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 (> 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.     

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.     

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 (S) tornone patient imaged during two different VT morphologies, the tachycardias had earliest phase at different borders of the same wall motion abnormality with differing progression of phase across the ventricles. RNA phase mapping of VT is feasible and appears to provide data consistent with the electrophysiology of this arrhythmia.     

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

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

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

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 patient's 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 < 0.03), with responders having received an average of 2.5 drugs compared with 4.2 for nonresponders. In addition to the logistic regression, 12 other clinical and electrophysiologic variables were not predictors of drug response. The question was also asked, “Does response or nonresponse to one class I drug predict response or nonresponse to the others?” Significant concordance of response and nonresponse was demonstrated for procainamide and quinidine, but not for either of these drugs and disopyramide. Drug therapy for inducible sustained VT therefore remains empiric.     

Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease

Results are reported of 24-hour ambulatory ECG recordings in 50 young women without apparent heart disease. During waking periods, maximum (sinus) rates ranged from 122 to 189 beats/min (bpm) (153 ± 14 mean ± SD) and minimum rates from 40 to 73 bpm (56 ± 7). During sleeping periods, maximum and minimum rates ranged from 71 to 128 bpm (105 ± 13) and from 37 to 59 bpm (48 ± 6), respectively. Thirty-two subjects (64%) had atrial premature beats, with only one subject (2%) having greater than 100 beats/24 hrs. Twenty-seven subjects (54%) had ventricular premature beats, with only three subjects (6%) having greater than 50 beats/24 hrs. One subject (2%) had one three-beat episode of ventricular tachycardia. Two subjects (4%) had transient type I second-degree atrioventricular block.     

Determination of left ventricular ejection fraction by visual estimation during real-time two-dimensional echocardiography

It has been shown that the measured reduction in the cross-sectional area of the left ventricle (LV), as viewed in the short axis, closely approximates its ejection fraction (EF). We assessed the reliability of using two-dimensional echocardiography (2DE) to visually estimate the EF during real-time viewing, without the need of digitizers, planimetry, or calculations. Twenty-five adult hospitalized patients with either suspected or known cardiac disease were evaluated prospectively. Each patient also had gated nuclear angiography during the same admission, and 14 had cardiac catheterization with left ventriculography. The EF was determined by 2DE using a visual estimate of the percent area reduction of the LV cavity in the short-axis view at the level of the papillary muscles. All 2 DE studies were read by two or more blinded reviewers, with a value for the EF to the nearest 2.5% determined by consensus. These values correlated closely to the values determined in all 25 patients with gated nuclear angiography (r = 0.927) and the 14 patients who had left ventriculography (r = 0.935). We believe that this method of visually estimating the LVEF will enable echocardiographers to easily use 2 DE for a reliable and instantaneous assessment of ventricular function, without the need of sophisticated analytical equipment.     

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.     

Effects of bundle branch block on experimental A-V reentrant tachycardia

The effects of bundle branch block on experimental A-V reentrant tachycardia (PSVT) were studied in 17 dogs using an anomalous pathway simulatory (APS). The APS was a programmable digital electronic circuit with ability for ventricular sensing, retrograde conduction with programmable conduction time, and atrial stimulation. Close bipolar electrodes were positioned at seven contiguous atrial and ventricular sites (V_l) along the A-V ring, these being; anterior, lateral, and posterior right (AR, LR, PR), septal (S), and posterior, lateral and anterior left (PL, LL, AL). Right (R) (seven dogs) and left (L) (10 dogs) bundle branch block (BBB) were produced with transcardiac needle. After BBB, cycle length (CL) of A-V reentrant PSVT was significantly increased only with ipsilateral sites. Thus, with RBBB, CL of PSVT increased by 37 ± 3 msec., 27 ± 3 msec., and 23 ± 4 msec. (P < 0.001), at AR, LR, and PR sites respectively. With LBBB, CL of PSVT increased only with left-sided sites. Thus, CL increased by 34 ± 2.6 msec., 38 ± 4.6 msec., and 32 ± 3.3 msec., (P < 0.001) with PL, LL, and AL sites, respectively. PSVT CL and septal site did not change significantly after either R or LBBB. The increase in CL was explicable in terms of corresponding increases in intraventricular conduction time (H-V_l). There were slight compensatory decreases in A-H intervals for the increases in H-V_l. These studies confirm findings suggested by clinical electrophysiological observation.     

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.     

Significance of site of origin of premature ventricular contractions.

One hundred and sixty-five inpatients with premature ventricular contractions (PVC's) were clinically evaluated in regard to the presence (130 patients) or absence (35 patients) of organic heart disease. PVC's were classified based on QRS morphology (bundle branch block pattern) in Lead V₁ as being either left ventricular (66 patients), right ventricular (71 patients), or of both ventricles (28 patients). The incidence of organic heart disease was significantly greater in patients with left ventricualr PVC's 60 of 66 (91 per cent) and biventricular PVC's 25 of 28 (89 per cent) than in patients with right ventricular PVC's 45 of 71 (63 per cent) (p < 0.001). Of the 130 patients with organic heart disease, 60 (46 per cent) had left ventricular PVC's, 25 (19 per cent) had biventricular PVC's, and 45 (35 per cent) had right ventricular PVC's. of the 35 patients without organic heart disease, six (17 per cent) had left ventricualr PVC's, four (9 per cent) had biventricular PVC's, and 26 (74 per cent) had right ventricular PVC's.These data suggest the following conclusions regarding inpatients with PVC's: (1) Organic heart disease is frequent in patients with right ventricular PVC's and almost universally present in patients with left ventricular and biventricular PVC's. (2) Patients without organic heart disease primarily have PVC's of right ventricular origin. The mechanism of the latter association is unknown.     

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.     

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.     

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.     

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.