The Role of Electrophysiologic Studies in the Management of Patients with Unexplained Syncope

We evaluated the frequency and type of electrophysiologic abnormalities in an unselected population of consecutive patients with unexplained syncope. Fifty patients were entered in the study; all had 24-hour dynamic electrocardiographs (Holter) recordings and underwent complete electrophysiological studies. An abnormal electrophysiologic study was found in 74% of the patients. Sinus node abnormality was observed in 30%, abnormal AV node function in 14%, long HV in 10%, block distal to H during rapid atrial pacing in 6%, paroxysmal supraventricular tachycardia in 12%, ventricular tachycardialfibrillation in 8%, and hypersensitive carotid sinus syndrome in 24%. There was no correlation between Holter and electrophysiologic study findings except for the presence of paroxysmal sustained supraventricular tachycardia. Based on clinical, Holter monitoring, and electrophysiologic findings, 38% were treated by antiarrhythmic drugs, 40% received permanent pacemakers, and. 22% were not treated at all. During follow-up (23 ± 13 months), 9 patients (18%) experienced recurrent syncope or death.     

The Value of Electrophysiology Study and Prophylactic Implantation of Cardioverter Defibrillator in Patients with Hypertrophic Cardiomyopathy

Fifty-three consecutive patients with hypertrophic cardiomyopathy (HCM) and no history of sudden death underwent electrophysiology (EP) study. Sustained polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF) was induced in 19 patients (35%). Patients with prior syncope or near syncope had a higher incidence of VT/VF inducibility. An implantable cardioverter defibrillator (ICD) was placed in 14 of the 19 patients. Of the remaining 5 patients with inducible VT/VF, three refused ICD implantation, while two underwent septal myectomy and VT/VF was no longer inducible afier the operation. None of the patients received antiarrhythmic drugs. During a mean follow-up period of 47 ± 31 (2–117) months, no events occurred in the 34 patients with negative EP study. Three events occurred among the 19 patients with inducible VT/VF. One patient died suddenly, one developed wide complex tachycardia which required resuscitation, and one patient received an appropriate ICD shock. In conclusion, sustained polymorphic VT/VF was inducible in about one-third of patients with HCM. Noninducibility of VT/VF appeared to predict a favorable prognosis. Although the overall event rate was low in patients with inducible VT/VF, prophylactic ICD implantation in patients with multiple risk factors may be appropriate.     

Role of Cardiac Electrophysiologic Studies in Patients with Unexplained Recurrent Syncope

Cardiac electrophysiologic studies (EPS) with programmed electrical stimulation (PES) were performed in 30 patients with recurrent syncope to uncover possible arrhythmic etiology. All patients had undergone thorough medical and neurologic evaluation prior to EPS without finding a definitive cause for syncope. In the majority of patients an arrhythmic etiology for syncope was suspected but could not be documented utilizing the 12-lead surface ECG, extended in-hospital and/or ambulatory monitoring (for ≥ 48 hours) and exercise testing prior to the EPS. The studies provided a clue to the possible underlying rhythm disturbance which could have caused syncope in 16/30 patients. Sustained or nonsustained ventricular tachycardia and/or ventricular fibrillation was induced in 11/30, sinus node dysfunction in 4/30 and intra-His block in the remaining one. Fourteen of the 16 have remained free of symptoms following therapy based on results of EPS during a follow-up period ranging from 6–30 months (mean 16.5 ± 7.8). In 2/16 syncope recurred (one arrhythmic and one non-arrhythmic) despite pacemaker therapy for sinus node dysfunction detected during EPS. In the remaining 14/30 patients, EPS and PES did not induce arrhythmia which could account for patient symptomatology and therefore no specific therapy could be recommended. Eleven of these 14 patients experienced a recurrence of symptoms within a 6–25 month period (mean 16.2 ± 6.8). Of the 16 patients with inducible arrhythmias considered clinically significant, 15 had associated structural heart disease. On the other hand, of the 14 patients without clinically significant arrhythmias, structural heart disease could be detected in only three. It is concluded that cardiac arrhythmias constitute a common cause of unexplained syncope, particularly in patients with structural heart disease, and that EPS with PES can uncover the type of arrhythmic disturbance in a significant number of cases.     

