Boris Strasberg

Torsade de pointes due to quinidine: Observations in 31 patients

We performed a mail solicitation and obtained the records of 31 patients with documented torsade de pointes (TDP) due to quinidine. All 31 patients had heart disease: ischemic = 11 patients (36%), rheumatic = five patients (16%), hypertensive = four patients (13%), cardiomyopathic = four patients (13%), other = seven patients (22%). Quinidine was administered to these patients for the following reasons: atrial fibrillation or flutter = 22 patients (71%), ventricular premature beats = six patients (19%), ventricular or supraventricular tachycardia = three patients (10%). The 31 patients were receiving quinidine, 650 to 2400 (mean 1097) mg/day, and 14 patients had serum quinidine levels of 1.4 to 10.6 (mean 3.7) micrograms/ml. TDP occurred within 1 week of initiation of quinidine therapy in 23 (74%) of the patients. Twenty-eight (90%) of the 31 patients were receiving digoxin, and 5 (24%) of 21 patients had hypokalemia at the time of TDP. Off of quinidine therapy, corrected QT (QTc) intervals in 24 patients ranged from 390 to 580 (mean 470) msec and were prolonged in 17 patients (71%). On quinidine therapy, QTc intervals in 23 patients ranged from 390 to 630 (mean 510) msec and were prolonged in 21 patients (91%). In summary, patients with TDP due to quinidine usually had heart disease complicated by atrial fibrillation, were receiving digoxin, and were receiving moderate dosages of quinidine for less than 1 week prior to TDP. Approximately two thirds of patients with TDP due to quinidine had long QT intervals while off of quinidine.

Procainamide-lnduced polymorphous ventricular tachycardia

Seven cases of procainamide-induced polymorphous ventricular tachycardia are presented. In four patients, polymorphous ventricular tachycardia appeared after intravenous administration of 200 to 400 mg of procainamide for the treatment of sustained ventricular tachycardia. In the remaining three patients, procainamide was administered orally for treatment of chronic premature ventricular contractions or atrial flutter. These patients had Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In four patients, the arrhythmia was rapidly diagnosed and treated with disappearance of further episodes of the arrhythmia. In two patients, the arrhythmia degenerated into irreversible ventricular fibrillation and both patients died. In the seventh patient, a permanent ventricular pacemaker was inserted and, despite continuation of procainamide therapy, polymorphous ventricular tachycardia did not reoccur. These seven cases demonstrate that procainamide can produce an acquired prolonged Q-T syndrome with polymorphous ventricular tachycardia.

Paroxysmal atrial fibrillation in the wolff-parkinson-white syndrome

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.

Treadmill exercise testing in the Wolff-Parkinson-White syndrome

Abstract Graded treadmill exercise testing was performed in 54 patients with the Wolff-Parkinson-White syndrome and preexcitation (persistent in 36, intermittent in 9 and concealed in 9). Forty-eight patients had previous paroxysmal supraventricular arrhythmia (spontaneous or induced or both). At initiation of treadmill testing, the nine patients with intermittent and the nine with concealed preexcitation had normal conduction. None manifested preexcitation during exercise. Thirty-six patients had preexcitation at initiation of exercise; exercise produced no change in preexcitation in 2, partial normalization of the QRS complex in 16 (due to enhanced atrioventricular [A-V] nodal conduction), and total normalization of the QRS complex in 18 (due to enhanced A-V nodal conduction in 14 and to rate-dependent anomalous pathway block in 4). Exercise-provoked block of the anomalous pathway reflected prolonged anomalous pathway refractoriness, as measured with atrial stimulation. All 18 patients with either total or partial preexcitation at peak exercise manifested more than 1 mm flat or downsloping S-T segment depression. None had evidence of ischemic heart disease. None of the 54 patients manifested either paroxysmal supraventricular tachycardia or atrial fibrillation during or after treadmill exercise. Treadmill exercise testing in patients with preexcitation frequently produces partial or total normalization of the QRS complex due to enhanced A-V nodal conduction and, less commonly, total normalization due to rate-dependent block of the anomalous pathway. False positive S-T segment changes (suggesting ischemia) are always present in patients manifesting preexcitation during treadmill testing. Treadmill exercise testing in patients with preexcitation does not provoke paroxysmal supraventricular tachycardia or atrial fibrillation and is not useful as a provocative test for arrhythmia.

