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Biomedical subjects

B Strasberg

Publications and source records attributed to B Strasberg.

At least 181 records · Page 10Linked to original sources
PubMed1981

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 second-degree block; five patients also had periods of 2:1 block. Prospective follow-up 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.

Adolescent↗
PubMed1981

Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia.

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.

Administration, Oral↗
PubMed1981

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 85%). Spontaneous trifascicular block (TFB) developed in two patients (0.6%) with NHV and nine patients (4.5%) with PHV (p less than 0.05). Cumulative 7-year incidence of TFB was 3% with NHV and 12% with PHV (p less than 0.01). Seven-year cumulative cardiovascular mortality was 32% in NHV patients and 57% in PHV patients (p less than 0.005). In conclusion, PHV in patients with chronic BFB was associated with a greater incidence and severity of OHD, and higher total and sudden death mortalities. The risk of spontaneous TFB was small in patients with either NHV or PHV, although it was significantly higher in the latter.

Angina Pectoris↗
PubMed1980

Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the Lown-Ganong-Levine syndrome.

Sixty-five patients with dual pathway atrioventricular (A-V) nodal reentrant paroxysmal tachycardia were studied. Of these 65 patients, 11 (17 percent) had a short P-R interval (0.12 second or less) and 3 (5 percent) had a short A-H interval (53 ms or less) during sinus rhythm, suggesting the Lown-Ganong-Levine syndrome. Frequency distribution analyses of P-R and A-H intervals in the 65 patients demonstrated continuous unimodal functions, suggesting a continuum of A-V nodal properties. Regression analyses of P-R and A-H (fast pathway) intervals versus cycle length of paroxysmal tachycardia revealed an r value of 0.11 and 0.10, respectively (not significant). The cycle length of paroxysmal tachycardia did not differ between the 11 patients with a short P-R interval (370 +/- 20 ms) and the 54 patients without a short P-R interval (382 +/- 11 ms). Regression analysis of the slow pathway A-H interval versus cycle length of paroxysmal tachycardia revealed an r value of 0.68 (p less than 0.001). The cycle length of dual pathway A-V nodal reentrant paroxysmal tachycardia is a function of the slow pathway A-H interval and not the P-R or A-H interval during sinus rhythm. Identification of short P-R intervals in patients with A-V nodal reentrant paroxysmal tachycardia has little significance.

Adult↗
PubMed1980

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.

Administration, Oral↗
PubMed1980

Myotonia dystrophica and mitral valve prolapse.

Two siblings are described, both afflicted with myotonia dystrophica and mitral valve prolapse. This family supports the recent association of these two familial diseases. One of the siblings had severe conduction disease and recurrent ventricular tachycardia, possibly reflecting potentiation of arrhythmia, because of the association of these two familial diseases.

Adult↗
PubMed1980

Echocardiographic demonstration of porcine mitral valve vegetation and dehiscence.

The echocardiographic study of a patient with a malfunctioning porcine valve in the mitral position is presented. Echocardiography of the mitral valve revealed multiple, dense heterogeneous echoes behind and within the valve stent which were suggestive of vegetations. At the aortic valve level, a clear systolic echo in the left atrium was recorded. This echo probably represented the prolapsing anterior valve stent and was caused by a major dehiscence of the valve stent due to endocarditis.

Adult↗
PubMed1979

Polymorphous ventricular tachycardia: clinical features and treatment.

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.

Adult↗
PubMed1979

Left anterior hemiblock obscuring the diagnosis of right bundle branch block in acute myocardial infarction.

Thirty cases in which transient left anterior hemiblock (LAHB) obscured the diagnosis of right bundle branch block (RBBB) appearing during the first days of an acute myocardial infarction (AMI) are presented. Twenty-eight of the patients with AMI had a clear septal wall involvement, while the remaining two had an anterolateral and lateral wall AMI, respectively. These intraventricular conduction defects developed 2-120 hours (mean 64.9 +/- 26 hours) after the acute event, and persisted for 24 hours to 7 days (mean 63.1 +/- 35 hours). The ECG was characterized by a pure LAHB with wide QRS complexes and the presence of RBBB was shown by recording high V1 and right-sided chest leads. The vectorcardiogram was also useful in several cases. The clinical course of this type of bifascicular block was transient and benign, with an in-hospital mortality of 6.7%. No patient developed trifascicular or complete atrioventricular block and, therefore, we conclude that prophylactic installation of a temporary pacemaker is not indicated in this type of bifascicular block. The possible role of extracellular potassium released during acute myocardial necrosis in the pathophysiological mechanism of these blocks is discussed.

Acute Disease↗