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Biomedical subjects

B Strasberg

Publications and source records attributed to B Strasberg.

At least 145 records · Page 8Linked to original sources
PubMed1983

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.

Adolescent↗
PubMed1983

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.

Adult↗
PubMed1983

Electrophysiologic testing of bretylium tosylate in sustained ventricular tachycardia.

We used programmed ventricular stimulation to test intravenous bretylium tosylate in 10 consecutive patients with inducible sustained ventricular tachycardia (usually refractory to type I antiarrhythmic agents). These 10 patients had previously documented sustained ventricular tachycardia and/or ventricular fibrillation complicating stable heart disease. Following control inductions of sustained ventricular tachycardia, bretylium 10 mg/kg was infused over 30 minutes. Thirty minutes after this infusion, sustained ventricular tachycardia could be induced in 9 of the 10 patients (one of these nine patients also had bretylium-potentiated spontaneous ventricular tachycardia). Tachycardia induced in the nine patients after bretylium was similar to control tachycardia with respect to morphology and cycle length (333 +/- 16 msec after bretylium versus 330 +/- 16 msec during control). However, five of the nine patients tolerated induced tachycardia less well after bretylium (exacerbated hypotension). In one patient, ventricular tachycardia could not be induced after intravenous bretylium.

Administration, Oral↗
PubMed1983

Multiform accelerated idioventricular rhythm in acute myocardial infarction: electrocardiographic characteristics and response to verapamil.

Thirteen patients with acute myocardial infarction with multiform accelerated idioventricular rhythm (AIVR) occurring during the first 12 hours of monitoring in the coronary care unit are described. This arrhythmia, similar to the more common uniform AIVR, was intermittent, did not cause hemodynamic compromise, and was not related to more serious ventricular arrhythmias. There was no correlation between the bundle branch block pattern of the multiform AIVR and the electrocardiographic location of the myocardial infarction, but there was a perfect correlation between the frontal plane electrical axis of the multiform AIVR and the electrocardiographic location of the myocardial infarction. The presence of fusion beats between the different forms of AIVR suggests multifocality rather than multiformity. Intravenous verapamil (3 to 5 mg bolus) was administered to 6 patients with multiform AIVR in whom the arrhythmias were persistent enough to allow the evaluation of the effect of verapamil on the arrhythmia. Verapamil caused no change in the rate of AIVR in 1 patient, but in a second patient it decreased the rate by 20 beats/min. In 4 patients, verapamil abolished the arrhythmia: in 2 patients carotid sinus pressure (induced sinus slowing) allowed the emergence of the AIVR at a lower rate, and in the remaining 2 patients the arrhythmia was not observed.

Adult↗
PubMed1983

Sudden death in three teenagers: conduction system studies.

The pathologic substrate for sudden death in the middle-aged or elderly adult is usually ischemic heart disease. In contrast, few data are available regarding the pathology of sudden death in teenagers. This report describes three teenagers without clinically suspected heart disease dying suddenly. Patient 1 (age 15, male) was known to have right ventricular premature ventricular beats. Postmortem examination revealed marked premature aging, sclerosis of the cardiac skeleton extending to the right side of the summit with fibrosis of the left and right bundle branches. Patient 2 (age 17, male) was a trained athlete who died during football scrimmage. Autopsy revealed moderate mitral valve prolapse and marked premature aging, sclerosis of the left side of the cardiac skeleton, which extended to the right ventricular side, and secondary involvement of the trifascicular conduction system with mononuclear cell infiltration. Patient 3 (age 19, female) died suddenly at home. Autopsy revealed mitral valve prolapse, thrombosis of the sinoatrial (SA) node artery, and premature aging, sclerosis of the left side of the cardiac skeleton, with involvement of the ventricular septum more on the right ventricular side and involvement of the atrioventricular bundle and trifascicular conduction system. In conclusion, unexpected deaths in three teenagers occurred with demonstrable pathologic findings in the heart. Two of the three patients had mitral valve prolapse, one of whom also had thrombosis or embolism of the sinoatrial node artery. All three had sclerosis of not only the left side but also the right side of the ventricular septum with involvement of the conduction system. The anatomic substrate demonstrated in these three patients could relate to lethal bradyarrhythmia or tachyarrhythmia, or both.

Adolescent↗
PubMed1983

Familial inducible torsade de pointes with normal QT interval.