Prediction of response to class I antiarrhythmic drugs during electrophysiologic study of ventricular tachycardia

Abstract We have retrospectively examined data from 41 patients studied in our laboratory for symptomatic ventricular arrhythmia in order to test whether any clinical or electrophysiologic variables could be identified which would predict the patients response to class I antiarrhythmic drugs. All patients had (1) clinically documented paroxysmal sustained ventricular tachycardia (VT) or ventricular fibrillation remote from acute myocardial infarction, (2) inducible sustained VT during control electrophysiologic study (EPS), and (3) EPS after one or more of the following class I antiarrhythmic drugs: intravenous procainamide (36 patients), oral quinidine (30 patients), and oral disopyramide (36 patients). Initially, patients were divided into those who had noninducible or only nonsustained VT after any of the tested drugs (responders), and those who continued to have inducible sustained VT after all tested drugs (nonresponders). A logistic regression technique demonstrated no independent contribution to drug response by any of the following variables: sex, arteriosclerotic heart disease, cardiomegaly, age, time since the initial episode of VT, and cycle length of VT during control study. The number of antiarrhythmic drugs the patient had received prior to study was found to be a significant independent contributor ( p

Electrophysiologic drug testing in prophylaxis of sporadic paroxysmal atrial fibrillation: technique, application, and efficacy in severely symptomatic preexcitation patients.

Electrophysiologic drug testing was performed in nine patients with severely symptomatic sporadic (2 to 13 [mean 4.2] attacks/24 months) paroxysmal atrial fibrillation (PAF). All patients had control inductions of sustained (greater than 30 seconds) AF by high right atrial stimulation, and attempted inductions following serial administration of drugs. Drugs tested were intravenous procainamide (1.0 to 1.5 gm) (five patients), intravenous propranolol (0.1 mg/kg) (three patients), oral quinidine (1.6 to 2.4 gm/day) six patients), oral disopyramide (1.2 to 1.6 gm/day) (four patients), and oral aprindine (100 to 250 mg/day) (four patients). In all patients, one or more drugs prevented induction of sustained AF: procainamide (one patient), quinidine (five patients), disopyramide (four patients), and aprindine (four patients). All patients were treated with drugs which prevented induction of sustained AF and followed for 8 to 40 (mean 24) months. Seven patients tolerated their drugs: six had no AF and one had several short nonsustained attacks. Two patients did not tolerate their drugs: one had paroxysmal palpitation (on decreased aprindine dosage), and one had AF (while off of aprindine). In conclusion, electrophysiologic drug testing is feasible in patients with sporadic PAF. Inability to induce sustained AF following drug administration suggests successful prophylaxis of spontaneous PAF with the same drug.

Symptomatic spontaneous paroxysmal AV nodal block due to localized hyperresponsiveness of the AV node to vagotonic reflexes

Two apparently healthy patients had recurrent syncope with documented paroxysmal AV block. In both patients the site of AV block was demonstrated to be in the AV node. Coronary angiography (in both patients) and sustained deep inspiration (one patient) reproducibly initiated episodes of paroxysmal AV nodal block (identical to spontaneous episodes). Atropine abolished further attempts of AV block induction. Vagal hyperresponsiveness was limited to the AV node, since the interventions provoking paroxysmal AV nodal block produced only appropriate sinus slowing. This syndrome reflects hyperresponsiveness of the AV node to vagotonic reflexes, and exists as a clinically significant entity producing recurrent syncope.

Lack of effectiveness of oral mexiletine in patients with drug-refractory paroxysmal sustained ventricular tachycardia: A study utilizing programmed stimulation

Abstract Recent studies indicate that oral administration of mexiletine is useful in the therapy of recurrent ventricular tachycardia (VT). To further define the clinical usefulness of this drug, mexiletine was administered to 13 men and 4 women with a mean age ± standard deviation of 62 ± 8 years who had drug-refractory paroxysmal sustained VT associated with chronic ischemic heart disease in 14, valvular heart disease in 1, and primary myocardial disease in 1. One patient had no heart disease. All 17 patients had inducible sustained VT during the control electrophysiologic study and during serial electrophysiologic study on conventional drugs. Eleven patients tolerated a mean maximal daily dose of 1,073 ± 149 mg of mexiletine and underwent programmed ventricular stimulation; sustained VT was inducible in 10 patients and nonsustained VT in 1. in 10 patients with inducible sustained VT on mexiletine, the VT cycle length was longer during mexiletine therapy than during control (mean ± standard error of the mean, 342 ± 22 versus 268 ± 14 ms, respectively) (p

Sequential regional phase mapping of radionuclide gated biventriculograms in patients with sustained ventricular tachycardia: Close correlation with electrophysiologic characteristics

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.

Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia

Ten patients are described with two discrete discontinuities in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean +/- SD, 48 +/- 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion, triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.