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Biomedical subjects

P Denes

Publications and source records attributed to P Denes.

At least 19 recordsLinked to original sources

The importance of derived 12-lead electrocardiography in the interpretation of arrhythmias detected by Holter recording.

Holter monitoring has been used extensively for the detection, diagnosis, and evaluation of therapy for cardiac arrhythmias. The availability of three-channel monitors allows for the recording of vectorcardiographic leads X, Y, and Z. One method, which was recently described by Dower et al., (J Electrocardiol 1988;21:5182-7), uses modified vectorcardiographic leads and allows for the acquisition of a derived 12-lead ECG of selected rhythm strips during the recording. In the present study, we evaluated the usefulness of the derived 12-lead ECG in the detection of P-wave and ST-segment shifts, assessment of QRST changes, and distinction between ventricular ectopic and aberrant supraventricular complexes. Our preliminary findings indicate that careful analysis of the derived 12-lead ECG provides additional information for a more accurate diagnosis of arrhythmias that are detected by the Holter monitor. The clinical importance and cost-effectiveness of the derived 12-lead ECG needs further evaluation.

Arrhythmias, Cardiac

Permanent pacemaker placement in chronic atrial fibrillation associated with intermittent AV block and cerebral symptoms.

We examined the hypothesis that a greater than or equal to 2 second pause detected on 24-hour Holter monitoring in patients with persistent atrial fibrillation and complaints of syncope or dizziness lacked sufficient specificity to warrant implantation of a permanent pacemaker. We retrospectively reviewed cases from our 24-hour electrocardiographic (Holter) monitoring data base. A total of 411 consecutive Holter monitoring records demonstrating persistent atrial fibrillation obtained during a 5-year period (1982 to 1987) were examined. One hundred and five (26%) patients had cerebral symptoms (dizziness or syncope) as a primary indication for monitoring 80 (76%) patients were identified with documented ventricular pauses of greater than or equal to 2 seconds. Three hundred and six patients (74%) underwent 24-hour monitoring without cerebral symptoms as an indication and 209 (68%) patients had greater than or equal to 2-second pauses. Clinical information was available in 164 (50 symptomatic and 114 asymptomatic) patients. There were no significant differences in the clinical or Holter findings between the two groups. Of the 50 symptomatic patients, 15 (30%) underwent permanent pacemaker placement and the remaining 35 (70%) were managed conservatively during a mean follow-up of 23 +/- 5 months. Eleven of 15 paced (73%) and 31 of 35 (89%) nonpaced patients experienced resolution of their cerebral symptoms (NS). The sensitivity of Holter monitoring in detecting pauses of greater than or equal to 2 seconds in patients with cerebral symptoms was high (76%), but the specificity (32%) and positive predictive values (28%) were low.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

Multiple reentrant tachycardias due to retrograde conduction of dual atrioventricular bundles with atrioventricular nodal-like properties.

A patient is presented who had two paroxysmal supraventricular tachycardias, one slow and incessant and the other fast. Both paroxysmal tachycardias appeared to be atrioventricular (A-V) reentrant, with anterograde conduction by way of a normal A-V pathway. Two pathways conducting in retrograde manner were demonstrated, characterized by different conduction times (fast and slow), identical abnormal atrial activation sequence and A-V nodal-like properties (retrograde Wenckebach periodicity with rapid ventricular pacing, and depression with ouabain and propranolol). Thus, there appeared to be two anomalous A-V bundles with nodal-like properties conducting in retrograde fashion. Whether the paroxysmal tachycardia was fast or slow depended on which of these pathways was utilized. Spontaneous cure of incessant paroxysmal tachycardia was observed and coincided with unexplained total loss of ability for ventriculoatrial conduction.

Atrioventricular Node

Incidence and site of atrioventricular block in patients with chronic bifascicular block.

Four hundred fifty-two patients with chronic bifascicular block and initially intact atrioventricular (AV) conduction were detected, studied, and prospectively followed between January 1970 and March 1978. There were 360 males and 92 females, ages 18--93 years (mean +/- SD, 62 +/- 15 years). Follow-up ranged from 29-2804 days (mean 1066 +/- 97 days). AV block (2 degrees or 3 degrees) developed in 29 patients, nine with apparent cause and spontaneously in 20. Cumulative annual incidence of all heart block for 1--5 years was, respectively, 4%, 5.9%, 8.7%, 10.1% and 11.3%, and for spontaneous block was 2%, 3.1%, 5.2%, 6.7%, and 7.1%. Sites of spontaneous block were probably or definitely AV nodal in ten, His bundle in one, and trifascicular in nine. Cumulative incidence of AV block in surviving bifascicular block patients is 11% at 5 years, with 7% reflecting spontaneous block. The probable or definite site of AV block varies and is trifascicular in less than half of the patients. The small incidence of trifascicular block probably explains the difficulty in predicting this complication with electrophysiological studies.

Adolescent

Congenital abnormalities of the conduction system in two patients with tachyarrhythmias.

Serial sections of the conduction system (CS) were performed in two patients with recurrent tachyarrhythmias. Case 1, a 34-year-old female who had dual atrioventricular (AV) nodal pathways with recurrent paroxysmal supraventricular tachycardia, committed suicide. Autopsy revealed an abnormally formed atrial septum with insertion of eustachian valve on the AV part of the pars membranacea. The intercuspid portion of the pars membranacea was muscular. The AV node was located adjacent to the membranous part of the ventricular septum rather than the central fibrous body. In addition, there was an accessory anterior AV node on the parietal wall of the right atrium. Case 2, a 13-year-old boy with history of recurrent ventricular tachycardia, died suddenly. CS revealed a right-sided, markedly septated bundle. The first part of right bundle branch was divided into three parts, which later joined together. Both cases showed fatty infiltration of the atrial septum, more than normal for the age of the patients. The relationship of the recurrent tachyarrhythmias to the congenital abnormalities in the CS in the two cases and the fatty infiltration is reviewed.

