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Atrial fibrillation is the most common sustained arrhythmia, increases with age, and presents with a wide spectrum of symptoms and severity Paroxysmal, persistent, and permanent forms require very individualized approaches to management. New information about electrical and anatomic remodeling emphasizes the importance of time-related thrombogenicity and progressive interference with mechanical function of the atria and ventricles. The most important aspect of diagnosis is risk stratification with respect to risk of thromboembolism. The general goals in treatment are, in order of importance: prevention of thromboemboli, control of ventricular response, restoration of sinus rhythm, and maintenance of sinus rhythm by preventing recurrences. This review focuses on the above issues. The therapeutic choices are discussed under each category Antiarrhythmic drugs, radiofrequency ablation techniques, and device therapy are reviewed with respect to prevention of recurrent atrial fibrillation.

A case of severe constrictive pericarditis resulting from an indolent Pseudomonas aeruginosa infection of the automatic internal cardiac defibrillator is described. Total explanation of the device was attempted after nine months but was unsuccessful because of dense adhesions under the patch electrodes. The patient subsequently developed clinical and hemodynamic findings of constrictive pericarditis and a second desperate attempt to remove the patches resulted in operative death. Diagnostic modalities for detecting infection of the AICD are reviewed. As soon as there is infection involving any component, the entire lead system and pulse generator should be removed.

Radiofrequency current was utilized to mark the anatomic location of earliest endocardial activation during catheter mapping of ventricular tachycardia. Intraoperative identification of the radiofrequency lesion allowed validation that the site of earliest endocardial activation determined by a catheter mapping study was the same as assessed by a computerized balloon mapping system. Radiofrequency current may be a useful method of marking areas of endocardium thought to be potential sites for ablative surgery as well as allowing correlation between different mapping techniques.

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.

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.

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.

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 +/- 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.

A patient is described with drug-resistant recurrent paroxysmal atrial flutter. Electrophysiologic studies demonstrated that flutter was inducible with rapid atrial stimulation (stimulation rates of 375 to 400/min) and convertible with rapid atrial stimulation (rates of 400 to 460/min). Because of the latter response, a radio-frequency atrial pacemaker was implanted, which allowed self-initiated conversion of flutter episodes with rapid stimulation.

Pulmonary toxicity developed in 15 (17%) of 89 patients treated with amiodarone during a follow-up period of 2 weeks to 54 (mean 20 +/- 15) months. Prospective evaluation of serial pulmonary function tests in 67 patients demonstrated both a significant decrease from baseline in three of six variables in patients with toxicity at the time of diagnosis and a significant difference compared with the same variables in patients without toxicity. The most significant of these was the diffusing capacity for carbon monoxide (DLCO). An individual decrease in DLCO greater than or equal to 15% gave an optimal sensitivity of 100% and a specificity of 89% for the diagnosis of pulmonary toxicity. However, a decrease in DLCO greater than or equal to 15% did not alone warrant a change in therapy in asymptomatic patients. Although higher maintenance doses of amiodarone appeared to be related to the development of this complication, an abnormal baseline DLCO (less than 60% of predicted) with or without an initial abnormal chest roentgenogram did not predispose to pulmonary toxicity.

Radionuclide (RNA) gated studies were performed during sinus rhythm and during spontaneous or induced sustained ventricular tachycardia (VT) in six patients with clinical VT. Fourier analysis of time-activity variation was used to calculate a RNA phase value for each pixel in the image. Color coding of each pixel according to its calculated phase resulted in a RNA phase map of the ventricles. The following results were considered to be consistent with the known electrophysiology of VT: (1) the phase map correlated with QRS morphology and axis in most but not all tachycardias; (2) earliest phase usually demonstrated the VT origin to be at the border of the ventricular wall motion abnormality; (3) endocardial mapping (available in one patient) showed close correlation with RNA phase mapping; (4) in three patients with ischemic heart disease, VT with left bundle branch block (LBBB) pattern had earliest LV phase along the septum; and (5) for one patient imaged during two different VT morphologies, the tachycardias had earliest phase at different borders of the same wall motion abnormality with differing progression of phase across the ventricles. RNA phase mapping of VT is feasible and appears to provide data consistent with the electrophysiology of this arrhythmia.

