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Biomedical subjects

R A Bauernfeind

Publications and source records attributed to R A Bauernfeind.

16 recordsLinked to original sources
PubMed1990

Cumulative effects of cycle length on ventricular refractoriness in man.

This study examined the time course of changes of ventricular effective refractory period (VERP) following an abrupt change of cycle length (CL) in man. Stimulation at the right ventricular apex consisted of 19 cycles of an initial CL, followed by a variable number of cycles (0 to 50 cycles) of a new CL, and an extrastimulus to test for VERP. Fifteen patients were enrolled in each part of the study. In part A, initial CLs were long (mean +/- standard error, 650 +/- 20 msec) and new CLs were short (325 +/- 10 msec). VERPs were 259 +/- 6 msec after the long cycles, 238 +/- 6 msec after one short cycle (p less than 0.05), 224 +/- 5 msec after 10 short cycles, and 210 +/- 6 msec after 50 short cycles (p less than 0.05 versus 1 or 10 short cycles). Thus 43% of total shortening of VERP occurred in the first short cycle and 57% occurred in subsequent short cycles. In part B, initial CLs were short and new CLs were long. VERPs were 212 +/- 7 msec after the short cycles, 237 +/- 7 msec after one long cycle (p less than 0.05), 239 +/- 7 msec after 10 long cycles, and 247 +/- 7 msec after 50 long cycles (p less than 0.05 versus 1 or 10 long cycles). Thus 71% of total lengthening of VERP occurred in the first long cycle and 29% occurred in subsequent long cycles. In conclusion, following an abrupt change of CL in man, VERP changes markedly in the first new cycle (immediate effect) and then undergoes further, more gradual change over a large number of subsequent cycles (cumulative effects). Cumulative effects appear to be greater following shortening of CL than following lengthening of CL.

Adult↗
PubMed1989

Enhancement of sympathetic nerve activity by single premature ventricular beats in humans.

This is the first systematic study of the effects of ventricular premature beats on sympathetic nerve activity in humans. Microneurographic techniques were used to record efferent sympathetic activity from the peroneal nerve, and an intracardiac electrode catheter was used to introduce ventricular premature beats after every 6 to 10 sinus heartbeats. Studies were performed in eight patients, aged 22 to 74 years (mean 57), undergoing cardiac electrophysiologic studies. Three patients did not have apparent heart disease and five had coronary artery disease. During sinus rhythm, 19 to 93% (mean 42%) of heartbeats were followed by a pulse-synchronous burst of sympathetic activity. Provoked ventricular premature beats had obvious effects on this activity. Premature beats with coupling intervals less than 80% of sinus cycle length were consistently followed by a burst of sympathetic activity, and this activity was greater in amplitude, duration and area (all p less than 0.05) than were burst of such activity during sinus rhythm. The magnitude of this burst of activity increased as the coupling interval of the ventricular premature beat decreased (p less than 0.0001). In contrast, postextrasystolic beats were followed by nearly complete neural silence. These effects were seen in all patients regardless of baseline burst incidence and the presence or absence of heart disease. Total nerve activity per 10 heartbeats was 6,520 +/- 770 U during ventricular extrastimulation and 5,720 +/- 440 U during normal sinus rhythm (difference not significant). It is concluded that single ventricular premature beats provoke fluxes of muscle sympathetic nerve activity in humans, comprising surges of sympathetic activity larger than those occurring during sinus rhythm, followed by neural silence.

Adult↗
PubMed1989

Shortening of ventriculoatrial intervals with left bundle branch block during orthodromic reciprocating tachycardia in three patients with a right-sided accessory atrioventricular pathway.

Previous studies of the effects of bundle branch block on ventriculoatrial (VA) intervals during orthodromic reciprocating tachycardia have focused on the timing of the atrial electrograms. However, left bundle branch block importantly affects the timing of initial ventricular activation, and this effect would also be expected to affect VA intervals during orthodromic reciprocating tachycardia. Presented here are three patients with a single right-sided accessory atrioventricular pathway exhibiting left bundle branch block during orthodromic reciprocating tachycardia. Each had shortening of the VA interval by 10 to 30 ms during left bundle branch block beats. This shortening was accompanied by a nearly equal increase in the HV interval, with the His bundle to atrial interval remaining constant. It is concluded that the timing of ventricular as well as atrial electrograms impacts on the VA intervals with left bundle branch block beats during orthodromic reciprocating tachycardia. With left bundle branch block, delay in initial left septal activation results in later onset of the QRS complex and, with right ventricular activation occurring normally, shortening of the VA interval occurs in patients with a right-sided pathway.

Adolescent↗
PubMed1989

Pericardial repair of endocardial defect following regional endocardial resection for ventricular tachycardia.

Regional endocardial resection is the accepted surgical treatment for sustained monomorphic ventricular tachycardia. In patients requiring extensive endocardial resection, or with large aneurysms involving the interventricular septum, the resulting defect may result in weakened myocardium and, ultimately, ventricular septal defect or ventricular rupture. A new approach for repair of the resulting defect is proposed using an autogenous pericardial patch sutured to normal endocardium and included in the aneurysm repair. This technique was performed in six patients undergoing surgery for drug refractory ventricular tachycardia. All patients had large anterior left ventricular aneurysms with endocardial scar extending onto the septum. The large endocardial defect left after endocardial resection and aneurysmectomy was repaired with a pericardial patch. No intraoperative complications (e.g., suture line bleeding) were observed as a result of this technique. All patients are alive, and five of the six patients no longer have inducible ventricular tachycardia. An improvement in congestive heart failure symptoms at 1-9 months of follow-up was noted following surgery. We conclude that the pericardium can be safely used to cover endocardial defects resulting from regional endocardial resection for sustained ventricular tachycardia.

