Nonpharmacologic therapy of tachycardias: the role of implanted devices.
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Atrial Fibrillation↗
Biomedical subjects
R A Winkle
Publications and source records attributed to R A Winkle.
Electrophysiology of Ethmozine (moricizine HCl) for ventricular tachycardia.
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%.
Adult↗
Role of extrastimulus prematurity and intraventricular conduction time in inducing ventricular tachycardia or ventricular fibrillation secondary to coronary artery disease.
The influence of extrastimulus prematurity and changes in intraventricular conduction time on ventricular tachycardia (VT) inducibility were evaluated in 78 patients with coronary artery disease undergoing electrophysiologic study. In a retrospective portion, the effect of adding ventricular extrastimuli vs shortening the ventricular drive cycle length on extrastimulus prematurity and VT inducibility was evaluated in 59 consecutive patients with inducible ventricular arrhythmias (group I). In a prospective component, changes in intraventricular conduction of the last ventricular extrastimulus and the relation to initiation of VT were evaluated in 19 consecutive patients undergoing programmed electrical stimulation (group II). Single (V2), double (V3) and triple (V4) ventricular extrastimuli were introduced during ventricular drive pacing (V1) at multiple cycle lengths. Although reduction of drive cycle length facilitated arrhythmia induction in 25% of patients, addition of an extrastimulus was a more potent method in group I patients. However, the mechanism of arrhythmia induction is not dependent on attainment of shorter coupling intervals with either method. In group II patients QRS duration and intraventricular conduction time of the extrastimuli increased as the coupling interval was reduced. Significant changes in QRS duration and intraventricular conduction time of the extrastimuli that initiated VT were not observed.
Cardiac Pacing, Artificial↗
The relationship between successful defibrillation and delivered energy in open-chest dogs: reappraisal of the "defibrillation threshold" concept.
The traditional assessment of the energy required for successful ventricular defibrillation involves the measurement of a "defibrillation threshold" (DFT), implying a clear-cut distinction between effective and ineffective energies. We examined the relationship between delivered energy and the likelihood of successful defibrillation in 10 open-chest pentobarbital anesthetized dogs, with the use of an internal spring/patch electrode system. An initial DFT was determined by decreasing the energy discharged until a failure first occurred (10.3 +/- 3.4 J). Six energy levels in 1 to 2 J increments were then selected surrounding this value and each was administered eight times in balanced random order (total 48 trials). The relationship between energy and percent success in defibrillation exhibited a shallow slope, with a gradual increase in success from 0% to 100% over several energy increments. The initial DFTs showed actual success rates varying from 25% to 87.5% (mean 71 +/- 26%). The results were fitted to a sigmoidal dose-response curve by logistic regression analysis and the energy associated with 50% success (E50) and 80% success (E80) was determined, as no single value for DFT could be defined in any animal. In 12 other dogs, a defibrillation curve was similarly constructed at baseline and was repeated after 90 minutes. No significant change in E50 (5.0 +/- 2.1 J vs 5.2 +/- 2.7 J) or E80 (6.3 +/- 2.5 J vs 6.6 +/- 3.2 J) was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of acute intravenous and chronic oral amiodarone on defibrillation energy requirements.
Amiodarone is commonly used with the automatic implantable defibrillator to treat recurrent ventricular tachyarrhythmias. The effects of acute intravenous and chronic oral amiodarone on the energy requirements for successful defibrillation were evaluated in 12 dogs chronically instrumented with right atrial spring and left ventricular patch defibrillation electrodes. Multiple shocks of varying energy were applied in balanced random order to construct curves of percent successful defibrillation vs energy (DF curves) on each test day. Dogs were studied on days 1, 11, 18, 25, and 32. On day 11, DF curves were determined before and after infusing saline (n = 6) or amiodarone (n = 6), 10 mg/kg loading and 0.33 mg/kg/min maintenance doses. Dogs administered intravenous amiodarone were continued on oral drug (300 mg twice daily) for the remainder of the study. Data were analyzed by logistic regression and the energy required for 50% (E50) and 80% (E80) successful defibrillation were compared. Differences between controls and animals receiving chronic oral amiodarone were not significant on any day. After acute intravenous infusion, dogs given amiodarone had a 21.7 +/- 12.8% decrease in E50 (p less than 0.01) and a 19.7 +/- 17.8% decrease in E80 (p less than 0.05), while controls had an 11.4 +/- 30.5% increase (p = NS) in E50 and 6.30 +/- 30.5 increase in E80 (p = NS). It is concluded that the energy required for successful defibrillation is decreased by acute intravenous amiodarone, while chronic oral administration has no significant effect.
