Edwin Palileo

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.

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

Tachyarrhythmias in young athletes.

Nineteen young athletes with documented symptomatic tachyarrhythmia were systematically evaluated. There were 15 men and 4 women, aged 14 to 32 years (mean 22 +/- 6). Documented tachyarrhythmias were paroxysmal atrial fibrillation in five patients, paroxysmal supraventricular tachycardia in five, paroxysmal ventricular tachycardia in eight (sustained in five, nonsustained in three) and ventricular fibrillation in one patient. Abnormal substrates were demonstrated in 15 (79%) of the 19 athletes: 5 had an anomalous atrioventricular (AV) pathway and 10 had heart disease (mitral valve prolapse in 9 patients and dilated cardiomyopathy in 1 patient). In 13 (68%) of the 19 athletes, all spontaneous attacks of tachyarrhythmia had started during strenuous exercise. Tachyarrhythmia that closely resembled clinical arrhythmia was induced by programmed cardiac stimulation in 13 athletes (68%) and was reproducibly provoked by treadmill exercise in 8 athletes (42%). In four of seven athletes with ventricular tachycardia, tachycardia closely resembling clinical arrhythmia was provoked by infusion of isoproterenol. In summary: young athletes can have any of several tachyarrhythmias; abnormal substrates can be demonstrated in many athletes with symptomatic tachyarrhythmia; and tachyarrhythmias in young athletes frequently occur during exercise.

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.

Retrograde dual atrioventricular nodal pathways

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type). Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual and unusual variety (one third of patients).

Analysis of Anterograde and Retrograde Fast Pathway Properties in Patients With Dual Atrioventricular Nodal Pathways Observations Regarding the Pathophysiology of The Lown-Ganong-Levine Syndrome

Anterograde and retrograde fast pathway properties were analyzed in 160 patients with anterograde dual atrioventricular (A-V) nodal pathways, with or without A-V nodal reentrant tachycardia. A-H intervals (reflecting anterograde fast pathway conduction) ranged from 46 to 234 ms (mean ± standard deviation 91 ± 30). The longest atrial paced cycle lengths at which block occurred in the anterograde fast pathway ranged from 231 to 857 ms (435 ± 112). Regression analysis of these cycle lengths versus A-H intervals revealed a correlation coefficient (r) value of 0.41 (p < 0.01). Retrograde fast pathway conduction was present (at a ventricular paced cycle length slightly shorter than sinus rhythm) in 84 of 125 patients: 15 of 16 with an A-H interval of less than 60 ms, 44 of 58 with an interval of 60 to 90 ms, 20 of 41 with an interval of 91 to 130 ms and 5 of 10 with an A-H Interval of more than 130 ms (p < 0.01). Retrograde fast pathway conduction was intact at a cycle length of 375 ms in 41 of 124 patients: 11 of 16 with an A-H interval of less than 60 ms, 22 of 57 with an interval of 60 to 90 ms, 7 of 41 with an interval of 91 to 130 ms and 1 of 10 with an A-H interval of more than 130 ms (p <0.01). Sustained A-V nodal reentrant tachycardia could be induced in 51 of 160 patients, being induced in 7 of 17 with an A-H interval of less than 60 ms, 27 of 72 with an interval of 60 to 90 ms, 15 of 59 with an interval of 91 to 130 and 2 of 10 with an interval greater than 130 ms (p < 0.05). In conclusion, in patients with dual A-V nodal pathways, there are relations between the A-H interval and the ability of the fast pathway to sustain sequential anterograde conduction, and between the A-H interval and the ability of the fast pathway to sustain sequential retrograde conduction. Among patients with dual pathways, patients with a shorter A-H interval are more likely to have A-V nodal reentrant tachycardia, because these patients are more likely to have excellent retrograde fast pathway sequential conduction (a requirement for the occurrence of reentrant tachycardia).

Ventricular tachycardia: Prediction of response to oral aprindine with intravenous aprindine

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