Reproduction of spontaneously occurring ventricular tachycardia (VT) and induction of previously undocumented VT were studied prospectively in 98 patients: 48 with documented sustained VT or ventricular fibrillation, 25 with nonsustained or exercise-induced VT, and 25 with no documented VT. Patients received 1 to 4 ventricular extrastimuli and ventricular burst pacing at 2 right ventricular (RV) sites, first at twice late diastolic threshold, and then at 10 mA using a prospective, tandem study design. Spontaneously occurring VT was reproduced in 37 of 48 patients (77%) at twice late diastolic threshold and in 1 other patient (2%) at 10 mA. VT was reproduced at both RV sites in 17 of 48 patients (35%) and at 1 site in 20 of 48 patients (42%) at twice late diastolic threshold. A previously undocumented VT was induced in 7 of 25 patients (28%) with no documented VT at twice diastolic threshold and 14 of 25 patients (56%) at 10 mA. A previously undocumented VT was induced in 33 of 73 patients (45%) with a history of sustained or nonsustained VT at twice late diastolic threshold and in 47 of 73 patients (64%) at 10 mA. In patients with documented sustained VT, the use of up to 4 ventricular extrastimuli at multiple RV sites increases the sensitivity of the test. In patients without documented VT, the induction of previously undocumented VT with more than 3 ventricular extrastimuli limits the specificity of the test. Increased current provides only a slight advantage over 4 ventricular extrastimuli at twice late diastolic threshold in terms of reproduction of spontaneously occurring VT, but leads to a marked increase in induction of previously undocumented VT.

Eighty-eight patients with preexcitation were studied to determine how 30 patients with documented spontaneous paroxysmal atrial fibrillation differed from 58 patients without this arrhythmia. Inducible reentrant tachycardia was present in 23 (77 percent) of the 30 patients with, versus 28 (48 percent) of the 58 patients without, atrial fibrillation (p less than 0.025). Heart disease was present in 13 (43 percent) of the 30 patients with, versus 15 (26 percent) of the 58 patients without, atrial fibrillation (not significant). Inducible reentrant tachycardia or heart disease, or both, were significant). Inducible reentrant tachycardia or heart disease, or both, were present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p less than 0.0005). Of 51 patients with inducible reentrant tachycardia, 23 patients with atrial fibrillation did not differ from 28 patients without this arrhythmia with respect to clinical features and atrial, sinus nodal, or anomalous pathway properties, or cycle length of induced reentrant tachycardia. Spontaneous degeneration of induced reentrant tachycardia to atrial fibrillation was observed in 6 (26 percent) of 23 patients with, versus none of 28 patients without, atrial fibrillation (p less than 0.025). In summary, patients with preexcitation and documented spontaneous paroxysmal atrial fibrillation almost always have inducible reentrant tachycardia or heart disease, or both. It is likely that in many patients with inducible reentrant tachycardia, spontaneously occurring reentrant tachycardia relates to induction of atrial fibrillation. However, it is unclear why some patients with inducible reentrant tachycardia have atrial fibrillation and others do not. In many patients with organic heart disease, atrial fibrillation could relate to hemodynamic changes.

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.

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.

