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 paced 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 or unusual variety (one third of patients).     

Aprindine-induced polymorphous ventricular tachycardia

Five cases of aprindine-induced polymorphous ventricular tachycardia (torsade de pointes) are presented. In four cases, polymorphous ventricular tachycardia appeared after the oral administration of 400 mg of aprindine. One patient had mild hypokalemia at the time of polymorphous ventricular tachycardia so that a direct cause and effect relation between the drug and the tachycardia cannot be established. All five patients manifested Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In all five, polymorphous ventricular tachycardia subsided once administration of aprindine was discontinued.     

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.     

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.     

Electrophysiologic demonstration of bilateral anomalous pathways in a patient with Wolff-Parkinson-White syndrome (type B preexcitation).

Pre- and postoperative electrophysiologic studies are described that were suggestive of two (right- and left-sided) anomalous atrioventricular (A-V) connections in a patient with type B Wolff-Parkinson-White syndrome and intractable arrhythmias, who underwent epicardial mapping and successful surgical ablation of the right-sided anomalous pathway. The presence of the right-sided anomalous pathway capable of both antegrade and retrograde conduction was suggested by the following observations: (1) Type B preexcitation on the surface electro-cardiogram; (2) maximal preexcitation and minimal stimulus-delta with low lateral right atrial pacing; (3) epicardial mapping of the atria and ventricles; and (4) disappearance of ventricular preexcitation after surgical ablation of the right-sided anomalous pathway. The presence of an additional left-sided anomalous pathway capable of only retrograde conduction (concealed on the surface electrocardiogram) was sugg-sted by the following observations: (1) Left to right retrograde atrial activation sequence during reentrant tachycardia and ventricular pacing at rapid rates and with coupled ventricular pacing postoperatively; (2) spontaneous conversion of wide ORS tachycardia utilizing the anomalous pathway for antegrade conduction to narrow QRS tachycardia with significant slowing in rate; and (3) smooth antegrade A-V nodal conduction curves with echo zone postoperatively. The demonstration of bilateral anomalous pathway in patients with preexcitation has important electrophysiologic and surgical implications.     

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 < 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 present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p < 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 < 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.     

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).     

Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation

Electrophysiologic effects of intravenous propranolol, 0.1 mg/kg, were evaluated in 18 patients with anomalous pathways utilizing intracardiac stimulation and recording. Fourteen patients had Wolff-Parkinson-White syndrome and four had concealed ventricular preexcitation. Anomalous pathway effective refractory period could be measured during the control period and after propranolol administration in nine patients and was 304 ± 7.5 (mean ± standard error of the mean) and 304 ± 8.3 msec, respectively (difference not significant). Ventricular paced 1:1 ventriculoatrial (V-A) conduction (reflecting retrograde anomalous pathway conduction) measured in 12 patients was intact during both the control period and after propranolol at rates of 170 to 200/min. Sustained paroxysmal supraventricular tachycardia was induced in 14 patients during the control period and in 10 after propranolol (in 4 of whom the tachycardia could not be sustained because of atrioventricular [A-V] nodal refractoriness). Mean cycle length of tachycardia in these 10 patients was 328 ± 18 (control) and 352 ± 19 msec (propranolol) (P < 0.01). The increase in tachycardia cycle length reflected an increase in A-V nodal conduction time (A-H interval).In conclusion: (1) Propranolol has an insignificant effect on both anterograde and retrograde anomalous pathway properties. (2) In most cases, propranolol does not interfere with induction of sustained circus movement tachycardia. However, it does produce a statistically significant but slight slowing of the rate of tachycardia. (3) In a minority of cases, propranolol inhibits induction of sustained paroxysmal supraventricular tachycardia by increasing A-V nodal refractoriness.     

Comparative actions of hydralazine, nifedipine and amrinone in primary pulmonary hypertension

