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Biomedical subjects

C D Swerdlow

Publications and source records attributed to C D Swerdlow.

71 records · Page 4Linked to original sources
PubMed1986

Results of operations for ventricular tachycardia in 105 patients.

Operations to treat ventricular tachycardia refractory to antiarrhythmic drugs were performed in 105 patients. Intraoperative epicardial activation sequence maps were completed in 83% and endocardial maps in 57%. Mapping could be used to guide 79% of operations. When no useful mapping data were obtained, patients had visually guided antiarrhythmic operations (17%) or conventional cardiac operations (4%). The most frequently performed antiarrhythmic procedures, alone or in combination, were endomyocardial resection (45%), cryothermal destruction (44%), and encircling procedures (20%). Operative mortality was 16%, including 6% from heart failure and 4% from ventricular tachycardia. Emergency operation (p = 0.002) and New York Heart Association heart failure class (p = 0.01) were independent preoperative risk factors for cardiac operative mortality in the 98 patients with coronary artery disease. At postoperative electrophysiologic study performed in 79 patients, ventricular tachycardia could not be induced in 75% of patients who had map-guided operations and 36% who had visually guided ones (p = 0.001). During follow-up of 23 +/- 21 months, results of postoperative electrophysiologic study predicted ventricular tachycardia recurrence. At 2 years the actuarial incidence of freedom from arrhythmia recurrence was 50% +/- 10% in patients with and 78% +/- 6% in patients without inducible ventricular tachycardia (p = 0.001); it was 71% +/- 5% in patients who had map-guided operations and 37% +/- 12% in patients who had visually guided ones (p = 0.004). Ventricular tachycardia recurrence was infrequent in survivors of map-guided operations; benefits of surgical treatment for ventricular tachycardia were limited by high operative mortality and frequent arrhythmia recurrence when no useful mapping data were obtained.

Actuarial Analysis↗
PubMed1985

Prospective comparison of Holter monitoring and electrophysiologic study in patients with coronary artery disease and sustained ventricular tachyarrhythmias.

Baseline 24-hour Holter monitoring (HM) and electrophysiologic study (EPS) were compared in 43 consecutive patients with coronary artery disease who had sustained ventricular tachyarrhythmias to determine the fraction of patients in whom each could be performed and the fraction in whom each could be used to guide therapy. Patients were excluded from HM if sustained ventricular tachycardia (VT) requiring termination occurred and from EPS if heart failure was sufficiently severe to cause excessive risk. More patients completed EPS than HM (90% vs 71%), but this difference was not statistically significant (p = 0.12). Overall, HM detected arrhythmias suitable for antiarrhythmic drug assessment in 50% of patients: 30 or more ventricular premature complexes (VPCs) per hour in 50%, 10 or more VPC pairs in 44%, 5 or more runs in 19%, and 10 or more pairs and runs in 44%. Sustained monomorphic VT suitable for electropharmacologic testing was induced at EPS in 82% (p = 0.003 vs HM). Drug efficacy could be assessed in 70% of patients evaluated by HM, compared with 96% evaluated by EPS (p = 0.02). Thus, in consecutive coronary patients with sustained ventricular tachyarrhythmias, EPS could be used to guide therapy more frequently than HM.

Aged↗
PubMed1984

Facilitation of ventricular tachyarrhythmia induction by isoproterenol.

Ventricular tachyarrhythmia induction was facilitated during infusion of isoproterenol in 21 of 60 patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) in whom programmed electrical stimulation alone failed to reproducibly induce sustained ventricular tachyarrhythmias. Of 44 patients with no ventricular tachyarrhythmias induced before isoproterenol infusion, 11 had a sustained ventricular tachyarrhythmia and 1 patient had unsustained VT induced by isoproterenol alone or by programmed stimulation during the infusion. In 9 of 16 patients in whom nonreproducible or unsustained ventricular tachyarrhythmias were induced before isoproterenol infusion, more reproducible or more sustained ventricular tachyarrhythmias were induced during the infusion. Tachyarrhythmia induction was facilitated by isoproterenol in 20 of 40 patients with sustained VT clinically, but in only 1 of 20 patients with unsustained VT or VF clinically. Among patients with sustained VT clinically, those with exercise-provoked VT and those who had not been tested with stimulation at a second right ventricular site or in the left ventricle were more likely to have induction facilitated by isoproterenol. Drugs effective against induction of isoproterenol-facilitated ventricular tachyarrhythmias were identified in 13 of 25 trials. These drugs were effective during a mean follow-up of 17 months in 7 of 9 long-term trials.

