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.

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).

Electrophysiologic effects of ouabain in patients with preexcitation and circus movement tachycardia.

Effects of intravenous ouabain were evaluated in 19 patients with an anomalous conduction pathway (14 with manifest and 5 with concealed preexcitation (utilizing intracardiac stimulation and recording. Anterograde conduction through the anomalous pathway was present in all 14 patients with manifest preexcitation at a maximal atrial paced rate of 140 to 250 beats/min (mean +/- standard error of the mean 214 +/- 7.2) before and at 150 to 240 beats/min (mean 206 +/- 7.1) after ouabain (difference not significant [NS]). The anterograde effective refractory period of the anomalous pathway, measured at an equivalent atrial paced rate in 10 patients, was 250 to 450 ms (mean 309 +/- 19.7) before and 260 to 450 ms (mean 300 +/- 17.2) after ouabain (NS). Retrograde conduction through the anomalous pathway was possible at maximal ventricular paced rates (17 patients) of 160 to 250 beats/min (mean 222 +/- 6.6) before and 190 to 250 beats/min (mean 221 +/- 4.4) after ouabain (NS). Sustained atrioventricular (A-V) reentrant paroxysmal supraventricular tachycardia was inducible in all 19 patients before and in 17 patients (89 percent) after ouabain (tachycardia could not be induced in two patients because of increased A-V nodal refractoriness). The mean cycle length of tachycardia in the 17 patients was 320 +/- 6.7 ms before and 340 +/- 8.1 ms after ouabain (p < 0.01). In conclusion, ouabain has no significant effect on either anterograde or retrograde anomalous pathway refractoriness. Although ouabain slightly increases the cycle length of tachycardia, it does not interfere with induction of tachycardia in most patients with preexcitation. Oral cardiac glycosides alone would appear to be of limited value in patients with preexcitation and recurrent supraventricular 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.

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.

Chronic nonparoxysmal junctional tachycardia.

We describe an adult with chronic (three years' duration) acquired nonparoxysmal junctional tachycardia, a previously undescribed rhythm. Ambulatory monitoring revealed junctional rates ranging from 75 to 110 beats/min. Electrophysiologic studies demonstrated intact atrioventricular and ventriculoatrial conduction with a normal H-V interval (43 msec) and narrow QRS. Underlying sinus node function appeared to be normal (recovery time of 900 msec). Junctional rate increased with administration of atropine and isoproterenol, suggesting that the junctional pacemaker was located in the proximal His bundle. Electrocardiographic and electrophysiologic observations suggested that this case of chronic nonparoxysmal junctional tachycardia was benign, not necessitating therapy.

Familial inducible torsade de pointes with normal QT interval.

A familial presentation of torsade de pointes is described. The propositus had recurrent syncope, documented torsade de pointes, a normal Q-T, and close coupled premature ventricular beats initiating the paroxysmal arrhythmia. The mother had sporadic syncope without documented torsade de pointes, a normal Q-T, and closely coupled premature ventricular beats. Electrophysiological studies demonstrated reproducible inducible torsade de pointes tachycardia in both patients. Serial drug testing in both revealed suppression of induced torsade de pointes with oral propranolol. Chronic oral propranolol resulted in clinical cure in both patients.

Postoperative electrophysiological studies with a modified radiofrequency system. Technical aspects and clinical usefulness.

Two patients who underwent a ventricular aneurysmectomy for treatment of ventricular tachycardia are presented. In both patients, a radiofrequency pacemaker was implanted at surgery (for therapeutic use if surgery should fail). In both patients, electrophysiological studies were performed before discharge utilizing a radiofrequency pacemaker without recourse to repeat catheterization. This was possible by modifying the transmitter and coupling it to a commercially available programmable stimulator.

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.

Angiographic correlates of recurrent sustained ventricular tachycardia in chronic ischemic heart disease.

We report the angiographic studies of 53 consecutive patients with angiographic coronary artery disease (CAD) and recurrent sustained ventricular tachycardia occurring at least 6 weeks remote from an acute myocardial infarction. Triple-vessel disease was present in 25 patients (47%), double-vessel disease in 19 patients (36%), and single-vessel disease in nine patients (17%). All patients with single-vessel disease had left anterior descending coronary artery obstruction. Patients under 50 years old had significantly fewer diseased vessels than those over 50 years old (1.4 vs 2.4 vessels diseased; p less than 0.025). Left ventricular ejection fraction ranged from 0.15 to 0.61 (mean 0.34 +/- 0.11) and was 0.25 or less in 14 patients (26%). All patients had regional wall motion abnormalities. There was akinesia and/or dyskinesia in 49 patients (92%). Akinesia or dyskinesia was inferior in 17 patients (32%), anteroapical in 14 patients (26%), inferoapical in 10 patients (19%), and anteroapicoinferior in 6 patients (11%). Involvement of the septum was noted in 19 patients (36%) and of basal segments in 26 patients (49%). An average of 2.7 (out of seven) segments per patient were dyskinetic or akinetic. Thus multivessel disease, markedly reduced ejection fraction, and severe and extensive regional wall motion abnormalities are generally present. These findings have pathophysiologic as well as clinical and therapeutic implications. The nautral history of these patients as well as the results of therapy should be related to the underlying coronary anatomy and left ventricular function.

