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Biomedical subjects

B Strasberg

Publications and source records attributed to B Strasberg.

At least 163 records · Page 9Linked to original sources
PubMed1982

Postoperative electrophysiological studies with a modified radiofrequency system. Technical aspects and clinical usefulness.

Two patients who underwent a ventricular aneurysmectomy for treatment of ventricular tachycardia are presented. In both patients, a radiofrequency pacemaker was implanted at surgery (for therapeutic use if surgery should fail). In both patients, electrophysiological studies were performed before discharge utilizing a radiofrequency pacemaker without recourse to repeat catheterization. This was possible by modifying the transmitter and coupling it to a commercially available programmable stimulator.

Electrocardiography↗
PubMed1982

Anatomic substrate for congenital atrioventricular block in middle-aged adults.

Congenital atrioventricular block is usually a benign disorder not necessitating pacing. In some patients slowing of rate and/or mortality have been noted with aging. However an anatomic substrate has not been established for the progressive slowing of the escape rate. In this study we report an anatomic substrate in two such patients who were dying in congestive heart failure, ages 49 and 42, respectively. Multiple pre-mortem ECG's in both cases revealed wide QRS escape rhythms, and escape rates of approximately 35 and 28 beats/minute, respectively. Conduction system examination by serial section in both cases revealed lack of connection between the atrial septum with the peripheral conduction system with total replacement by fat of the AV nodal approaches and AV node, and advanced sclerosis of the summit of the ventricular septum which was more marked on the right side. In addition, the His bundle showed marked septation in case one and fragmentation in case two. Sclerosis of the summit of the ventricular septum involved the branching bundle and the bundle branches in both cases. In conclusion, both patients had the characteristic lesions of congenital atrioventricular block, namely replacement of the AV node and AV nodal approaches by fat, with lack of connection to the peripheral conduction system, and one also had a fragmented His bundle. In addition premature aging of the summit of the ventricular septum may have reflected the long-standing hemodynamic stresses of chronic bradycardia. This in turn resulted in trifascicular involvement of the conduction system leading to a shifting of the escape rhythm distally eventuating in a slower idioventricular escape rhythm.

Adult↗
PubMed1982

Slowing of paroxysmal tachycardia with loss of functional bundle-branch block.

Electrophysiological studies in a patient with paroxysmal supraventricular tachycardia disclosed anterograde dual atrioventricular nodal pathways, and a concealed left-sided anomalous atrioventricular pathway which was used as the retrograde limb of two circus movement tachycardias. Tachycardia No.1, reflecting anterograde fast pathway conduction, was characterised by functional left bundle-branch block and a stable cycle length of 330 ms. Paroxysmal loss of bundle-branch block resulted in tachycardia No.2, which reflected anterograde slow pathway conduction, and was characterised by narrow QRS and a stable cycle length of 355 ms. Tachycardia No.2 had a longer cycle length than tachycardia No.1 because the increment in AH interval (slow pathway instead of fast pathway condition) more than compensated for the decrement in ventriculoatrial interval (narrow QRS instead of bundle-branch block).

Adult↗
PubMed1981

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 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 and unusual variety (one third of patients).

Adult↗
PubMed1981

Procainamide-induced 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.

Administration, Oral↗
PubMed1981

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.

Adolescent↗
PubMed1981

Ventricular fibrillation complicating temporary ventricular pacing in acute myocardial infarction: significance of right ventricular infarction.

Five patients with acute myocardial infarction had ventricular fibrillation as a complication of indicated temporary pacing. All five patients had evidence of right ventricular infarction (three patients with postmortem confirmation). The presence of right ventricular infarction seems to be a contributing mechanism involved in the induction of ventricular fibrillation during temporary pacing for bradyarrhythmia complicating acute myocardial infarction.

Adult↗
PubMed1981

Paroxysmal atrial flutter and fibrillation associated with preexcitation syndrome: treatment with ajmaline.

Ajmaline was administered intravenously to six patients with the Wolff-Parkinson-White syndrome for the acute management of paroxysmal atrial flutter (three patients) or fibrillation (three patients) with a fast ventricular response (over the accessory pathway). Ajmaline increased refractoriness in the accessory pathway in all three patients with atrial flutter and stopped the flutter in one. The drug completely abolished preexcitation in two of the three patients with atrial fibrillation, decreasing the means ventricular rate of 240 and 300 beats/min to 110 and 180 beats/min, respectively. In the third patient with atrial fibrillation, ajmaline increased refractoriness over the accessory pathway, decreasing the mean ventricular rate of 300 beats/min to 160 beats/min. In two patients ajmaline was continued as an intravenous maintenance infusion until sinus rhythm was restored. It is concluded that ajmaline is an effective drug for the acute management of atrial flutter or fibrillation with a fast ventricular response in patients with the Wolff-Parkinson-White syndrome.

Adult↗
PubMed1981

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.

Adolescent↗
PubMed1981

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.

Administration, Oral↗