Administration, Oral↗
Internal cardiac defibrillation: histopathology and temporal stability of defibrillation energy requirements.
The automatic implantable cardioverter/defibrillator is tested intraoperatively to ensure effectiveness by performing a number of induced fibrillation-defibrillation trials. The temporal stability of defibrillation energy requirements and the histopathologic effects of multiple defibrillating shocks were studied in 12 dogs chronically instrumented with an internal spring-patch lead system identical to that used in humans. Dogs were studied on days 1, 11, 18, 25 and 32. Data were analyzed by logistic regression and the energy required for 50% (E50) and 80% (E80) success was compared. On day 32 the dogs were killed and the heart was removed for gross and microscopic pathologic examination. There was a significant decrease in energy requirements from day 1 to day 11, as the E50 decreased from 6.9 +/- 4.5 to 4.9 +/- 2.5 J (p less than 0.02) and the E80 decreased from 8.5 +/- 5.2 to 6.1 +/- 3.4 J (p less than 0.02). The energy requirements then remained stable over the remainder of the experiment. The dogs were administered 209 +/- 18 shocks (range 1 to 24 J) for a total cumulative dose of 1,524 +/- 571 J. In all cases, both grossly and microscopically, there was no evidence of pathologic changes in the myocardium or coronary vessels. In all cases there was a fibrous plaque beneath the patch electrodes, at times containing an area of patchy hemorrhage; in a single specimen a mixed inflammatory infiltrate accompanied the hemorrhage. Endothelialization of the spring electrode with mild right atrial endocardial fibrosis was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Long-term electrocardiographic and event recorders for the diagnosis and treatment of cardiac arrhythmias.
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Arrhythmias, Cardiac↗
Esophageal electrocardiography: a new technology revives an old technique.
This study evaluates the clinical use of an easily swallowed bipolar electrode for recording an esophageal electrocardiogram (ECG). Fourteen patients were selected for bedside diagnosis (ECG group) because of arrhythmias difficult to evaluate using a standard 12-lead ECG. A second group of 27 non-selected patients scheduled for routine 24-hour ambulatory electrocardiographic recordings (ambulatory ECG group) had an esophageal ECG recorded as the "third channel." All 14 patients (100%) in the ECG group had excellent-quality tracings, and the esophageal ECG was diagnostic in 12 cases (86%). Of 27 patients in the ambulatory ECG group, 19 (70%) had fairly good to excellent-quality 24-hour esophageal pill tracings, with the esophageal ECG contributing to correct arrhythmia diagnosis in 11 patients (41%). It is concluded that this easily swallowed esophageal electrode provides an excellent-quality short-term ECG and often permits proper arrhythmia diagnosis in selected patients with arrhythmias. Good-quality 24-hour esophageal ambulatory electrocardiographic recordings can also be obtained that contribute to arrhythmia diagnosis in a limited number of unselected patients, and should be even more clinically useful in carefully selected patients.
Arrhythmias, Cardiac↗
Ethmozine: electrophysiology, hemodynamics, and antiarrhythmic efficacy in patients with life-threatening ventricular arrhythmias.
Thirteen patients with drug-resistant, life-threatening ventricular arrhythmias and inducible sustained ventricular tachycardia (VT) at electrophysiologic study received moricizine HC1 (ethmozine), 10 mg/kg/day orally. Eight patients underwent electrophysiologic study before and after drug administration; the arrhythmia became noninducible in one. In five other patients, spontaneous sustained VT occurred after 1 to 5 days of drug therapy, and one patient had a worsening of arrhythmias on ethmozine. Ethmozine prolonged infranodal conduction time (HV interval) (51.4 +/- 13.8 msec to 69.3 +/- 17.7 msec [mean +/- SD]), PR interval (201 +/- 28.1 msec to 244 +/- 62.2 msec), and QRS interval (123 +/- 27 msec to 147 +/- 32 msec). Ventricular refractory periods were not consistently affected, and only the one patient who became noninducible had an increase in effective ventricular refractory period (280 to 310 msec). The drug had no significant effect on sinus cycle length or sinus node recovery time, atrial conduction or refractoriness, or atrioventricular nodal refractoriness. Ethmozine had no effect on radionuclide ejection fraction (25.5 +/- 12.7% to 28.2 +/- 13.8%) or cardiac index (2.4 +/- 0.7 to 3.0 +/- 0.6 ml/min/m2) and caused no significant changes in mean aortic, right atrial, pulmonary arterial, or pulmonary capillary wedge pressures. Although the drug is well tolerated and produces no untoward hemodynamic effects, ethmozine is relatively ineffective in patients with sustained VT refractory to conventional antiarrhythmic agents.