Anti-Arrhythmia Agents↗
PubMed1984

Clinical efficacy and electrophysiology of imipramine for ventricular tachycardia.

Invasive electrophysiologic studies were performed before and during treatment with imipramine in 18 patients with inducible ventricular tachycardia (VT). All received imipramine, 50 mg twice daily for 3 days, and then 100 mg twice daily for 3 days. Imipramine increased the infranodal conduction times (HV) (from 58 +/- 7.8 to 65 +/- 10 ms) and QRS duration (from 133 +/- 21 to 153 +/- 39 ms) and significantly decreased sinus cycle length (from 875 +/- 145 to 711 +/- 116 ms) and maximal corrected sinus nodal recovery time (from 457 +/- 656 to 380 +/- 603 ms). The Wenckebach cycle length tended to decrease and the QT interval to increase, but these changes were not statistically significant. Atrial and ventricular refractory periods, atrioventricular nodal conduction times and induced VT cycle length did not change significantly. Imipramine prevented induction of VT in 2 patients, and VT was more difficult to induce in 1 patient. These 3 patients received chronic imipramine therapy. The 2 patients in whom no VT could be induced while taking imipramine have had no recurrence of arrhythmia at 6 and 12 months of follow-up. The third patient died suddenly 4 months after discharge from the hospital. One patient had worsening of arrhythmias while taking imipramine and 61% had minor adverse effects. The mean combined plasma imipramine and desmethylimipramine concentration at the time of the repeat electrophysiologic study was 227 +/- 114 ng/ml. Imipramine is effective against VT in some patients; however, like other type I antiarrhythmic drugs, the rate of efficacy is low.

Adult↗
PubMed1983

Determinants of survival in patients with ventricular tachyarrhythmias.

We analyzed data from 239 patients with sustained ventricular tachycardia or ventricular fibrillation to determine prognosis, predictors of survival, and the prognostic value of inducing arrhythmia and assessing therapy at the time of electrophysiologic study. Therapy predicted to be effective on the basis of electrophysiologic study was administered over a sustained period. There were 71 cardiac deaths, including 44 sudden deaths, during a mean (+/- S.D.) follow-up period of 14.8 +/- 13.9 months (range, one day to 67 months). At one, two, and three years, the actuarial incidence of sudden death was 17 +/- 3, 25 +/- 4, and 34 +/- 6 per cent, and that of cardiac death was 28 +/- 3, 37 +/- 4, and 50 +/- 6 per cent. Multivariate regression analyses demonstrated that the two strongest predictors of both sudden death and cardiac death were a higher New York Heart Association functional class (P less than 0.0001 for sudden death and P less than 0.0001 for cardiac death) and the failure of any therapy to be identified as potentially effective on the basis of electrophysiologic study (P = 0.0019 and P = 0.0003). The majority of deaths in patients with ventricular tachyarrhythmias were sudden, but the severity of heart failure was the strongest independent predictor of mortality. Response to therapy during electrophysiologic study was also an independent predictor of survival.

Adult↗
PubMed1983

The automatic implantable defibrillator: local ventricular bipolar sensing to detect ventricular tachycardia and fibrillation.

The first-generation automatic implantable defibrillator implanted in man sensed arrhythmias by monitoring a transcardiac electrocardiographic signal. This sensing system reliably detected ventricular fibrillation and sinusoidal ventricular tachycardia but failed to sense all nonsinusoidal ventricular tachycardias. To solve this problem, a new ventricular tachycardia detection scheme was developed using a local ventricular bipolar electrogram and electronic circuits using rate averaging and automatic gain control to permit sensing of electrograms down to 0.1 mV. This detection scheme was tested during electrophysiologic studies in 11 patients with ventricular tachycardia and fibrillation. All 22 episodes of induced ventricular tachycardia with a rate above the selected cutoff were detected after an average of 5.1 +/- 1.8 seconds. No episodes below the rate cutoff were detected. The bipolar circuits also reliably detected ventricular fibrillation. Arrhythmia detection and signal quality in 9 patients receiving automatic defibrillators using the new bipolar rate detection circuit were compared with the findings in 5 patients previously receiving units that sensed arrhythmias using the transcardiac electrocardiographic signal. Compared with the transcardiac monitoring units the newer bipolar units had shorter and more uniform sense times (5.5 +/- 1.4 versus 12.2 +/- 7.1 seconds). It is concluded that malignant ventricular tachyarrhythmias can be sensed accurately using bipolar rate detection and that this system has numerous advantages over the previously used transcardiac electrocardiographic signal.