The effects of 3 types of vasoactive agents, hydralazine, nifedipine and amrinone, were evaluated in 7 patients with primary pulmonary hypertension (PPH). Hemodynamic values were measured before and after drug administration in every patient. All drugs increased cardiac output and reduced both systemic and pulmonary resistance in the patients studied. Only nifedipine significantly reduced pulmonary artery (PA) pressure (6 +/- 5 mm Hg). In addition, it decreased pulmonary resistance to a greater degree than systemic resistance in 2 of the 7 patients, suggesting that nifedipine can cause selective pulmonary vasodilation in some patients. Hydralazine appeared to increase cardiac output and stroke volume by reducing systemic resistance. There was no evidence of direct pulmonary vasodilating effects; it decreased systemic resistance more than pulmonary resistance in every case. The increase in cardiac output from amrinone was secondary to a decrease in systemic arterial pressure with reflex tachycardia; stroke volume was unchanged. Amrinone had little pulmonary effect in all but 1 patient, in whom it substantially reduced PA pressure and pulmonary resistance. The mechanism of action of these 3 drugs in PPH differs. Nifedipine holds the most promise as an effective pulmonary vasodilator. A study of the effects of long-term administration of nifedipine in PPH is warranted.     

Radionuclide regurgitant index: Value and limitations

The radionuclide regurgitant index, defined as left ventricular/right ventricular stroke counts obtained from gated equilibrium studies, has been reported to predict the presence and severity of left-sided valve regurgitation. This study evaluated the radionuclide regurgitant index in 100 patients in whom left-sided valve regurgitation was angiographically graded (0 to 4+) with regard to most severe mitral or aortic regurgitation. Regurgitation was graded 0 in 44 of the 100 patients, 1+ in 22, 2+ in 8, 3+ in 6 and 4+ in 20.The radionuclide regurgitant index was 0.9 to 1.5 in 51 patients, 1.6 to 2.4 in 23 and 2.5 to 12.0 in 26. The mean radionuclide regurgitant index was 1.34 in the group with no regurgitation and 1.60 in those with 1+, 2.01 in those with 2+, 2.80 in those with 3+ and 3.85 in those with 4+ regurgitation. There was a significant difference (p <0.05) in the radionuclide regurgitant index between patients with no regurgitation and each group with regurgitation and between groups with regurgitation separated by two or more grades of angiographic regurgitation.Twelve patients had a discordant radionuclide regurgitant index; their index either predicted clinically significant or severe regurgitation when they had no or trivial regurgitation, or predicted no or trivial regurgitation when they had clinically significant regurgitation. Eight of 10 patients with a left ventricular ejection fraction of less than 0.30 had a discordant index (p < 0.0005). All three patients with mitral valve prolapse associated with frequent ventricular extrasystoles had a discordant index (p <0.0005).     

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.     

Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease.

Results are reported of portable 24 hour dynamic electrocardiographic monitoring in 50 male medical students without cardiovascular disease, as defined by normal clinical and noninvasive cardiovascular examination. During waking periods, maximal sinus rates ranged from 107 to 180 beats/min (mean +/- 5). Twenty-five subjects (50 percent) had episodes of marked sinus arrhythmia as defined by spontaneous changes in adjacent cycle lengths of 100 percent or more. Fourteen subjects (28 percent) had sinus pauses of more than 1.75 seconds, usually during sinus arrhythmia. Transient nocturnal type I second degree atrioventricular (A-V) block was noted in three subjects (6 percent). Of 28 patients (56 percent) having atrial premature beats, only 1 (2 percent) had more than 100 such beats (141) in 24 hours. Of 25 patients (50 percent) having premature ventricular contractions, only 1 (2 percent) had more than 50 such contractions (86) in 24 hours. In conclusion, frequent atrial and ventricular premature beats are unusual in a young adult male population. In contrast, bradyarrhythmias (including marked sinus arrhythmia with sinus pauses, sinus bradycardia and nocturnal A-V block) are common. These findings are useful in evaluating the clinical significance of arrhythmias detected with portable monitoring.     

Self-initiated conversion of paroxysmal atrial flutter utilizing a radio-frequency pacemaker

A patient is described with drug-resistant recurrent paroxysmal atrial flutter. Electrophysiologic studies demonstrated that flutter was inducible with rapid atrial stimulation (stimulation rates of 375 to 400/min) and convertible with rapid atrial stimulation (rates of 400 to 460/min). Because of the latter response, a radio-frequency atrial pacemaker was implanted, which allowed self-initiated conversion of flutter episodes with rapid stimulation.     

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.     