A familial presentation of torsade de pointes is described. The propositus had recurrent syncope, documented torsade de pointes, a normal Q-T, and close coupled premature ventricular beats initiating the paroxysmal arrhythmia. The mother had sporadic syncope without documented torsade de pointes, a normal Q-T, and closely coupled premature ventricular beats. Electrophysiological studies demonstrated reproducible inducible torsade de pointes tachycardia in both patients. Serial drug testing in both revealed suppression of induced torsade de pointes with oral propranolol. Chronic oral propranolol resulted in clinical cure in both patients.

Adult↗
PubMed1983

Long-term follow-up of patients receiving aprindine. Safety and efficacy.

Aprindine hydrochloride is an antiarrhythmic agent presently undergoing clinical trials in the United States. Because of the narrow therapeutic-toxic ratio observed for aprindine, the long-term follow-up of these patients is important in determining the potential clinical effectiveness of this drug. In this report we examine our experience with 30 patients with drug-resistant arrhythmias who were discharged receiving aprindine and who were followed up for a mean period of 25 months.

Adolescent↗
PubMed1982

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.

Aged↗
PubMed1982

M-mode echocardiography in left bundle branch block: significance of frontal plane QRS axis.

M-mode echocardiograms were obtained in 48 patients with complete left bundle branch block (LBBB). Of these 48 patients, 28 had LBBB with normal frontal plane QRS axis (-20 degrees to +90 degrees, mean +/- SD 18 degrees +/- 34 degrees), and 20 had LBBB with a left axis deviation (LAD) (-30 degrees to -60 degrees, mean +/- SD -48 degrees +/- 11 degrees). In the group with LBBB and normal axis, 25 patients had typical early mean +/- SD -48 degrees +/- 11 degrees). In the group with LBBB and normal axis, 25 patients had typical early systolic posterior septal motion characteristic of LBBB. Septal motion following early posterior septal motion (through the ejection period) was posterior in 24 patients (86%), anterior (paradoxical) in 2 (7%), and flat in 2 (7%). In the group with LBBB and LAD, 16 patients had the typical early systolic posterior septal motion; subsequent septal motion was posterior in 3 (15%), anterior (paradoxical) in 13 (65%), and flat in 4 (20%). Patients with LBBB and normal axis had a higher frequency of posterior septal motion, and patients with LAD had a higher frequency of anterior septal motion (p less than 0.001). The correlation of abnormal axis and paradoxical septal motion may be explained by the activation pattern producing LAD or by a septal disease process producing both abnormalities of axis and abnormal septal motion.

Adolescent↗
PubMed1982

Exercise provocable right ventricular outflow tract tachycardia.

During the past 5 years, we have seen six patients who met inclusion criteria of exertional palpitations, reproducible treadmill (TM) provocable ventricular tachycardia (VT), and performance of electrophysiologic (EP) studies including isoproterenol (ISO) infusion. There were five males and one female, aged 15 to 55 years (mean +/- SD, 31 +/- 18 years). Three patients were trained athletes, two patients had mitral valve prolapse, three had enlarged right ventricular (RV) volumes (all trained athletes), and two had no evidence of organic heart disease. TM testing in all patients demonstrated reproducible exercise-provocable VT of at least 20 beats' duration. TM VT was characterized by left bundle branch block pattern ORS morphology and rates of 150 to 230 bpm (186 +/- 30 bpm). EP did not reproduce VT in five of six patients while ISO at a dose of 2 to 4 micrograms/min (2.5 +/- 0.8 micrograms/min) reproduced VT in all patients. ISO VT was characterized by QRS morphology identical to TM VT and rates of 165 to 230 bpm (191 +/- 26 bpm). Endocardial mapping of ISO VT revealed earliest activity in RV outflow tract. Serial TM testing revealed suppression of TM VT in all six patients on propranolol therapy. Responses to class I drugs were variable and less successful. In summary, we describe a group of patients with common clinical, ECG, and electrophysiologic features who may share a common pathophysiology of VT. Possible mechanisms are discussed.

Adolescent↗
PubMed1982

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 (5) for one 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.

Adult↗
PubMed1982

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.

Adult↗
PubMed1982

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

Ten patients are described with two discrete discontinuities 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.

Adolescent↗
PubMed1982

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 (greater than 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.

Administration, Oral↗