Dual Chamber Rate Responsive Pacing to Allow Sotalol Therapy for Ventricular Tachycardia

In order to allow the use of sotalol to control ventricular tachycardia (VT), dual chambe rate responsive (DDDR) pacemakers were implanted in ten patients aged 6 to 73 years (mean 50 years) Nine presented with monomorphic VT (seven inducible at baseline electrophysiological study (EPS)) ant one with syncope (monomorphic VT at EPS). On sotalol, VT was initiated in only one. This patien received sotalol in the absence of an effective alternative agent. The mean dose was 468 ± 269 mg/day Indications for pacing were symptomatic sotalol induced bradycardia (7), sinus node dysfunction (1) postoperative complete heart block (1), and infra-His block at baseline EPS (1). At least five of these patients would have been candidates for an implantable cardioverter defibrillator had sotalol required discontinuation. Initially, nine patients were paced in DDDR mode and one, with normal AV conduciioi on sotalol, in AAIR. One patient was unable to tolerate sotalol despite pacing. One patient died suddenly after 35 months of symptom-free follow-up. There was a significant improvement in symptomatic statu, (P = 0.03) after pacing among the other eight patients with no recurrence of VT. The implantation of DDDR pacemaker may be indicated in selected patients with serious cardiac arrhythmias. With such < device programmed to an appropriate mode, sotalol can be used successfully where otherwise contraindi cated by bradycardia or preexisting conduction disease. For some patients this may obviate the expense inconvenience, and attendant risks of implantable cardioverter defibrillator implantation.     

Results of Electrophysiological Testing and Long-Term Follow-Up in Patients Sustaining Cardiac Arrest Only While Receiving Type IA Antiarrhythmic Agents

Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. In conclusion: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.     

Electrophysiologic studies of patients with hypertrophic cardiomyopathy presenting with syncope of undetermined etiology

Patients with hypertrophic cardiomyopathy (HC) have a high risk of sudden death. The best clinical predictors of sudden death from HC are young age, strong family history of sudden death, ventricular tachycardia (VT), and progression of symptoms such as syncope. We performed 24-hour Holter monitoring and electrophysiologic studies (EPS) on 26 patients with HC, some with the obstructive form of the disease and some with syncope, in order to predict their vulnerability to syncope and to potentially malignant arrhythmias. Holter monitoring demonstrated supraventricular tachycardia (SVT) in 9/26 patients whereas atrial programmed electrical stimulation induced SVT in 17/26 patients. Of the 17 patients, nine had symptomatic hypotension with SVT while lying supine. Holter monitoring demonstrated nonsustained VT in 7/26 patients whereas ventricular programmed electrical stimulation induced VT or ventricular fibrillation (VF) in 6/26 patients. The patient who had the longest run of nonsustained VT on Holter had VF induced by ventricular programmed electrical stimulation. He was cardioverted to normal sinus rhythm with no untoward effects. We found that atrial programmed electrical stimulation induced SVT with hypotension best predicted a history of syncope in these patients. Although one patient required direct current cardioversion, EPS was conducted safely in all patients. Further long-term studies are needed to demonstrate the value of clinical decisions based upon EPS in patients with HC.     