Aged↗
PubMed1983

Efficacy of verapamil in chronic, recurrent ventricular tachycardia.

Verapamil, 0.25 mg/kg, was given to 24 patients with chronic, recurrent ventricular tachycardia (VT) whose clinical tachyarrhythmias were reproduced at electrophysiologic study. Seven patients (29%) responded acutely to verapamil: VT was not inducible in 5 and spontaneously terminated within 5 seconds of induction in 2 patients in whom it was previously sustained. Four of the 7 responders had no identifiable structural heart disease, and 3 had coronary artery disease. Responders were younger and had better left ventricular function than did nonresponders. Long-term therapy with verapamil, attempted in 5 of the 7 responders, was effective in 3, ineffective in 1, and of uncertain efficacy in 1. Verapamil therapy was discontinued because of worsened congestive heart failure in 2 patients. The short-term efficacy of verapamil in these patients compares favorably with the efficacy of other antiarrhythmic agents against VT induction in patients with long-term, recurrent, drug-refractory VT. The short-term efficacy of verapamil correlated with its long-term efficacy. These observations provide preliminary evidence that verapamil may be useful in the treatment of some patients with recurrent VT. When standard drugs are not effective, verapamil should be given a trial, especially in young patients with good left ventricular function.

Adult↗
PubMed1983

Safety and efficacy of intravenous quinidine.

The safety and efficacy of intravenous quinidine were evaluated in a patient population with a high prevalence of left ventricular dysfunction and intraventricular conduction delays. Quinidine gluconate (mean dose 9.1 +/- 1.6 mg/kg) was administered during electrophysiologic study to 100 patients with ventricular or supraventricular tachyarrhythmias. Clinical heart failure was present in 68 percent of the patients. Left ventricular end-diastolic pressure, cardiac index, and left ventricular ejection fraction were abnormal in 62, 48, and 70 percent, respectively. Major intraventricular conduction delays (QRS of 120 msec or more) were present in 27 percent, and the H-V interval was prolonged (over 55 msec) in 28 percent. Despite the prevalence of these abnormalities, quinidine was discontinued because of hypotension in only 10 patients. Saline solution was infused to maintain preload in 37 percent, and hypotension responded promptly to saline solution infusion or discontinuation of quinidine infusion in all subjects. Hypotension was not more common in patients with more severe left ventricular dysfunction. QRS duration, H-V interval, QTc, and right ventricular effective refractory period increased significantly (p less than 0.001) after quinidine administration. Heart block or QRS widening of 50 percent or more did not occur. Quinidine prevented arrhythmia induction in 26 percent of patients who received full doses. Ventricular tachycardia cycle length increased in all 41 patients in whom identical forms were induced before and after quinidine (287 +/- 71 msec versus 361 +/- 93 msec, p less than 0.001). Intravenous quinidine may be administered safely to patients with intraventricular conduction delays and moderate heart failure. When antiarrhythmic efficacy is assessed by electrophysiologic study, quinidine compares favorably with other antiarrhythmic agents.

Arrhythmias, Cardiac↗
PubMed1983

Clinical factors predicting successful electrophysiologic-pharmacologic study in patients with ventricular tachycardia.

Data from 142 patients who had sustained ventricular tachycardia or ventricular fibrillation were analyzed to determine if clinical variables predict response to antiarrhythmic drugs at electrophysiologic study. Effective antiarrhythmic drugs were identified for 43 patients (30%). Ten of 25 variables analyzed were univariate predictors of drug response at the probability (p) level of less than 0.05. Stepwise logistic regression identified three variables independently predictive of drug response: fewer coronary arteries with 70% or greater stenosis (p less than 0.001), female sex (p less than 0.002) and fewer episodes of arrhythmia (p less than 0.03). A function incorporating these three variables was constructed to predict the probability of drug response, and ranges of the predictor function corresponding to high, intermediate and low probabilities of drug response were identified. Response rates in the high (greater than 50%), intermediate and low (less than 10%) probability ranges were 28 (58%) of 48, 10 (27%) of 37 and 5 (9%) of 57, respectively. Thus 40% of the patients who had a less than 10% likelihood of benefit from electrophysiologic-pharmacologic study were classified into the low probability range. When the predictor function was applied prospectively to 25 additional patients, response rates in the three probability ranges were 3 (50%) of 6, 1 (12%) of 8 and 0 (0%) of 11. These data show that analysis of clinical variables can be used to estimate the probability of benefit from electrophysiologic-pharmacologic study.

Anti-Arrhythmia Agents↗
PubMed1983

Amiodarone: clinical efficacy and toxicity in 96 patients with recurrent, drug-refractory arrhythmias.