Adolescent

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.

Adult

Significance of chronic bifascicular block without apparent organic heart disease.

Eighty-six of 452 patients (19%) with chronic bifascicular block were found to have no clinically apparent associated organic heart disease (OHD) and were defined as having primary conduction disease (PCD). Comparison of patients with PCD and OHD revealed a significantly lower incidence of the following clinical variables in the PCD patients (p less than 0.001): exertional angina, dyspnea, congestive heart failure, cardiomegaly, functional class I (all by study design), left bundle branch block and premature ventricular contractions. Both mean AH and HV intervals were significantly shorter in patients with PCD (p less than 0.01). The incidence of HV prolongation was 21% in PCD and 41% in OHD patients (p less than 0.001). All patients were prospectively followed for 21-2998 days with a mean +/- SEM of 1209 +/- 66 days for PCD and 1172 +/- 36 days for OHD. Atrioventricular (AV) block developed in three patients from the PCD group and 26 from the OHD group (NS), with spontaneous block occurring in one (1%) PCD patient and 19 (5%) OHD patients (p less than 0.05). Annual mortality due to sudden death as well as total cardiovascular mortality (including sudden death) for the 5-year follow-up was significantly lower in patients with PCD. Patients with PCD have significantly lower incidence of electrophysiologic abnormalities and subsequent spontaneous AV block as well as cardiovascular and sudden death mortality. The diagnosis of PCD based on clinical criteria probably underestimates the presence of underlying OHD, as suggested by a small but definite risk of cardiovascular mortality.

Adult

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

Twenty-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 (lond 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).

Adolescent

Evaluation of criteria for diagnosis of myocardial infarction: study of 256 patients with intermittent left bundle branch block.

In an attempt to elucidate the specificity and sensitivity of atypical findings during left bundle branch block (LBBB) with respect to myocardial infarction (MI), we analyzed ECGs from patients with intermittent LBBB obtained by mail solicitation of cardiologists. The group consisted of 256 patient files fulfilling the following criteria: 1) complete LBBB present on one or more 12-lead ECGs, and 2) at leat one 12-lead ECG taken subsequent to a LBBB tracing exhibiting absence of LBBB (non-LBBB). The sensitivity of atypical LBBB for predicting presence of MI was 0.41, the specificity 0.64, and the accuracy 0.59. No specific atypical finding was significantly better than any other in predicting MI. We conclude that atypical findings present during LBBB are of little value in predicting the presence of MI (as diagnosed by significant Q waves present during non-LBBB conduction).

Bundle-Branch Block

Paroxysmal supraventricular tachycardia induction in patients with Wolff-Parkinson-White syndrome.

In 54 patients with pre-excitation, 30 (56%) had inducible A-V re-entrant paroxysmal tachycardia. Of these 30, 20 had spontaneous paroxysmal tachycardia (four also had atrial fibrillation), four had spontaneous paroxysmal atrial fibrillation, five had a history of palpitation without arrhythmia, and one was asymptomatic. In 24 patients (44%), paroxysmal tachycardia was not inducible. Of these 24, none had documented paroxysmal tachycardia, four had atrial fibrillation, none had palpitation without arrhythmia, and 11 were asymptomatic. The incidence of documented paroxysmal tachycardia was higher in the patients with inducible tachycardia (P less than 0.001). Tachycardia induction was noted in 20 of 20 patients with spontaneous paroxysmal tachycardia, eight of 12 patients with paroxysmal atrial fibrillation, five of 14 patients with palpitation and no arrhythmia, and one of 12 asymptomatic patients. The frequency of ability to induce paroxysmal tachycardia was significantly higher in both the patients with documented spontaneous paroxysmal tachycardia and the patients with paroxysmal atrial fibrillation than in the asymptomatic group (P less than 0.01).

Adolescent

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.

Adolescent

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.

Arrhythmias, Cardiac

Electrophysiologic effects of lidocaine on sinus node and atrium in patients with and without sinoatrial dysfunction.

Electrophysiological studies were conducted in 13 patients with normal sinus node function and 14 with sinus node dysfunction before and after intravenous lidocaine. Mean +/- SEM sinus cycle length significantly shortened from 810 +/- 34.3 to 774 +/- 34.3 msec in patients with normal sinus node (P less than 0.001) and from 1061 +/- 67.6 to 1016 +/- 64.5 msec in patients with sinus node dysfunction (P less than 0.025) after lidocaine. Mean sinus recovery time was 1027 +/- 49.4 before and 1026 +/- 52.5 msec after lidocaine in patients with normal sinus node (NS) and 1269 +/- 97.7 before and 1170 +/- 73.8 msec after lidocaine in patients with sinus node dysfunction (P less than 0.05). Mean calculated sinoatrial conduction time was 87 +/- 9.5 before and 90 +/- 9.2 msec after lidocaine in patients with normal sinus node (NS) and 80 +/- 10.3 before and 96 +/- 10.2 msec after lidocaine in patients with sinus node dysfunction (P less than 0.001). Mean atrial effective and functional refractory periods were not significantly changed with lidocaine. Thus lidocaine shortened sinus cycle length in both groups, without affecting atrial refractoriness. Lidocaine appeared to depress perinodal tissue only in patients with sinus node dysfunction. The abbreviation of sinus recovery time in patients with sinus node dysfunction could reflect increased sinus automaticity and/or increased perinodal refractoriness, allowing entrance block to occur. This mechanism may explain why sinus arrest has been noted in some patients during lidocaine administration.

Adult