Ten-Years Follow-Up of 20 Patients with Idiopathic Ventricular Tachycardia

The follow-up and characteristics of 20 patients with ventricular tachycardia (VT) and no detectable heart disease is reported. These were 16 men and four women with a mean age of 44 years. Symptoms were present in 18 patients (eight had syncope and ten palpitations or dizziness), VT was sustained in 11 patients and a left bundle branch block morphology with inferior axis was found in 17 patients. In three patients, VT had a right bundle branch block morphology and left-axis deviation. The VT was inducible in 13 patients during the electrophysiological testing (EP) and was sustained in five patients. Medical treatment was introduced in 19 patients. During a mean follow-up of 10 years from the onset of the symptoms and 6 years from the EP testing, one patient died suddenly. He had stopped taking amiodarone 5 months before. In seven patients symptoms recurred and were due to discontinuation of therapy in two cases and inefficacy of previous effective treatment in five patients. After modification of the treatment (three cases), implantation of a pacemaker (one case) and catheter ablation (one case), all patients became asymptomatic. Eleven patients became asymptomatic with the first administered antiarrhythmic therapy. One patient continues to be asymptomatic in spite of discontinuation of his medical therapy. We conclude that patients with VT and no detectable heart disease have a good long-term prognosis and that appropriate therapy can be found in almost all patients.     

Induced Sustained Ventricular Tachycardia in Nonischemic Dilated Cardiomyopathy: Dependence on Clinical Presentation and Response to Antiarrhythmic Agents

Thirty-one patients with nonischemic dilated cardiomyopathy either idiopathic or due to regurgitant valvular disease were studied in the cardiac electrophysiology lab. The indications for study were sustained ventricular tachycardia (VT) in 26, ventricular fibrillation (VF) in 11, and syncope of unknown etiology in 4. Sustained VT was reproducibly induced in 17 patients, including 12 with a history of sustained VT, 2 with VF and 3 with syncope. Of 15 patients undergoing serial antiarrhythmic drug studies, sustained VT was rendered noninducible or nonsustained in 23. Three had recurrent arrhythmic events while on therapy predicted to be effective. One of 2 patients discharged on a regimen predicted to be ineffective had a recurrence of sustained VT that resulted in cardiac arrest. Of 14 patients in whom sustained VT could not he reproducibly induced, 2 subsequently had spontaneous occurrences of sustained VT, and 2 experienced aborted sudden death. These results suggest the following; (1) the induction of sustained VT in the setting of nonischemic dilated cardiomyopathy is dependent on the clinical presentation; (2) antiarrhythmic drugs frequently render sustained VT noninducible or nonsustained; (3) antiarrhythmic drug suppression of inducible sustained VT predicts long-term prevention of spontaneous recurrences; and (4) noninducibility of sustained VT in the baseline state does not predict freedom from subsequent episodes of VT or sudden death.     

Electrophysiological Evaluation of Sustained Ventricular Tachyarrhythmias in Idiopathic Dilated Cardiomyopathy

Sustained ventricular tachyarrhythmias and sudden death are particularly prevalent in patients with idiopathic dilated cardiomyopathy (IDC). In contrast to patients with ischemic heart disease, the value of electrophysiological stimulation (EPS) in patients with IDC has not yet been established. To clarify the role of EPS in these patients, we studied 19 patients (58 +/- 11 years) with IDC who had symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF). The mean left ventricular ejection fraction was 26 +/- 9%. Ten patients had survived out-of-hospital cardiac arrest, eight had documented sustained monomorphic VT and one patient had non-sustained VT associated with syncope. Thirteen of the 19 patients (68%) had their clinical ventricular tachyarrhythmias induced at EPS (12 VT, 1 VF). In nine of 13 patients (69%), the arrhythmias were subsequently suppressed during serial electrophysiological drug testing. During 17 +/- 11 months of follow-up, 10/19 (53%) patients experienced recurrence of their arrhythmias and nine out of 19 (47%) patients died; six died suddenly and three secondary to heart failure. There was no difference in arrhythmia recurrence between patients with and without inducible ventricular tachyarrhythmias at initial study. Furthermore, suppression of arrhythmia during serial testing did not predict outcome; recurrences were observed in five out of nine patients whose arrhythmias were suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Recurrent Symptoms after Ventricular Pacing in Unexplained Syncope