Ninety-six patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for 8.0 +/- 7.5 months (range 1 day to 27 months): 77 for recurrent ventricular tachycardia or ventricular fibrillation (VT/VF), two for complex ventricular ectopy, and 17 for supraventricular tachyarrhythmias. The actuarial incidence of successful amiodarone therapy was 52 +/- 7% at 12 months and 28 +/- 9% at 24 months for patients with VT/VF. Neither patient with complex ventricular ectopy was successfully treated. Among the patients with supraventricular tachyarrhythmias, 64.7% were successfully treated for 7.7 +/- 7.6 months (range 1 to 22 months). Amiodarone toxicity occurred in 66 of 91 patients (72.5%) treated for more than 1 week. Fourteen patients had therapy-limiting toxicity. Of these 14, six had pulmonary toxicity, four had arrhythmia exacerbation, one had hepatitis, one had renal toxicity, one had rash, and one had erythema nodosum. The actuarial incidence of therapy-limiting side effects was 27 +/- 7% at 15 months. We conclude that amiodarone is useful in the treatment of refractory tachyarrhythmias but that the rate of efficacy in VT/VF is lower and the incidence of significant toxicity is higher than has been generally appreciated.

Adult↗
PubMed1983

Prognostic significance of the number of induced ventricular complexes during assessment of therapy for ventricular tachyarrhythmias.

We analyzed 255 long-term trials of antiarrhythmic therapy, each of which had been evaluated at electrophysiologic study, to identify the maximum number of induced ventricular complexes consistent with the long-term efficacy of antiarrhythmic therapy. All patients had spontaneous and inducible sustained ventricular tachycardia or ventricular fibrillation. The incidence of therapeutic efficacy at 1 month and throughout follow-up was similar for trials in which zero, one, two, three, four, five, six to 10, and 11 to 15 complexes were induced, but significantly lower (p less than .001) for trials in which 16 or more complexes were induced. The cumulative incidence of efficacy at 1 year was 75 +/- 5% for 0 to 5 induced complexes, 72 +/- 11% for six to 10 complexes, 83 +/- 15% for 11 to 15 complexes, 42 +/- 10% for 16 complexes to 15 sec, and 48 +/- 6% for sustained ventricular tachycardia. At 1 year, the incidence of "sudden death-free" survival was higher for patients in trials that prevented initiation of sustained ventricular tachycardia than for those in trials that permitted initiation of sustained ventricular tachycardia (91 +/- 3% vs 75 +/- 6%; p = .01). The duration of the arrhythmia induced at therapy assessment was in the range of 11 to 20 complexes for only 4% of trials. Antiarrhythmic therapy is likely to be effective if as many as 15 complexes are induced at therapy assessment. The best cutoff, between 11 and 20 complexes, is difficult to identify because of the small fraction of trials in this range. Patients in whom initiation of sustained ventricular tachycardia is not prevented are at high risk for arrhythmia recurrence and sudden death.

Adult↗
PubMed1982

Decreased incidence of antiarrhythmic drug efficacy at electrophysiologic study associated with the use of a third extrastimulus.

Drug trials during electrophysiologic study were performed in 166 patients with sustained ventricular tachycardia (VT) or ventricular fibrillation. In the first 21 patients (group I), a maximum of two extrastimuli was used. In 145 subsequent patients (group II), drug efficacy was assessed using three extrastimuli if one or two failed to induce VT. The incidence of acute drug efficacy was 15 of 21 (71%) in group I, but only 44 of 145 (30%) in group II (p less than 0.01). To assess the influence of the third extrastimulus on the differing incidence of acute drug efficacy, we examined the 69 group II patients whose VT was initially induced by one or two extrastimuli. Acutely effective agents were identified for 19 of these 69 patients using up to three extrastimuli to define efficacy. In 24 of te 50 patients for whom no effective drug could be found, VT was induced with one or two extrastimuli during all drug trials. In the remaining 26 patients VT could be induced after drug administration only with use of three extrastimuli. If efficacy had been defined using a maximum of two extrastimuli, these 26 patients would have been considered responsive to drug testing. Overall, 45 to 69 (65%) rather than 19 of 69 (28%) would have had a favorable response (p less than 0.001). Fourteen group I patients and 17 group II patients in whom VT was initially induced by one or two extrastimuli received chronic therapy with agents predicted effective during acute drug trials. At 18 months, the cumulative percent of patients free of arrhythmia recurrence by actuarial analysis was 79 +/- 14% in group I and 80 +/- 14% in group II (NS). Use of three extrastimuli during drug trials is associated with a lower incidence of acute drug efficacy. Limited data suggest that prophylaxis against VT induction by three, rather than two, extrastimuli may not be a stronger predictor of chronic efficacy in patients whose VT is initially induced by one or two extrastimuli. Further study is needed to identify optimal pacing methods for antiarrhythmic drug assessment.

