Robert A. Bauernfeind

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.

Torsade de pointes due to quinidine: Observations in 31 patients

We performed a mail solicitation and obtained the records of 31 patients with documented torsade de pointes (TDP) due to quinidine. All 31 patients had heart disease: ischemic = 11 patients (36%), rheumatic = five patients (16%), hypertensive = four patients (13%), cardiomyopathic = four patients (13%), other = seven patients (22%). Quinidine was administered to these patients for the following reasons: atrial fibrillation or flutter = 22 patients (71%), ventricular premature beats = six patients (19%), ventricular or supraventricular tachycardia = three patients (10%). The 31 patients were receiving quinidine, 650 to 2400 (mean 1097) mg/day, and 14 patients had serum quinidine levels of 1.4 to 10.6 (mean 3.7) micrograms/ml. TDP occurred within 1 week of initiation of quinidine therapy in 23 (74%) of the patients. Twenty-eight (90%) of the 31 patients were receiving digoxin, and 5 (24%) of 21 patients had hypokalemia at the time of TDP. Off of quinidine therapy, corrected QT (QTc) intervals in 24 patients ranged from 390 to 580 (mean 470) msec and were prolonged in 17 patients (71%). On quinidine therapy, QTc intervals in 23 patients ranged from 390 to 630 (mean 510) msec and were prolonged in 21 patients (91%). In summary, patients with TDP due to quinidine usually had heart disease complicated by atrial fibrillation, were receiving digoxin, and were receiving moderate dosages of quinidine for less than 1 week prior to TDP. Approximately two thirds of patients with TDP due to quinidine had long QT intervals while off of quinidine.

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.

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...

Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block.

SUMMARYTwenty-one of 496 (4%) patients with chronic bifascicular block, studied and followed prospectively, had block distal to the His bundle (BDH) induced by atrial pacing during initial electrophysiologic studies. In six, BDH was noted during pacing-induced atrioventricular (AV) nodal Wenckebach periods (at paced rates of 150–190 beats/min), with BDH in the short HH cycles after the AV nodal blocked P (long cycle). The AH interval was normal in all six patients and HV was normal in four. None of the six patients has developed AV block during a mean follow-up of 5.33 ± 0.48 years.In 15 patients, pacing-induced BDH was noted during intact AV nodal conduction (paced rate of 80–200 beats/min). The AH interval was prolonged in one, and HV was prolonged in 10 of the 15 patients. During a mean follow-up of 3.4 ± 0.59 years, seven of these patients developed AV block, one had treadmill-provoked AV block, and two died suddenly (major morbid event in 10 of 15 patients).In conclusion, BDH induced by atrial pacing is an infrequent finding in patients with bifascicular block, and can be a functional as well as a pathologic response. The latter is associated with a high risk of major morbid events (AV block and sudden death).

Chronic nonparoxysmal sinus tachycardia in otherwise healthy persons.

Seven patients had chronic, unexplained, nonparoxysmal sinus tachycardia. The clinical, electrocardiographic, and electrophysiologic characteristics of these cases are described. In each case electrocardiographic and electrophysiologic observations suggested that tachycardia was nonparoxysmal and due to increased automaticity of the sinus node (or of an automatic atrial focus located very near the sinus node). The mechanisms of increased sinus node automaticity in these patients were explored using drugs affecting the autonomic nervous system. In each patient these studies suggested a defect in either sympathetic or vagal nerve control of resting heart rate, with or without an abnormality of intrinsic heart rate. Data are also presented on baroreceptor reflex arc function in these patients.

Natural history of chronic second-degree atrioventricular nodal block.

This report details our experience with documented chronic second-degree atrioventricular (AV) nodal block (proximal to His [H]) in 56 patients. Forty-six men (82%) and 10 women (18%), ages 18–87 years, were studied. Nineteen of the patients (34%) had no organic heart disease (including seven trained athletes) and 37 (66%) had organic heart disease. ECGs in all patients demonstrated episodes of type I seconddegree block; five patients also had periods of 2:1 block. Prospective follow-up of patients with no organic heart disease (157–2280 days, mean 1395 636 days) revealed one patient with clear indication for permanent pacing because of bradyarrhythmic symptoms (permanently placed on day 220 of follow-up). Two patients died nonsuddenly.In patients with organic heart disease (prospective follow-up of 60–2950 days, mean 1347 ± 825 days), pacemakers were implanted in 10 patients, primarily for treatment of congestive heart failure in eight and syncope in two. Sixteen patients died three suddenly, seven with congestive heart failure, two of an acute myocardial infarction and four of causes unrelated to cardiac disease.In summary, chronic second-degree AV nodal block has a relatively benign course in patients without organic heart disease. In patients with organic heart disease, prognosis is poor and related to the severity of underlying heart disease.

Serial electrophysiologic testing of multiple drugs in patients with atrioventricular nodal reentrant paroxysmal tachycardia.

Serial electrophysiologic testing of multiple drugs was performed in 21 patients with recurrent atrioventricular (AV) nodal reentrant paroxysmal supraventricular tachycardia (PSVT). All patients had reproducible sustained PSVT induced before drug administration. Serial daily PSVT induction was attempted after administration of i.v. ouabain (0.01 mg/kg) (16 patients), i.v. propranolol (0.1 mg/kg (17 patients), i.v. ouabain + propranolol (same dosages) (12 patients), i.v. procainamide (600-1000 mg) (17 patients) and oral quinidine (1600-2400 mg/day) (nine patients). In two of 21 patients (10%), no tested drug prevented induction of sustained PSVT. In 19 of 21 patients (90%), one or more drugs prevented induction of sustained PSVT: ouabain seven patients, propranolol seven patients, ouabain + propranolol seven patients, procainamide - 11 patients, quinidine - seven patients. The site of action of ouabain and/or propranolol was either the antegrade limb or the retrograde limb (RL) of the circus movement. The site of action of procainamide or quinidine was always the RL. These 19 patients were treated with oral drugs, based on results of serial testing. Eighteen patients were successfully followed for 6-50 months. In 13 of these 18 patients PSVT did not recur. Two patients (11%) had > 95% reduction in frequency of PSVT recurrences, and three (17%) did not respond to chosen oral drugs.Serial electrophysiologic testing of multiple drugs is feasible in patients with AV nodal reentrant paroxysmal tachycardia. Drug responses are variable. In most but not all patients, serial electrophysiologic testing defines effective prophylactic drug therapy. This method of defining prophylactic drug therapy appears most suitable for patients with poorly tolerated tachycardias that occur only sporadically.

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.

Treadmill exercise testing in the Wolff-Parkinson-White syndrome

Abstract 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.