Animals↗
PubMed1986

Long-term therapy with disopyramide phosphate: side effects and effectiveness.

In this study, the safety and efficacy of long-term therapy with disopyramide phosphate were evaluated in 40 patients with documented, recurrent, symptomatic tachyarrhythmias. Twenty-one (53%) of the patients had organic heart disease, and nine of these patients had compensated congestive heart failure. The tachyarrhythmias which were treated were paroxysmal supraventricular tachycardia (21 patients), paroxysmal atrial fibrillation (six patients), and paroxysmal ventricular tachycardia (13 patients). In each patient there was evidence, from continuous ECG monitoring or electrophysiologic testing, that disopyramide would be effective therapy, and each patient was able to tolerate disopyramide (no side effects or tolerable side effects) during an initial trial period of 1 to 2 weeks. Dosages of disopyramide were 400 to 1600 mg/day (994 +/- 320 mm/day). During long-term therapy, side effects were reported by 28 (70%) of the patients. The side effects were usually anticholinergic, and were usually a continuation of side effects noted during the initial trial period. None of the patients had idiosyncratic reactions to disopyramide. Most of the patients found side effects to be tolerable; however, in seven patients it was necessary to discontinue disopyramide after 1 to 8 (6 +/- 3) months. Actuarial incidence of intolerable side effects was 21 +/- 7% at 12 months. Nine (22%) of the 40 patients had symptomatic recurrences of tachyarrhythmia after 3 to 32 (15 +/- 9) months of therapy. Actuarial incidence of drug ineffectiveness was 32 +/- 10% at 24 months. Disopyramide was both effective and tolerated in 24 (60%) of the patients, who were followed for 2 to 64 (23 +/- 16) months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Paroxysmal fascicular tachycardia and ventricular tachycardia due to mechanical stimulation by a mitral valve prosthesis.

Electrophysiologic studies were performed in a woman who had two varieties of paroxysmal wide QRS tachycardia after mitral valve replacement with a Starr-Edwards prosthesis. One tachycardia originated in the left anterior fascicle; QRS complexes were 100 ms wide and resembled right bundle branch block with left posterior fascicular block, and a His bundle potential preceded each QRS by an interval of 20 ms (compared with 50 ms during sinus rhythm). The other tachycardia originated in the left ventricle. Clinical and echocardiographic observations suggested that the tachycardias were caused by mechanical stimulation of the interventricular septum by the mitral prosthesis.

Adult↗
PubMed1986

Tachyarrhythmias in young athletes.

Nineteen young athletes with documented symptomatic tachyarrhythmia were systematically evaluated. There were 15 men and 4 women, aged 14 to 32 years (mean 22 +/- 6). Documented tachyarrhythmias were paroxysmal atrial fibrillation in five patients, paroxysmal supraventricular tachycardia in five, paroxysmal ventricular tachycardia in eight (sustained in five, nonsustained in three) and ventricular fibrillation in one patient. Abnormal substrates were demonstrated in 15 (79%) of the 19 athletes: 5 had an anomalous atrioventricular (AV) pathway and 10 had heart disease (mitral valve prolapse in 9 patients and dilated cardiomyopathy in 1 patient). In 13 (68%) of the 19 athletes, all spontaneous attacks of tachyarrhythmia had started during strenuous exercise. Tachyarrhythmia that closely resembled clinical arrhythmia was induced by programmed cardiac stimulation in 13 athletes (68%) and was reproducibly provoked by treadmill exercise in 8 athletes (42%). In four of seven athletes with ventricular tachycardia, tachycardia closely resembling clinical arrhythmia was provoked by infusion of isoproterenol. In summary: young athletes can have any of several tachyarrhythmias; abnormal substrates can be demonstrated in many athletes with symptomatic tachyarrhythmia; and tachyarrhythmias in young athletes frequently occur during exercise.

Adolescent↗
PubMed1986

Distal atrioventricular conduction system function.

This article addresses electrophysiologic evaluation of the distal AV conduction system in patients with chronic bifascicular block. It was formerly thought that progression to complete AV block was a common cause of morbidity and even sudden death in this condition, and it was hoped that electrophysiologic evaluation, including measurement of the H-V interval, would facilitate prospective identification and prophylactic treatment of patients prone to these complications. However, a decade of clinical investigation has revealed that progression to complete AV block is rare and that although cardiovascular mortality, including sudden death, is substantial, this mortality usually relates to underlying organic heart disease. The current role for electrophysiologic studies in chronic bifascicular block is limited to delineation of the site of electrocardiographically documented second- or third-degree AV block and to the evaluation of unexplained syncope.

Atrioventricular Node↗
PubMed1979

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.

Adolescent↗
PubMed1978

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 (slow 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.

Atrioventricular Node↗