We report clinical and hemodynamic data in two cases of recurrent syncope. Both patients received permanent demand ventricular pacing (VVI) for unexplained syncope. Both patients experienced recurrent syncope after pacemaker implantation. They later underwent 60 degrees head-up tilt testing, initially noninvasively and then with hemodynamic profile. A vasovagal response to tilt occurred with bradycardia and was complicated by the onset of ventricular pacing and retrograde atrioventricular conduction (RAVC) with hemodynamic deterioration and rapid reproduction of syncope. Limited intracardiac electrophysiological study (EPS) excluded atrioventricular (AV) conduction disease, sinus node disease, and carotid sinus syndrome, and confirmed RAVC. Both patients were upgraded to dual chamber pacing, DDI mode, with 50/80 rate hysteresis. One patient was asymptomatic at repeat tilt testing; the other experienced continued symptoms due to the vasodepressor component of vasovagal syncope. Cardiac pacing alone is ineffective treatment for this phenomenon, and no proven therapy is presently available. Ventricular pacing applied to patients with unexplained syncope may lead to an increase in or continuation of symptoms rather than an amelioration. There is a need for full investigation of such patients, which must include tilt testing, to allow for the most accurate diagnosis possible and guide the most appropriate therapy.     

Uncommon cause of syncope in patient with bundle branch block and negative electrophysiological study

We report a case study of a patient with bifascicular block, episodes of syncope, and negative electrophysiological study (EPS) who diagnosed to have sinus arrest with the help of an implantable loop recorder. This case emphasizes that atrioventricular (AV) block is not the only mechanism of syncope in patients with bundle branch block (BBB) and negative EPS.     

Fulguration of Ventricular Tachycardia Using High Cumulative Energy: Results in Thirty-one Patients with a Mean Follow-Up of Twenty-seven Months

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 31 patients (57 ± 15 years) who had refractory recurrent VT. Fifteen patients had coronary artery disease, seven had arrhythmogenic right ventricular dysplasia, four had cardiomyopathy and five had no structural heart disease. Ten patients were NYHA class III-IV. Ten patients experienced cardiac arrest or syncope during VT. Twenty-two patients had only one documented morphologic type of spontaneous VT. Whereas nine patients had more than one: the VT was incessant or daily in 17 patients. One to 16 shocks (mean 5.6) of 160 to 240 joules each (1162 ± 1060 joules) were delivered to the endocardial exit site of VT—as identified by endocardial activation mapping (29 patients) and pacemapping (31 patients)—during one (22 patients) or more than one session (nine patients). Cumulative delivered energy was 840 ± 558 joules for right ventricular VT (11 patients) and 1362 ± 1240 joules for left ventricular VT (20 patients). Reversible side effects occurring immediately after shocks included: nonclinical VT (two patients), ventricular fibrillation (two patients), AV block (three patients). Mean CK—MB fraction 6 hours after shocks was 93 ± 46 IU/1. An electrophysiology study performed 7 to 10 days later demonstrated that the original clinical VT was inducible in seven patients, nonclinical monomorphic VT was inducible in eight patients and no VT was inducible in 13 patients. The procedure was successful in 25/29 patients (86%) who had no recurrence of the original VT (or sudden death) either on no antiarrhythmic therapy (16 patients) or on the same regimen that was ineffective before ablation (nine patients) over a follow-up period of 27 ± 11 months. A nonclinical VT occurred in two patients. The ablation result was not interpretable in two patients and unsuccessful in four patients: the endocardial activation time at site of shocks was –5 ± 5 ms in the failures versus ?43 ± 29 ms in the successes (P < 0.05).     