This study investigates the relation of spontaneous ventricular arrhythmia on ambulatory electrocardiographic (ECG) monitoring to the subsequent inducibility of ventricular tachycardia during programmed electrical stimulation. Eighty patients (65 men, 15 women), whose mean age was 58 years, presented with one of the following: sustained ventricular tachycardia (n = 54); sudden death requiring resuscitation (n = 4); ventricular fibrillation (n = 11); or syncope thought to be of cardiac origin (n = 11). All patients had 24 hour ambulatory electrocardiograms and programmed electrical stimulation while receiving no antiarrhythmic therapy. Programmed electrical stimulation resulted in inducible sustained ventricular tachycardia (defined as a rate of greater than or equal to 120 beats/min for greater than or equal to 1 minute or requiring intervention) in 53 of the 80 patients. There was no measure of frequency or complexity of spontaneous arrhythmia detected on ambulatory ECG that could identify the degree of subsequent ventricular tachycardia inducibility during programmed electrical stimulation. In fact, 25% of patients who had inducible sustained ventricular tachycardia had little or no spontaneous arrhythmia on ambulatory ECG. Furthermore, of the 53 patients with inducible sustained ventricular tachycardia, 28 and 55% had no couplets or nonsustained ventricular tachycardia, respectively, during ambulatory monitoring. The combination of a clinical presentation of sustained ventricular tachycardia, confirmed coronary artery disease and a left ventricular ejection fraction of less than 30% had a better positive predictive value than did any ambulatory ECG criterion in predicting the inducibility of sustained ventricular tachycardia.

In patients with dual atrioventricular (A-V) nodal pathways, atrial extrastimulus testing induces either no echoes, single atrial echoes (Ae), or repetitive re-entrance (repetitive atrial and ventricular beating). We examined the fast and slow pathways properties in 38 patients with dual pathways in order to delineate the determinants of re-entrance. Seventeen patients had no Ae. Of these, six had no V-A conduction and 11, intact V-A conduction. The mean paced ventricular cycle length producing retrograde V-A block (VABCL) in this group (a measure of retrograde fast pathway refractoriness) was 552 +/- 32 msec (mean +/- SEM; 10 pts). In contrast, all 21 patients with Ae had intact V-A conduction with mean VABCL of 382 +/- 21 msec (14 pts) (P less than 0.05). Repetitive re-entrance occurred only when Ae conducted to the ventricles. Seven patients had only single Ae. The mean paced atrial cycle length producing Wenckebach periodicity (CLAWP) in this group (a measure of antegrade slow pathway refractoriness) was 490 +/- 31 msec (5 pts). Fourteen patients had repetitive re-entrance. The mean CLAWP in this group was 399 +/- 18 msec (8 pts) (P less than 0.05). In conclusion, our results suggest that in patients with dual pathway, the occurrence of single or repetitive re-entry is dependent upon measurable slow and fast pathway properties.

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.

Between 1979 and 1984 the Cybertach-60, (Intermedics, Inc. Model 262-01), a programmable, automatic antitachycardia pacemaker was implanted in 11 patients who had drug-refractory supraventricular tachycardia (SVT). The patients have been followed for a total of 64-108 (mean 84 months). All patients were symptomatic and had failed two or more drugs and six patients had required prior DC cardioversion. The mechanism of supraventricular tachycardia was atrioventricular (AV) nodal reentry in six patients, AV reentry in four patients, and atrial tachycardia in one patient. Preoperatively all patients had reliable termination of the tachycardia without induction of atrial fibrillation by pacing methods available to Cybertach-60. Postimplant, Cybertach-60 reliably terminated all episodes of tachycardia without ancillary drug therapy. Nevertheless, at long-term follow-up antitachycardia pacing was effective and safe in the minority (36%), with only four patients out of eleven still using a pacemaker for supraventricular tachycardia. One of these four patients required additional drug therapy. In one of the patients, the Cybertach-60 was replaced after 78 months by a more advanced device, (Intertach, Intermedics, Inc.) because of a depleted Cybertach-60 battery. In seven patients who no longer use antitachycardia pacing for termination of tachycardia, one patient developed atrial fibrillation during tachycardia termination (at 58 months postimplant). Three patients experienced induction of tachycardia or atrial fibrillation by the pacemaker due to undersensing of sinus P waves (at 36, 48, and 51 months).(ABSTRACT TRUNCATED AT 250 WORDS)