Assessment of left ventricular function by radionuclide angiography during induced supraventricular tachycardia

Electrocardiographically synchronized radionuclide angiography was performed before, during and after induced paroxysmal Supraventricular tachycardia in 13 patients. Data were acquired with a computer-interfaced Anger camera in a left anterior oblique projection. No data were acquired during tachycardia until tachycardia had been sustained for 1 minute. Patients ranged in age from 20 to 64 years (mean ± standard deviation 42 ± 14.5). Three patients had organic heart disease and 10 did not. Baseline and tachycardia heart rates (beats/min) were 59 to 99 (73 ± 11) versus 141 to 228 (157 ± 22). Baseline and tachycardia left ventricular measurements (mean ± standard error) were as follows: ejection fraction 64 ± 2 versus 62 ± 4 percent (not significant), ejection rate 3.0 ± 0.1 versus 4.3 ± 0.4 mean ventricular counts/s (p < 0.001), normalized end-diastolic counts 72.7 ± 7.8 versus 48.7 ± 6.7 × 10³ counts (p < 0.001), normalized stroke counts 37.1 ± 3.4 versus 23.3 ± 2.7 × 10³ counts (p < 0.001) and normalized count cardiac output 2,717.5 ± 273.0 versus 3,620.2 ± 403.7 × 10³ counts/min (p < 0.005). Although ejection fraction for the whole group did not change significantly, it decreased during tachycardia by 5 percentage points or more in five patients. These were the three patients with heart disease and the two normal patients with the fastest heart rate during tachycardia (228 and 214 beats/min, respectively).In summary, paroxysmal Supraventricular tachycardia was characterized by a marked decrease in left ventricular end-diastolic and stroke volumes but increased ejection rate and cardiac output without significant change in ejection fraction. Heart disease or rapid heart rate during tachycardia appeared to have a deleterious effect on ejection fraction.     

H-V interval in patients with bifascicular block (right bundle branch block and left anterior hemiblock). Clinical, electrocardiographic and electrophysiologic correlations.

Electrophysiologic studies were performed in 119 adults with chronic bifascicular block manifested by right bundle branch block and left anterior hemiblock. The H-V interval was normal in 86 patients and prolonged in 33. The following clinical variables were more frequent (P less than 0.05) in patients with a prolonged H-V interval: cardiac third sound, mitral systolic murmur, cardiomegaly on chest roentgenogram, congestive heart failure and cardiac functional class III or IV (New York Heart Association criteria). The following differences in the electrocardiographic and electrophysiologic findings were found: Patients with a prolonged H-V interaval had a longer mean P-R interval, QRS duration and A-H interval (P less 0.02). All patients were followed up prospectively in a cardiac conduction disease clinic after initial evaluation. The mean follow-up periods were (mean plus or minus standard error of the mean) 514 plus or minus 49 and 563 plus or minus 34 days for the patients with a prolonged and normal H-V interval, respectively. Progression of conduction disease occurred in three patients (4 percent) with a normal H-V interval and in four (12 percent) with a prolonged interval. The cumulative 3 year mortality rate for the entire group was 25 percent. The patients with a prolonged H-V interval had a higher cumulative 2 year mortality rate than those with a normal H-V interval but the difference was not statistically significant. In summary, a prolonged H-V interval was often associated with serious myocardial dysfunction and a high mortality rate. The risk of progression of conduction disease was slight with either a prolonged or a normal H-V interval during this relatively short follow-up period.     

Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the lown-ganong-levine syndrome

Sixty-five patients with dual pathway atrioventrlcular (A-V) nodal reentrant paroxysmal tachycardia were studied. Of these 65 patients, 11 (17 percent) had a short P-R interval (0.12 second or less) and 3 (5 percent) had a short A-H interval (53 ms or less) during sinus rhythm, suggesting the Lown-Ganong-Levine syndrome. Frequency distribution analyses of P-R and A-H intervals In the 65 patients demonstrated continuous unimodal functions, suggesting a continuum of A-V nodal properties. Regression analyses of P-R and A-H (fast pathway) intervals versus cycle length of paroxysmal tachycardia revealed an r value of 0.11 and 0.10, respectively (not significant). The cycle length of paroxysmal tachycardia did not differ between the 11 patients with a short P-R Interval (370 ± 20 ms) and the 54 patients without a short P-R interval (382 ±11 ms). Regression analysis of the slow pathway A-H interval versus cycle length of paroxysmal tachycardia revealed an r value of 0.68 (p <0.001).

The cycle length of dual pathway A-V nodal reentrant paroxysmal tachycardia is a function of the slow pathway A-H Interval and not the P-R or A-H Interval during sinus rhythm. Identification of short P-R intervals in patients with A-V nodal reentrant paroxysmal tachycardia has little significance.