Mexiletine-quinidine combination: enhanced antiarrhythmic and electrophysiologic activity in the dog

Combination treatment with mexiletine and quinidine has been shown to be more effective than either monotherapy in the treatment of ventricular tachycardia in humans. The purpose of this study was to assess the electrophysiologic changes which correlated with enhanced antiarrhythmic activity during treatment with the monotherapies and this combination. Twenty-seven dogs with inducible sustained ventricular tachyarrhythmias (VT) late after ischemic injury were treated with mexiletine and quinidine, alone and in combination. Conscious but sedated animals were assigned randomly to receive serial drug treatments. Sustained VT was consistently inducible during serial placebo studies. In 13 dogs who received all four drug treatments (mexiletine, quinidine, combination and placebo) significantly greater antiarrhythmic efficacy was seen with combination therapy (8 of 13) than was seen with mexiletine alone (1 of 13), quinidine alone (3 of 13) and saline (0 of 13) (P less than .005). This enhanced antiarrhythmic activity was paralleled by greater prolongation of intraventricular conduction to the border zone and increase in excitability threshold at the border zone and increase in ventricular effective refractory period in the infarct zone. Serum concentrations of quinidine were 19 +/- 5 microM when given alone and 15 +/- 5 microM when given in combination. Mexiletine concentrations were 3.6 microM when given alone and 4.2 microM when given in combination. In conclusion, mexiletine and quinidine in combination produced enhanced antiarrhythmic activity which was paralleled by electrophysiologic changes occurring in the perinfarct zone. These electrophysiologic changes appear to be correlates of enhanced antiarrhythmic activity.     

Long-Term Outcome Following Programmed Electrical Stimulation in Patients with High-Grade Ventricular Ectopy

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.     

Ventricular Fibrillation Survivors in whom Tachyarrhythmia Cannot Be Induced: Outcome Related to Selected Therapy

Eight-five patients were studied to determine the prognosis of the ventricular tachyarrhythmias at the time of electrophysiologic study. Twenty-five patients (29%) were not inducible when we used a stimulation protocol consisting of up to four extrastimuli delivered at two right ventricular sites. Patients with no inducible arrhythmias were younger (53 vs 59 yrs; p = .06) and had higher ejection fractions (.49 vs .34; p less than .04) than the inducible ventricular fibrillation survivors. Sex, cardiac diagnosis, time from event to electrophysiologic study, and antiarrhythmic therapy at the time of event did not discriminate between those with and those without inducible ventricular tachyarrhythmias. Survival free of recurrent sudden death or ventricular tachycardia was .86 +/- .05 and .95 +/- .05 for patients with and without inducible tachyarrhythmias, respectively (p = .22). Nine of 25 (36%) patients with no inducible arrhythmias developed inducible ventricular tachyarrhythmias when testing was repeated with an antiarrhythmic drug. Ventricular fibrillation survivors not inducible at the time of programmed ventricular stimulation (using a stimulation protocol consisting of four extrastimuli delivered at two right ventricular sites) seem to have a good prognosis. Many "noninducible" patients develop inducible tachyarrhythmias when placed on antiarrhythmic therapy. Because it is possible that these drugs are proarrhythmic, empiric antiarrhythmic therapy should be avoided in these patients.     

Implantation of the Automatic Implantable Cardioverter Defibrillator (AICD): Practical Aspects

Most patients who are resuscitated from an episode of sudden cardiac death or one of sustained ventricular tachycardia (VT) can now be treated using serial electrophysiologic testing as a guide to drug therapy. Recurrence rates are low if an antiarrhythmic regimen can be found which prevents induction of VT. Patients failing serial drug testing have a high recurrence rate (approximately 50%/year). Most clinicians now refer such patients for either experimental antiarrhythmic therapy or electrical intervention. The most promising of the electrical interventions (including tachycardia converting pacemakers and intraoperative mapping)has been the automatic implantable cardioverter defibrillator (AICD). Only recently has the AICD been released from investigative status by the Food and Drug Administration. It can be implanted safely and with favorable clinical outcome if the techniques of implantation are well understood and used often. The text incorporates the authors' experience in implanting nearly 200 devices and is intended as a practical guide to the use of the AICD.     

