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Biomedical subjects

S Sclarovsky

Publications and source records attributed to S Sclarovsky.

At least 163 records · Page 9Linked to original sources
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

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

Acceleration of ventricular tachycardia induced by a chest thump.

Chest thump is accepted as a simple and effective maneuver for terminating a paroxysm of ventricular tachycardia. This report describes three patients receiving digitalis in whom chest thump caused an acceleration of the rate of ventricular tachycardia. Following discontinuation of digitalis therapy, chest thump converted to sinus rhythm recurrence of ventricular tachycardia in two patients and did not cause acceleration of the ventricular rate in the third. It is suggested that in patients taking digitalis with ventricular tachycardia, chest thump should be used with caution.

Aged↗
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↗
PubMed1979

Unusual electrocardiographic presentation of idiopathic hypertrophic subaortic stenosis.

A patient with idiopathic hypertrophic subaortic stenosis and normal coronary arteries, with dynamic electrocardiographic changes resembling acute myocardial ischemia, is presented. A definite association between the electrocardiographic changes and the idiopathic hypertrophic subaortic stenosis cannot be absolutely confirmed; however, the findings demonstrate the broad spectrum of electrocardiographic presentation in this disease.

Cardiomyopathy, Hypertrophic↗
PubMed1978

Coexistent Wenckebach phenomenon in the distal branches of the specialized conduction system.

A patient in whom Wenckebach phenomenon was observed to coexist in the three distal branches of the specialized ventricular conduction system, with an intermittent trifascicular block producing a second degree A-V block, is described. Surface electrocardiogram demonstrated the presence of this phenomenon in the right bundle branch (RBB) and the anterior division of the left bundle branch (LBB). Evidence of the presence of Wenckebach phenomenon in the remaining fascicle was provided by His bundle recording.

Aged↗
PubMed1978

Dissociation of the atrioventricular node in acute inferior wall myocardial infarction. 1. Transverse dissociation (alternate Wenckebach periods).

Two cases of alternate Wenckebach periods developing during the acute phase of inferior wall myocardial infarction are presented. In both cases, syncope occurred and severe bradyarrhythmia was recorded on the day of admission. Electrophysiologic study performed in one patient and a narrow QRS complex in the other patient during the alternate Wenckebach periods confirmed the atrioventricular node as the level of block. Transverse dissociation of the atrioventricular node with two (or more) levels of block is the most acceptable explanation for this phenomenon. We suggest that alternate Wenckebach periods occurring during the acute phase of inferior wall myocardial infarction is a severe bradyarrhythmia, and prophylactic temporary pacing is recommended.

Acute Disease↗
PubMed1978

Dissociation of the atrioventricular node in acute inferior wall myocardial infarction. 2. Longitudinal dissociation (dual atrioventricular nodal pathways).

Four cases of longitudinal dissociation of the atrioventricular node, with dual pathways developing during the acute phase of an inferior wall myocardial infarction (three cases) or during acute ischemia (one case), are presented. In all four cases, two grossly different P-R intervals were recorded, and in two cases, studies of the His bundle confirmed the location of the dissociation within the atrioventrcular node. In one case, premature atrial depolarization caused a bidirectional shifting of P-R intervals, while in the remaining three cases, premature ventricular depolarization (spontaneous or pacemaker-induced) was responsible for this phenomenon. In all cases, evidence of longitudinal dissociation of the atrioventricular node appeared during the acute phase of the infarction or ischemia, and in all of them the phenomenon was transient. This favors the assumption that this phenomenon is of a functional nature, most probably related to the ischemic lesion of the atrioventricular node.

Acute Disease↗