Over 6 years, recurrent drug-refractory supraventricular arrhythmias were treated by electrophysiologically guided surgical procedures in 67 patients. There were 57 patients, age 10-72 years, with accessory pathways who had 61 operations. The perioperative mortality rate was 3.5%, with deaths occurring in two patients with complex problems. Four patients with multiple but one or more silent accessory pathways had successful reoperation, and modified surgical technique has eliminated this problem. All patients are free of arrhythmias 2-70 months after operation. The survival and primary cure rates were 100% for 36 patients with solitary accessory pathways. Eight patients, age 10-53 years, were operated on for atrial focal tachycardia. Right atrial cryothermic lesions without excision or cardiopulmonary bypass were used in four patients: local excision was used in two patients and combined procedures were used in two patients. Because of recurrence in two of four patients treated by isolated cryoablation, a new technique was applied subsequently to one of these patients and two other patients: wide atrial excision and PTFE patch replacement during cardiopulmonary bypass. All patients are free of arrhythmias at a follow-up of 9-72 months. Intractable atrial flutter or fibrillation occurred in 11 patients who had 15 attempts at transvenous A-V node electroshock ablation. In three patients in whom this failed, subsequent open cryoablation of the A-V node during cardiopulmonary bypass and epicardial pacemaker implantation were performed successfully. Two patients had A-V nodal modification for control of A-V nodal re-entry tachycardia: one patient with cryothermia at the time of ablation of atrial focal tachycardia and the other patient with sharp dissection at the time of accessory pathway division. Of the initial 67 patients, 65 (97%) survived operation and all were cured of their presenting arrhythmia. Surgery for drug-refractory supraventricular arrhythmias is safe and effective in selected cases.

We describe an adult with chronic (three years' duration) acquired nonparoxysmal junctional tachycardia, a previously undescribed rhythm. Ambulatory monitoring revealed junctional rates ranging from 75 to 110 beats/min. Electrophysiologic studies demonstrated intact atrioventricular and ventriculoatrial conduction with a normal H-V interval (43 msec) and narrow QRS. Underlying sinus node function appeared to be normal (recovery time of 900 msec). Junctional rate increased with administration of atropine and isoproterenol, suggesting that the junctional pacemaker was located in the proximal His bundle. Electrocardiographic and electrophysiologic observations suggested that this case of chronic nonparoxysmal junctional tachycardia was benign, not necessitating therapy.

An experiment was designed to determine optimal methods of myocardial reperfusion after normothermic ischemic arrest in the in vivo pig heart. Four variables were studied: 1) ischemic arrest for 15 minutes repeated six times vs 30 minutes repeated three times: 2) coronary reperfusion between each arrest period lasting 5 or greater than or equal to 15 minutes (the latter duration dependent upon electrocardiographic reversal of ischemic); 3) perfusion pressure of 50, 75, or 100 mm Hg; and 4) a beating or fibrillating heart during reperfusion. The effects of perfusion were monitored by measuring the endocardial/epicardial perfusion ratio (with ratioactive microspheres), coronary blood flow, and coronary reactive hyperemia by measuring coronary vascular resistance during reperfusion. Electron micrographs were examined to determine if subtle distinctions between groups could be measured. A total of 78 pigs (60 experimental and 18 control) were evaluated. The experimental animals were divided into 10 groups of six pigs each. In each group only one of the four variables (beating or fibrillating ventricle, perfusion pressure, duration of ischemia, and duration of reperfusion) was altered to provide comparative data. Results are based on improved endocardial perfusion and a greater coronary reactive hyperemic response when comparing each experimental group to one another and to control animals. Reperfusion of a contracting rather than fibrillating ventricle resulted in improved endocardial flow as did reperfusion at a low (50 or 75 mm Hg) rather than a high (100 mm Hg) perfusion pressure. A short ischemic interval repeated six times rather than a longer ischemic interval repeated three times also allowed for improved subendocardial perfusion and a greater reactive hypermic response as did a longer reperfusion period between equal ischemic intervals. Electron microscopic studies showed a gradation of abnormalities ranging from little deviation from control in beating hearts and short ischemia and long duration, low pressure reperfusion to marked mitochondrial vacuolization in fibrillating hearts subjected to long ischemia, short reperfusion at high perfusion pressures. The best technique for myocardial reperfusion based on available data is to provide reperfusion of adequate duration in order to reverse the ischemic electrocardiogram in a beating heart, avoiding an excessively high perfusion pressure.