Value of Serial Electropharmacological Testing in Managing Patients Resuscitated from Cardiac Arrest

Electrophysiologic studies were performed in 11 patients (9 men, 2 women; mean age: 59.9 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose of the studies was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. Ten of the patients were suffering from chronic ischemic heart disease with one or more previous myocardial infarctions while one had no evidence of structural heart disease. A ventricular aneurysm was present in four of them. During control electrophysiologic study, a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths plus bursts of rapid ventricular pacing) in nine of the ten patients (90%) who were studied while not receiving antiarrhythmic drugs; a non-sustained VT was induced in one of them (10%). In three patients (30%) VT could be initiated only by right ventricular stimulation at a side different from the apex (outflow tract). No arrhythmia was observed in the only patient who was studied while taking amiodarone orally (400 mg/day for more than three months). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in seven of the ten patients (70%) who underwent this procedure and a partially effective drug regimen (a sustained VT was no longer inducible; it was easier to interrupt and it was considerably slower) was found in two patients (20%). None of the nine patients who received chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14 months (range: 3-28) and only one had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of follow-up. These results indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest.     

Phenytoin in the Treatment of Inducible Ventricular Tachycardia: Results of Electrophysiologic Testing and Long-Term FoUow-Up

Phenytoin treatment of inducible ventricular tachyarrhythmias was assessed by serial electrophysiologic studies (EPS) in 64 patients with spontaneous ventricular tachycardia, cardiac arrest, or symptoms compatible with a ventricular tachyarrhythmia. Coronary artery disease was the primary cardiac disease in 75% of the patients. All subjects had either inducible ventricular tachycardia (greater than or equal to 10 repetitive beats) or ventricular fibrillation at electrophysiologic study. Phenytoin was administered intravenously in 38 studies and orally in 31 studies. The mean serum phenytoin level was 19.5 +/- 4.7 mcg/ml. Only seven patients (11%) had a negative electrophysiologic study (less than or equal to 10 repetitive beats) after the administration of phenytoin and were classified as phenytoin responders (group I). The remaining 54 patients (89%) were classified as nonresponders (group II). For the nonresponders, phenytoin increased the cycle length of identical monomorphic ventricular tachycardias from a mean of 31 ms to a mean of 327 ms (p less than 0.001). For the four patients tested receiving both intravenous and oral phenytoin, the intravenous response always predicted the oral response. For the seven patients in whom electrophysiologic study indicated phenytoin efficacy, two are alive and arrhythmia-event free, two had sudden death when the regimen was changed (one case, quinidine added; one case, subtherapeutic serum level), and three died from nonarrhythmic causes. For the 10 patients treated empirically with phenytoin, either alone (seven patients) or in combination with another antiarrhythmic agent (three patients), four died secondary to an arrhythmic event.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Use of the Block Cycle Length as a Safe and Efficient Means of Interrupting Sustained Ventricular Tachycardia and Its Pharmacological Modification

In nine patients who had inducible monomorphic sustained ventricular tachycardia (VT), rapid pacing was performed in 11 episodes of morphologically distinct VT at progressively shorter cycle lengths and VT was interrupted at a critical cycle length. The VT interrupting critical cycle length was defined as the block cycle length (BCL) and the effect of Class I antiarrhythmic drugs were examined. Both the VT cycle length (VTCL) and the BCL were prolonged after administration of either drug. The overall mean ratio of the BCL to the VTCL was unchanged after procainamide administration, but increased after the use of mexiletine. The ratio, however, varied in individual VTs and the BCL after treatment with Class I antiarrhythmic drugs could not be predicted from the ratio baseline value, although the ratio was always > 60% and the hazard of VT acceleration might be avoided if the BCL is used.     

Amiodarone in the Management of Patients with Ventricular Tachycardia and Ventricular Fibrillation

Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximumtolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800–1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 ± 1.7 months (mean ± S. D.) of treatment with amiodarone at a mean daily dose of 588 ± 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5–9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 ± 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF overa follow-up period of 21.5 ± 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600–800 mg per day of amiodarone.