Electrophysiologic testing of bretylium tosylate in sustained ventricular tachycardia.

We used programmed ventricular stimulation to test intravenous bretylium tosylate in 10 consecutive patients with inducible sustained ventricular tachycardia (usually refractory to type I antiarrhythmic agents). These 10 patients had previously documented sustained ventricular tachycardia and/or ventricular fibrillation complicating stable heart disease. Following control inductions of sustained ventricular tachycardia, bretylium 10 mg/kg was infused over 30 minutes. Thirty minutes after this infusion, sustained ventricular tachycardia could be induced in 9 of the 10 patients (one of these nine patients also had bretylium-potentiated spontaneous ventricular tachycardia). Tachycardia induced in the nine patients after bretylium was similar to control tachycardia with respect to morphology and cycle length (333 +/- 16 msec after bretylium versus 330 +/- 16 msec during control). However, five of the nine patients tolerated induced tachycardia less well after bretylium (exacerbated hypotension). In one patient, ventricular tachycardia could not be induced after intravenous bretylium.

Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: clinical, hemodynamic, and angiographic findings.

Surgical cure of right ventricular tachycardia (RVT) has been recently described in patients with "arrhythmogenic right ventricular dysplasia," a disease characterized by abnormal electrical activation of the right ventricle and localized or generalized angiographic right ventricular (RV) wall motion abnormalities (WMA). In search of a selective RV cardiomyopathy complicated by chronic recurrent RVT, 38 consecutive patients (mean age 30.5 +/- 12 years) with RVT and no ischemic heart disease were studied clinically, noninvasively, and by cardiac catheterization including left and right ventriculography. RV volumes were as follow: end-systolic volume ranged from 23 to 103 (mean +/- SD, 45.8 +/- 20) cc/m2 and was abnormal in 14 patients (37%); end-diastolic volume ranged from 57 to 138 (90.5 +/- 26) cc/m2 and was abnormal in 15 patients (39%); ejection fraction (EF) ranged from 0.18 to 0.64 and was decreased in five patients (13%). Seventeen patients (45%) had abnormal RV volume, EF, and/or pressures (RVD), five (13%) of whom had abnormal LV volume, EF, and/or pressures (LVD), and 12 (32%) patients with RVD had no LVD. Twenty-one patients (55%) had no RVD, two of whom had LVD. Only two of the 17 patients had RV regional WMA, one with and one without LVD. Most patients with LVD five of seven (71%) also had RVD while 12 of 31 patients (39%) with no LVD had RVD. In conclusion, less than one half of patients with RVT had selective RV cardiomyopathy and more than one half of patients with RVT had normal RV hemodynamics and angiography.

Pharmacological observations in patients with nodoventricular pathways.

Three patients with accessory nodoventricular pathways and re-entry tachycardia are reported. In all three patients the accessory nodoventricular pathway formed the anterograde limb of the re-entry circuit while the His-Purkinje-atrioventricular node axis formed the retrograde limb of the tachycardia in two of the patients and a concealed accessory pathway formed the retrograde limb in the remaining patient. All three patients also manifested dual anterograde atrioventricular nodal pathways with conduction through the accessory nodoventricular pathways being associated with the atrioventricular nodal fast pathway. Type I antiarrhythmic drugs, especially disopyramide and quinidine, were effective for the treatment of the re-entry tachycardia because of their depressive action on the nodoventricular pathway. Beta blockers were also effective because of their action on the atrioventricular nodal portion of the re-entry circuit in one patient and most probably due to atypical (atrioventricular nodal like) properties of a retrogradely conducting accessory pathway in a second patient.

Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia.

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.

Significance of the HV interval in 517 patients with chronic bifascicular block.

In January 1975, we reported results of a prospective follow-up study (mean 538 +/- 42 days) of 119 patients with chronic bifascicular block (BFB), and concluded that BFB patients with normal and prolonged HV (NHV and PHV) had a similar incidence of atrioventricular (AV) block and mortality. In this report, we update these findings in 517 patients with a follow-up of 21 days to 9.8 years (mean 3.4 +/- 0.2 years). Three hundred nineteen patients (61%) had NHV and 198 (39%) had PHV (greater than 55 msec). The NHV and PHV groups were similar in regard to age (NHV vs PHV, 61 +/- 1 vs 62 +/- 1 years) and sex (80% male, 20% female vs 82% male and 18% female). The following were more common (p less than 0.05) in patients with PHV (percent of patients with finding in NHV vs PHV groups): angina (18% vs 27%), congestive failure (27% vs 42%), cardiomegaly (48% vs 66%), New York Heart Association functional class II-IV (34% vs 56%), premature ventricular complexes (20% vs 29%), and organic heart disease (OHD) (75% vs 85%). Spontaneous trifascicular block (TFB) developed in two patients (0.6%) with NHV and nine patients (4.5%) with PHV (p less than 0.05). Cumulative 7-year incidence of TFB was 3% with NHV and 12% with PHV (p less than 0.01). Seven-year cumulative cardiovascular mortality was 32% in NHV patients and 57% in PHV patients (p less than 0.005). In conclusion, PHV in patients with chronic BFB was associated with a greater incidence and severity of OHD, and higher total and sudden death mortalities. The risk of spontaneous TFB was small in patients with either NHV or PHV, although it was significantly higher in the latter.