentry. Verapamil administration to these patients led to an asymptomatic increase in activity of these junctional pacemakers. In patients with various chest pain syndromes, verapamil neither increased the frequency of junctional rhythms nor suppressed their role as escape rhythms under physiologically appropriate circumstances.
Ten patients with recurrent episodes of ventricular tachycardia (VT) had electrophysiologic studies in the basal state and on chronic oral ethmozin (12.1 +/- 0.6 SE mg/kg/day). Ethmozin significantly prolonged the AH interval (basal: 75 +/- 8 SE msec; ethmozin: 91 +/- 10 msec, p less than 0.05), the HV interval (51 +/- 3; 66 +/- 5 msec, p less than 0.01), and the QRS duration (101 +/- 4; 118 +/- 4 msec, p less than 0.001). Atrial and ventricular refractory periods and the corrected QT interval were not significantly affected by ethmozin. VT was induced in 7 of 10 patients in the basal state by means of programmed right ventricular extrastimulation or rapid burst ventricular pacing. On oral ethmozin nine patients had inducible VT. VT cycle length was consistently prolonged on ethmozin (250 +/- 13; 326 +/- 14 msec, p less than 0.001). Four of the seven patients with VT on basal ambulatory monitoring had total abolition of spontaneous VT on ethmozin. Ethmozin failed to prevent induction of VT in most patients despite significant reductions in ventricular arrhythmia on ambulatory monitoring. Further studies comparing VT induction with ambulatory monitoring in patients on ethmozin are needed to confirm these findings and to define the clinical significance of this dissociation.
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Electrophysiologic testing in patients after acute myocardial infarction may predict subsequent sudden death. We used a permanent pacemaker for repetitive electrophysiologic testing in a patient after acute infarction. Programmed, twice-threshold ventricular extrastimulation at two weeks after anteroseptal infarction failed to induce ventricular tachycardia. Subsequent programmed extrastimulation induced sustained ventricular tachycardia on four occasions (6, 16, 29 and 65 weeks) after infarction. As yet (20 months), spontaneous ventricular tachycardia has not occurred. Firm conclusions cannot be drawn from a single case. However, our patient developed a stable ventricular tachycardia circuit which was not apparent at two weeks. Thus, a single electrophysiologic study performed acutely after infarction may not accurately describe the potential for ventricular tachycardia or fibrillation. Serial electrophysiologic testing with an implantable externally triggered pacemaker may more accurately describe the potential for sudden death post-infarction in a few high-risk patients. This report shows that induction of ventricular tachycardia after acute infarction may not predict outcome.
The automatic implantable defibrillator is a valuable addition to the management of certain patients with ventricular tachycardia and/or fibrillation. The original technique required placement of two transvenous electrodes and an epicardial electrode via a left thoracotomy. We have successfully developed an all-epicardial approach using a left subcostal thoracotomy. Previous experience with epicardial pacemaker implantation by this approach suggested it would be a good technique for implantation of the automatic defibrillator. Early results with this approach have encouraged its continued use.
Currently available antiarrhythmic drugs possess very poor therapeutic-to-toxic ratios, and therefore, there is a great deal of interest in the development of new investigational agents to suppress ventricular rhythm disturbances. This article includes most of the investigational ventricular antiarrhythmic drugs in which there has been a great deal of recent active investigation and interest. It stresses the different patient populations that have been tested with each of these antiarrhythmic drugs, pointing out those drugs that have been documented to be effective in nonsustained ventricular tachycardia or sustained ventricular tachycardia and sudden cardiac death.
Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis. All patients received 1 to 4 extrastimuli (S2, S3, S4 and S5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S2 or S3 in 16 patients and by S4 or S5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), in 11 by S2 or S3 and in 13 by S4 or S5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S4 and S5 in the right ventricle increases the yield of inducible clinical VT compared with use of S2 and S3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.
Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.