Anti-Arrhythmia Agents↗
PubMed1982

Programmed ventricular stimulation in predicting vulnerability to ventricular arrhythmias and their response to antiarrhythmic therapy.

In predicting vulnerability to ventricular arrhythmias and their response to antiarrhythmic therapy, several factors and questions need to be considered, including the following. (1) Ventricular tachycardia (VT) can be induced in most patients who have recurrent sustained VT. (2) Because induced VT can often be pace terminated, termination by pacing should be attempted before cardioversion is applied. (3) Acutely effective antiarrhythmic agents are no longer being found for the majority of patients undergoing electrophysiologic-pharmacologic study in our series. (4) Specific VT-induction programs affect both the inducibility of VT and acute efficacy of drugs at electrophysiologic study; this point requires examination. (5) Arrhythmia-induction studies may not product high yield in patients with clinical ventricular fibrillation or unsustained VT. (6) It is as yet unclear whether some drugs, such as amiodarone, can be accurately evaluated by using arrhythmia-induction techniques. (7) Induction of the repetitive ventricular response by V2 stimulation is not a useful method for antiarrhythmic drug selection in patients with recurrent ventricular tachyarrhythmias. (8) Adequate data do not yet exist to identify either the ECG-monitoring technique or the arrhythmia-induction technique as the preferred method for selecting antiarrhythmic drugs for chronic therapy of patients with recurrent ventricular tachyarrhythmias. A study to compare the accuracies of the two techniques is both feasible and needed.

Amiodarone↗
PubMed1982

Antiarrhythmic drug combinations in the treatment of ventricular tachycardia.

Combinations of antiarrhythmic drugs are frequently used to treat refractory ventricular tachycardia (VT), but few scientific data support this practice. We examined the efficacy and electrophysiology of 110 antiarrhythmic drug combination trials at electrophysiologic study in 74 patients with recurrent ventricular tachycardia. Lidocaine was combined with quinidine in 33 trials, procainamide in 22 and encainide in 20. Propranolol was combined with quinidine in 17 trials, procainamide in 12 and encainide in six. All individual drugs tested (except propranolol, which was usually not tested individually) had failed at electrophysiologic study or clinically in the presence of usually accepted plasma concentrations. Lidocaine in combination with quinidine was effective in 3% of the trials, with procanamide in 5% and with encainide in none of the trials. Propranolol in combination with quinidine was effective in 18% of the trials, with procainamide in 17% and with encainide in none of the trials. The electrophysiologic effects of the tested drug combinations were dominated by the individual effects of the type 1 antiarrhythmic agents. We conclude that the tested antiarrhythmic drug combinations are infrequently effective in preventing VT induction at electrophysiologic study when each agent has failed individually. The addition of lidocaine or propranolol to quinidine, procainamide or encainide does not produce significant synergistic or new effects on the electrophysiologic variables analyzed.

Aged↗
PubMedDate not supplied

Prepulses reduce the pain of cutaneous electrical shocks.

OBJECTIVE: Both the startle reflex elicited by an intense acoustic or tactile stimulus and the perceived intensity of that stimulus can be diminished by a weak "prepulse" that precedes the startling stimulus. The present study examined whether prepulses can also diminish the pain produced by an intense electrical stimulus similar to that used to treat life-threatening cardiac arrhythmias in conscious patients with implantable cardioverter/defibrillators or transcutaneous pacemakers. METHODS: Perceptual and pain thresholds for electrical shocks to the arm were determined in 20 adults. Participants then rated the painfulness of 25 electrical shocks that were 1.5 times the pain threshold (mean shock intensity, approximately 160 V) and either presented alone or preceded (at 40-60 ms) by weak electrical prepulses equal to or 25% above the perceptual threshold. RESULTS: Prepulses significantly reduced the pain produced by the intense shocks. Individuals with the lowest pain thresholds experienced the greatest pain reduction with prepulses. In these more sensitive individuals, the most effective prepulses reduced perceived pain by 26% across the entire test session and by 54% in the initial block of five shocks. CONCLUSIONS: Prepulses may be useful in diminishing the pain associated with the therapeutic electrical shocks used to treat cardiac arrhythmias.

Adult↗