Adult↗
Effect of quinidine and bretylium on defibrillation energy requirements.
We examined the effect of bretylium and quinidine on the energy requirements for internal defibrillation in 14 pentobarbital-anesthetized dogs. Bretylium, 6 or 10 mg/kg (n = 6), did not affect the relation between energy and the likelihood of successful defibrillation. The mean energy required to achieve 50% success (E50) or 90% success (E90) in defibrillation was not significantly altered; E50 was 5.3 +/- 1.9 J (X +/- s.d) before and 6.1 +/- 3.5 J after bretylium (n.s.), and E90 was 7.2 +/- 2.1 J before and 8.6 +/- 3.3 J after drug (n.s.). Quinidine was administered in a series of two loading and maintenance infusions to achieve mean plasma concentrations of 2.4 +/- 0.63 and 2.95 +/- 0.88 microgram/ml, respectively (n = 8). No significant effect on defibrillation energy requirement was observed; mean E50 before and after treatment was 6.3 +/- 3.3 J and 6.2 +/- 2.9 J, respectively, and mean E90 was 8.3 +/- 4.4 J and 8.3 +/- 4.1 J, respectively. Similarly, saline administration to control dogs (n = 12) resulted in no change in E50 or E90. At concentrations or doses similar to those in patients with serious arrhythmias, neither quinidine nor bretylium appears to have consistent effects on the energy requirements for internal defibrillation in our dog model.
Animals↗
Lidocaine causes a reversible, concentration-dependent increase in defibrillation energy requirements.
To investigate the influence of lidocaine on the energy requirements for internal defibrillation, lidocaine (n = 8) or saline solution (n = 12) was administered by intravenous infusion to 20 pentobarbital-anesthetized dogs, and the likelihood of successful defibrillation was examined at various shock energy levels before and after treatment. After lidocaine administration to a mean steady state concentration of 5.6 +/- 2.7 micrograms/ml, the mean energy required to achieve 50 and 90% success in defibrillation (E50 and E90) increased by 61.1 +/- 34.1% (mean +/- SD, p less than 0.005) and 47.1 +/- 28.6% (p less than 0.005), respectively. The steady state log lidocaine concentration correlated positively with the observed increase in E50 (r = 0.887, p less than 0.01) over a concentration range from 1.95 to 9.8 micrograms/ml. In a related experiment, lidocaine infusion was administered to five dogs and then abruptly discontinued. At energy levels achieving a mean 90.0 +/- 10.0% success in defibrillation before treatment, only 43.3 +/- 23.4% success was achieved after 60 minutes of the lidocaine infusion (p less than 0.01) at a mean plasma concentration of 8.4 +/- 2.1 micrograms/ml. The percent of successful defibrillations returned to baseline value (92.0 +/- 18.0%, p less than 0.01) after drug washout at a time when mean lidocaine concentration had declined to 1.8 +/- 0.5 microgram/ml. Lidocaine causes a reversible, concentration-dependent increase in the energy requirements for successful defibrillation; recommendations to administer lidocaine to patients with ventricular fibrillation resistant to defibrillation may need to be reviewed.
Animals↗
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.
Electric Countershock↗
Effects of encainide and its metabolites on energy requirements for defibrillation.
Encainide, a class IC antiarrhythmic agent, has been associated with proarrhythmic responses of ventricular tachycardia and fibrillation requiring defibrillation in patients. We examined the short-term effects of intravenous encainide and its two major metabolites, O-demethyl-encainide (ODE) and 3-methoxy-ODE (MODE), on the energy requirements for successful defibrillation in 25 pentobarbital-anesthetized, open-chest dogs. Truncated exponential (60% tilt) defibrillation shocks were administered through right atrial spring and left ventricular epicardial patch electrodes identical to those used in man with the automatic implantable defibrillator. At baseline multiple shocks of varying energy were applied to construct curves of percent successful defibrillation as a function of energy (DF curves) for each animal. Encainide, ODE, or MODE was then infused in loading and maintenance doses to achieve QRS widening of 20% to 50%. Saline was administered to animals serving as controls. Determination of the DF curve was repeated, after which the infusion was discontinued. After 1 hr washout period, an additional DF curve was constructed. The data were analyzed by logistic regression, and the energies required for 50% successful defibrillation (E50) were compared. No significant differences existed between the four groups in body or heart weight, extent of QRS widening, or baseline E50 values. After administration of encainide and ODE, the E50 increased by 129 +/- 43% (p less than .001) and 76 +/- 34% (p less than .005), respectively. Return of E50 toward baseline was observed after the washout periods in both groups (p less than .025), demonstrating the reversibility of the drugs' effects.(ABSTRACT TRUNCATED AT 250 WORDS)
Anilides↗
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↗
Chronic lorcainide therapy for symptomatic premature ventricular complexes: efficacy, pharmacokinetics and evidence for norlorcainide antiarrhythmic effect.