Moricizine HCl, an antiarrhythmic phenothiazine drug, was investigated for its efficacy against ventricular tachycardia (VT) in a group of 60 patients from 8 institutions using electrophysiologic testing before and after oral administration. Moricizine HCl significantly prolonged PR, QRS, AH and HV intervals and cycle length for atrioventricular nodal block, but had minimal or no effect on repolarization or cardiac refractory periods. Induction of sustained VT (in 33 patients) and nonsustained VT (in 14 patients) occurred at baseline. During moricizine HCl therapy, sustained VT was induced in 31 patients and nonsustained VT in 7 patients. In individual patients, suppression of VT induction was obtained in 18% of patients with sustained VT and in 27% of patients with nonsustained VT. Cycle length of induced VT was significantly prolonged by moricizine HCl therapy. During prospective follow-up of 37 patients, electrophysiologic study predicted recurrence of nonrecurrence of VT with a sensitivity value of 82% and specificity of 65%.

In a patient with two morphologic forms of ventricular tachycardia, rapid pacing from different ventricular sites produced two distinctively different patterns of entrainment. Pacing from sites contralateral to the site of emergence of ventricular tachycardia caused progressive fusion. Following pacing, the interval (return interval) between the first tachycardia beat (return beat) and the preceding beat was equal to the pacing cycle length. Near the site of emergence, the local electrogram of the return beat was morphologically identical to that of the preceding paced beats. In contrast, pacing from sites ipsilateral to the site of emergence did not cause fusion. The return intervals increased with decreasing pacing cycle lengths. The local electrogram of the return beat was morphologically different from that of the preceding paced beats. Using a model of ventricular reentrance, both patterns of responses can be explained. Pacing impulses arising from sites contralateral to the site of emergence activate the latter orthodromically. Fusion occurs between the emerging tachycardia wavefront and the next pacing wavefront. In contrast, pacing impulses arising from sites ipsilateral to the site of emergence activate the latter antidromically. Fusion is not observed because collision within the area of slow conduction prevents the emergence of the tachycardia during pacing.

Fifty-four patients with previous myocardial infarction and sustained ventricular tachycardia on fibrillation underwent two electrophysiologic studies in the drug-free state within 72 hours. Although the concordance of overall ventricular tachycardia induction over the 2 days was good (87% of patients), there was variability in the number of extrastimuli needed to induce sustained ventricular tachycardia on each day in 60% of patients. Of those in whom ventricular tachycardia was inducible on both days, 40% required additional extrastimuli and 20% required fewer extrastimuli. A change by two or more extrastimuli was found in 12% of patients. There was no correlation between the variability observed and multiple clinical and laboratory parameters (including the aggressiveness of the stimulation protocol); however, the direction of the variability (easier or harder to induce) correlated with changes in ventricular refractoriness. Inherent day-to-day variability may affect the reproducibility of electrophysiologic studies and influence the results of serial drug testing.

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.

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.

Electrophysiological studies with atrial extrastimulus technique suggested the presence of dual atrioventricular (A-V) nodal pathways in a patient with hypothyroidism, as evidenced by a sudden increase of H1-H2 intervals at critical A1-A2 coupling intervals. Following the atrial extrastimulus (A2), a third impulse (A3) occurred spontaneously. During slow pathway conduction of A2, and A3, appearing at a critically timed interval allowed fast pathway conduction, resulting in an earlier than expected QRS (a form of supernormal conduction). This demonstration of fast pathway conduction during slow pathway conduction adds strong evidence for the existence of dual A-V nodal pathways.

