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

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 < 0.005). Programmed stimulation was not possible in 1 patient with severe neurologic side effects and in 5 patients with mexiletine-related worsening of ventricular arrhythmia. Seven other patients had severe neurologic or gastrointestinal side effects, necessitating dose reduction in 5. This 47 % incidence of noncardiovascular side effects is similar to that in previous reports, but the 29 % incidence of arrhythmia potentiation by mexiletine is unexpectedly higher. Limited follow-up reveals recurrence of VT in 3 of 4 patients treated with oral mexiletine on a long-term basis. In conclusion, oral mexiletine does not appear useful in the therapy of patients with drug-refractory, paroxysmal sustained VT. In addition, its use is associated with a high incidence of adverse effects, cardiovascular (arrhythmic) and noncardiovascular, some of which can be serious and life-threatening.     

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.     

Electrophysiologic observations in a patient with bradycardia-dependent atrioventricular block

In a patient with atrioventricular (A-V) block distal to the His bundle (H), 1:1 A-V conduction with right bundle branch block and an H-V interval of 70 msec was established with atrial pacing at rates of 120 to 150/min, suggesting that the A-V block was bradycardia-dependent. Advanced second degree A-V block distal to the H deflection occurred with atrial pacing at 160/min after completion of A-V nodal Wenckebach periodicity proximal to the H deflection because of the long H-H encompassing the blocked P wave. Atrial extrastimulus testing coupled with sinus rhythm (with A-V block) demonstrated that critical H₁-H₂ intervals of less than 545 msec allowed conduction to the ventricles. The H₂-V₂ interval shortened progressively from 290 to 70 msec with shortening of these critical H₁-H₂ intervals. Atrial extrastimulus testing coupled with an atrial driven cycle length of 500 msec (with intact A-V conduction) revealed block of the H₂ deflection with an H₁-H₂ interval longer than 540 msec.In conclusion, at critical diastolic intervals, impulses were blocked, creating a state of decreased responsiveness. If a cycle length of subsequent impulses was shorter than the critical diastolic blocking interval, membrane responsiveness gradually improved and conduction resumed. If a cycle length of subsequent impulses was longer than the critical blocking diastolic interval, A-V block was sustained. Blocked impulses continually penetrated to the site of block and reset the state of membrane responsiveness.     

Significance of left axis deviation in patients with chronic left bundle branch block

Forty-nine patients with chronic left bundle branch block and a normal frontal axis were compared with 53 patients with left bundle branch block and left axis deviation. The following clinical variables were more frequent (P < 0.05) in patients with left axis deviation: greater age, exertional angina, congestive heart failure, cardiomegaly, cardiac functional class II to IV, coronary artery disease and presence of organic heart disease. Absence of organic heart disease (primary conduction disease) was seen only in patients with a normal axis. Patients with left axis deviation had longer (P < 0.05) mean P-R, A-H and H-V intervals and atrial and atrioventricular (A-V) nodal effective refractory periods. All patients were prospectively followed up for 30 to 2,271 days with a mean ± standard error of the mean follow-up period of 538 ± 72 for the group with a normal axis and 604 ± 72 days for the group with left axis deviation (difference not significant). A-V block developed in three patients (6 percent) with left axis deviation and in none of those with a normal axis. The cumulative 4 year mortality rate for the entire group approached 75 percent. The patients with left axis deviation had greater cardiovascular mortality (P < 0.05).In conclusion, among patients with left bundle branch block, those with left axis deviation have a greater incidence of myocardial dysfunction, more advanced conduction disease and greater cardiovascular mortality than those with a normal axis.     

Clinical,electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined In 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia.In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.     

Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia

There are limited reported data regarding the occurrence of retrograde block during dual pathway atrioventricular (A-V) nodal reentrant paroxysmal tachycardia. This study describes two patients with this phenomenon. The first patient had 2:1 and type 1 retrograde ventriculoatrial block during the common variety of A-V nodal reentrance (slow pathway for anterograde and fast pathway for retrograde conduction). Fractionated atrial electrograms suggested that the site of block was within the atria. The second patient had type 1 retrograde block (between the A-V node and the low septal right atrium) during the unusual variety of A-V nodal reentrance (stow pathway for retrograde and fast pathway for anterograde conduction). The abolition of retrograde block by atropine suggested that the site of block was within A-V nodal tissue. Both cases demonstrate that intact retrograde conduction is not necessary for the continuation of A-V nodal reentrant paroxysymal tachycardia. Case 2 supports the hypothesis that the atria are not a requisite part of the A-V nodal reentrant pathway.     