Chronic premature ventricular complexes (PVCs) have been effectively suppressed by oral lorcainide as reported in previous short-term studies. The plasma level-effect relation of lorcainide may be affected by the possible cardioactivity of norlorcainide, a metabolite that accumulates after repeated oral doses. This study evaluated the long-term efficacy of lorcainide in suppressing chronic symptomatic PVCs, and examined the relation of arrhythmia suppression to plasma concentrations of lorcainide and norlorcainide. Fourteen patients were treated with lorcainide, 200 to 400 mg/day, 12 of whom achieved nearly complete suppression of arrhythmias after treatment for 1 year. Chronic lorcainide treatment was well tolerated; no patient discontinued treatment because of adverse effects. Lorcainide and norlorcainide plasma concentrations remained stable after the first week of therapy. Antiarrhythmic activity persisted throughout the year. Upon drug withdrawal, the mean lorcainide washout half-life was 14.3 +/- 3.7 hours and the mean norlorcainide washout half-life was 31.9 +/- 8.9 hours. The return of arrhythmias occurred well after the lorcainide plasma concentration had decreased to subtherapeutic levels, suggesting an antiarrhythmic effect of norlorcainide. Thus, long-term lorcainide therapy is effective in treating chronic symptomatic PVCs and is well tolerated by most patients. The metabolite norlorcainide appears to have antiarrhythmic activity independent of lorcainide.
Benzeneacetamides↗
Treatment with oral lorcainide in patients with sustained ventricular tachycardia and fibrillation.
Fifty patients with drug-refractory (failed 7 +/- 2 other drug trials) sustained ventricular tachycardia or fibrillation were treated with oral lorcainide. Twenty-three patients underwent programmed stimulation both before and after oral lorcainide, and all 23 remained inducible, although ventricular tachycardia cycle length was prolonged and mean arterial pressure was higher. Lorcainide was discontinued in 23 patients prior to hospital discharge because of death in four patients, side effects in five patients, spontaneous clinical arrhythmia recurrence in six patients, and ventricular tachyarrhythmias induced at electrophysiologic study in eight patients. Twenty-seven patients were discharged on an average dose of 169 +/- 56 mg twice a day, including 15 in whom ventricular tachycardia remained inducible. During long-term follow-up the drug was discontinued in 15 patients; three because of side effects, three because of clinical nonfatal arrhythmia recurrence, two who selected other alternative therapy, and seven patients who died suddenly due to ventricular tachyarrhythmias. Twelve patients remain on long-term lorcainide. The actuarial 1-year chance of being arrhythmia free was 38.9%, and 1-year cardiovascular and arrhythmia survival rates were 56.8% and 60.4%, respectively. Based on our data we conclude that: In this extremely drug-resistant patient population the clinical efficacy of lorcainide is low; lorcainide should not be used empirically in such highly drug-resistant patients; persistent ventricular tachyarrhythmia inducibility at electrophysiologic study implies a poor prognosis in patients treated with oral lorcainide; the incidence of becoming noninducible during oral lorcainide therapy in highly drug-resistant patients appears low; and for patients in whom the drug seems partially beneficial it could be used in conjunction with a backup automatic implantable cardioverter/defibrillator.
Administration, Oral↗
The mechanisms of ventricular tachycardia in humans determined by intraoperative recording of the electrical activation sequence.
We recorded ventricular activation sequence during ventricular tachycardia in 76 patients who underwent surgical therapy of refractory ventricular tachycardia. Ventricular tachycardia arose from a discrete site (focal origination) in 28 patients (37%) or resulted from reentry around scar (macroreentry) in 22 patients (29%). The mechanism responsible for ventricular tachycardia was not discernable in the remaining 26 patients (34%), usually because of inadequacy of activation data. We conclude: (1) although focal originating of ventricular tachycardia is common, more frequently the mechanism is either macroreentry or uncertain, as assessed by conventional recording techniques; thus, a search for the "site of earliest activation" during ventricular tachycardia frequently may fail to direct rationally the operative procedure; (2) conventional techniques for intraoperative study of electrical activation during ventricular tachycardia are inadequate.
Cardiac Pacing, Artificial↗
Amiodarone and the American Way.
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Amiodarone↗