Paroxysmal supraventricular tachycardia may result from re-entrance in the AV node, the normal A-V pathway with an accessory AV connection, in the sino-atrial node, in the atria, or else reflect ectopic impulse formation in a spontaneously automatic supraventricular focus. Electrocardiographic criteria which are helpful in differentiating these mechanisms involve an analysis of cycle length, changes in cycle length with intermittent bundle branch block, P wave morphology and the relationship of P wave to QRS complex, P-R interval, the presence of A-V block during tachycardia and the influence of autonomic tone on the tachycardia. Electrophysiologic studies further elucidate mechanism by demonstrating the mode of induction and termination of the tachycardia, the characteristics of antegrade and retrograde A-V conduction curves and refractory periods, atrial activation sequence of echo beats and the influence of premature beats introduced during tachycardia. These features are summarised in Table 1. Therapy can be accurately planned according to the results of experimental administration of antiarrhythmic agents and of pacing sequences upon induction and termination of tachycardia in the catheterisation laboratory.

Serial electrophysiologic testing of multiple drugs was performed in 21 patients with recurrent atrioventricular (AV) nodal reentrant paroxysmal supraventricular tachycardia (PSVT). All patients had reproducible sustained PSVT induced before drug administration. Serial daily PSVT induction was attempted after administration of i.v. ouabain (0.01 mg/kg) (16 patients), i.v. propranolol (0.1 mg/kg (17 patients), i.v. ouabain + propranolol (same dosages) (12 patients), i.v. procainamide (600-1000 mg) (17 patients) and oral quinidine (1600-2400 mg/day) (nine patients). In two of 21 patients (10%), no tested drug prevented induction of sustained PSVT. In 19 of 21 patients (90%), one or more drugs prevented induction of sustained PSVT: ouabain--seven patients, propranolol--seven patients, ouabain + propranolol--seven patients, procainamide--11 patients, quinidine--seven patients. The site of action of ouabain and/or propranolol was either the antegrade limb or the retrograde limb (RL) of the circus movement. The site of action of procainamide or quinidine was always the RL. These 19 patients were treated with oral drugs, based on results of serial testing. Eighteen patients were successfully followed for 6-50 months. In 13 of these 18 patients PSVT did not recur. Two patients (11%) had > 95% reduction in frequency of PSVT recurrences, and three (17%) did not respond to chosen oral drugs. Serial electrophysiologic testing of multiple drugs is feasible in patients with AV nodal reentrant paroxysmal tachycardia. Drug responses are variable. In most but not all patients, serial electrophysiologic testing defines effective prophylactic drug therapy. This method of defining prophylactic drug therapy appears most suitable for patients with poorly tolerated tachycardias that occur only sporadically.

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.

Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal QRS axis more negative than -45 degrees, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior "fascicle" of the left bundle branch.

To determine whether the slow onset of action of amiodarone might result in a delayed effect on the inducibility of sustained ventricular arrhythmias, 45 patients with ischemic heart disease and inducible sustained monomorphic ventricular tachycardia were prospectively studied. Each patient had at least one initial repeat study on amiodarone and those with persistently inducible arrhythmias were rescheduled for further studies over the following 24 weeks. After 2-3 weeks of amiodarone therapy, nine patients no longer had inducible tachycardias, and tachycardia in another eight patients (18%) later became noninducible. Using life-table methods, analysis based on the results of the first re-study showed 18-month recurrence rates of 43% in the inducible vs 17% in the noninducible groups (p = 0.056). When the results of additional testing were then used to reclassify patients, the recurrence rates for these two groups were 50% and 17%, respectively (p = 0.004). Observation of blood pressure and level of consciousness during induced arrhythmias was also predictive of clinical tolerance in patients having recurrences; 16 of 19 patients experienced symptoms of similar severity to those produced during testing. We conclude: (1) early testing of amiodarone may result in misclassification of some patients as remaining inducible; (2) re-testing at a later time more accurately predicts tachycardia recurrence; (3) observation of hemodynamic response also provides important prognostic information.

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.