Prevalence of high-risk thallium-201 scintigraphic findings in left main coronary artery stenosis: comparison with patients with multiple- and single-vessel coronary artery disease

To determine the prevalence of high-risk thallium-201 (Tl-201) scintigraphic findings in patients with left main (LM) coronary artery disease (CAD), quantitative exercise Tl-201 scintigrams were analyzed in 295 consecutive patients with angiographic (greater than or equal to 50% stenosis) CAD, of which 43 (14%) had greater than or equal to 50% LM stenosis. A high-risk scintigram was defined as one that demonstrated (1) a LMCAD scintigraphic pattern (greater than or equal to 25% homogeneous decrease in Tl-201 activity in the middle and upper septal and posterolateral walls on the 45 degree left anterior oblique projection); (2) abnormal Tl-201 uptake or washout in multiple vascular scan segments indicative of multivessel disease; and (3) increased lung Tl-201 uptake on the initial anterior projection image. Of the 43 patients with LMCAD, 41 (95%) had an abnormal scintigram. Thirty-three (77%) had 1 or more high-risk scintigraphic findings, including 29 (67%) with a multivessel CAD scan pattern, of which 6 (14%) demonstrated a typical LMCAD pattern; and 18 (42%) with abnormal lung Tl-201 uptake. The prevalence of a high-risk scintigram in patients with LMCAD was significantly greater than that in 53 patients with 3-vessel disease (58%) (p = 0.05), 99 patients with 2-vessel disease (60%) (p = 0.04) and 100 patients with 1-vessel disease (41%) (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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).     

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.     

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.     

Influence of coronary artery disease on pulmonary uptake of thallium-201

An increased pulmonary thallium-201 concentration has been observed in exercise stress thallium perfusion imaging in patients with coronary artery disease. To understand the cause of this lung uptake, studies were performed in experimental animals and in patients undergoing stress thallium perfusion imaging. The extraction fraction of thallium-201 by the lungs was measured in a group of eight dogs using a dual isotope technique. Basal thallium-201 extraction fraction at rest was 0.09 ± 0.009. After administration of isoproterenol, it decreased to 0.06 ± 0.02 (difference not significant). After balloon obstruction of the left atrium (which increased mean left atrial pressure and pulmonary transit time) and after administration of acetylcholine as a bolus injection (which prolonged pulmonary transit time only) it increased to 0.19 ± 0.02 (p <0.01).Lung thallium-201 activity was measured in 86 patients who had undergone cardiac catheterization and stress-redistribution myocardial perfusion imaging. The initial/final lung activity ratio was 1.41 ± 0.03 in patients with no significant coronary artery disease, 1.52 ± 0.03 (difference not significant) in patients with single vessel coronary disease, 1.60 ± 0.05 (p <0.05) in those with two vessel disease and 1.59 ± 0.05 (p <0.05) in those with triple vessel disease. Quantitation of lung activity in 30 of these patients indicated that the increased ratio in patients with multivessel coronary artery disease was due to a transient absolute increase in the thallium-201 concentration immediately after maximal exercise. The data imply that increased pulmonary concentration of thallium-201 during exercise is a consequence of left ventricular failure.     

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.     

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).     

Treadmill exercise testing in the Wolff-Parkinson-White syndrome

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.     

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.     

Effect of age on atrioventricular conduction in patients with chronic bifascicular block

Five hundred thirty-one patients with chronic bifascicular block and intact atrioventricular (A-V) conduction were studied and prospectively followed up to ascertain the effect of age on both severity of conduction defect and life history. The patients were subdivided into a younger group, aged 18 to 59 years, and an older group, aged 60 and above. They were further separated into those with primary conduction disease (118 patients) and those with organic heart disease (413 patients). In the patients with primary conduction disease, the findings were as follows (younger group, 60 patients, versus older group, 58 patients) (mean ± standard error of the mean): age 43 ± 1.4 versus 73 ± 1.1 (p < 0.001); A-H Interval 92 ± 3.8 versus 100 ± 3.8 ms (not significant); H-V interval 48 ± 1.6 versus 49 ± 1.6 ms (not significant). Progression to spontaneous A-V block was noted in no younger patient and one older patient (not significant) over a mean follow-up period of 3.5 ± 0.3 years. The 5 year total cumulative mortality was significantly higher in the older group with no difference in the incidence of sudden death in the two groups.In patients with organic heart disease, the findings were as follows (younger group, 170 patients, versus older group, 243 patients): age 48 ± 0.9 versus 71 ± 0.5 (p < 0.001); A-H interval 105 ± 2.3 versus 114 ±3.1 ms (p < 0.05); H-V interval 54 ± 1.3 versus 55 ± 0.9 ms (not significant). Progression to spontaneous A-V block was seen in six patients (3 percent) in the younger group and 15 (5 percent) in the older group (not significant). The 5 year total cumulative mortality was significantly higher in the older group with no difference in the incidence of sudden death in the two groups. With the exception of the A-H interval in the group with organic heart disease, the severity and progression of conduction disease were independent of advanced age in patients with chronic bifascicular block.     

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).     

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.