A 41-year-old man had chronic, recurrent, drug-resistant paroxysmal right atrial tachycardia. Electrophysiologic studies revealed features suggesting atrial reentrance, including induction and termination of tachycardia with rapid atrial pacing and atrial extrastimuli. Endocardial catheter mapping localized the origin of tachycardia to the right atrial appendage. Intraoperative epicardial mapping refined the localization to the posterolateral rim of the appendage. The appendage was excised and the tachycardia was permanently cured. Microelectrode studies on the excised tissue revealed an inducible rhythm localized to a small area of the atrial endocardium, characterized by rapid pacing induction, rhythmicity generated from a suprathreshold afterdepolarization, low maximum diastolic potential, low overshoot potential and a smooth transition from phase 4 to phase 0, suggesting triggered automaticity. This is the first observation in man of probable triggerable atrial automaticity, which may be a direct counterpart of the clinical arrhythmia. The successful surgical outcome indicates that a focal atrial tachycardia can be excised in selected patients.

Atrial pacing at multiple sites was used in an attempt to predict the site of pre-excitation in 5 patients with Wolff-Parkinson-White syndrome with 5 different anomalous pathway locations (right anterior, right posterior, septal, left posterior, and left lateral). At least 3 atrial pacing sites were tested in each patient. Pacing sites tested included high right atrium, low lateral right atrium, low septal right atrium, proximal coronary sinus, and distal coronary sinus. Atrial stimulation sites with shortest and longest stimulus-delta intervals could be identified in each patient, the shortest stimulus-delta interval in each case ranging from 60 to 80 ms. The difference between the shortest and longest stimulus-delta interval in each case ranged from 60 to 110 ms. It was suggested that the site with the shortest stimulus-delta interval corresponded to a site close to the atrial insertion of the anomalous pathway. This hypothesis was confirmed in all cases (3 with epicardial mapping and 2 with retrograde atrial activation data). In conclusion, atrial pacing at multiple sites is helpful in predicting the site of anterogradely conducting anomalous pathways, and appears particularly useful for differentiation of right posterior, left posterior, and septal pre-excitation.

Prospective follow-up studies of 277 patients with chronic bifascicular block showed that 30 patients developed sudden cardiac death (SCD). Cumulative one-, two-, and three-year SCD mortality was computed. The patients that developed SCD were compared with the remaining patients (209 alive and 38 dead). The groups were similar in regard to age, sex, AH, and HV intervals. The following were more frequent in the SCD group (P less than .05): angina, previous myocardial infarction, heart failure, cardiomegaly, left bundle-branch block, premature ventricular beats, and ventricular tachycardia. Ventricular fibrillation was the cause of death in four cases of SCD where terminal ECG documentation was available. We concluded that SCD is a major cause of mortality in patients with chronic bifascicular block. The association of SCD with coronary disease and ventricular dysrhythmia suggested ventricular fibrillation as a frequent mechanism.

To describe the epicardial ventricular activation sequence in the intact human heart, we obtained epicardial maps from 11 patients with normal QRS undergoing open heart surgery. Epicardial breakthrough (EBT), defined as the emergence of a radially propagating epicardial wavefront, occurred in three to five sites in each patient, and was earliest in the anterior right ventricle, 7--25 msec (mean 17 msec) after the onset of the QRS in all patients. Subsequent EBT occurred in the inferior right ventricle (10 sites in 10 patients), in the anterolateral left ventricle (13 sites in 10 patients), and the inferior left ventricle (eight sites in seven patients). Latest epicardial activation (LEA), defined as the latest site of recordable epicardial activity, occurred in the basal segments in all patients, anteriorly in the right ventricle in five patients, and inferiorly in six patients, four on the right and two on the left. LEA occurred 63--96 msec (mean 77 msec) after the onset of the QRS, and was recorded within 20 msec of the end of the QRS in all patients. Sequence of epicardial activation reflected a fusion process among the wavefronts. This descriptive and quantitative data should provide a suitable basis for comparison of abnormal ventricular activation sequences in patients undergoing surgery for preexcitation or ventricular tachycardia.

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)

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.