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Biomedical subjects

M M Scheinman

Publications and source records attributed to M M Scheinman.

At least 253 records · Page 14Linked to original sources
PubMed1981

ECG diagnostic pearls and pitfalls. 1. Acute myocardial infarction and pseudoinfarction.

An accumulation of valuable empirical data supports the clinical usefulness of the ECG in diagnosis of cardiac disorders and electrolyte disturbances. Although the patterns in some conditions are sufficiently characteristic to be diagnostic, many ECG abnormalities fit several conditions and many mimic the findings in myocardial infarction. Thus, interpretation presents many pitfalls, and each ECG must be carefully scrutinized in light of the complete clinical picture and laboratory data. ECGs may be used to diagnose, date, and locate the site of myocardial ischemia or infarction and many afford clues to pseudoinfarction patterns as described here. The ECG is also valuable in assessment of fascicle block and ventricular hypertrophy (part 2, page 136) and in diagnosis of drug-induced and electrolyte disturbances (part 3, page 145).

Adult↗
PubMed1981

Atrial and ventricular vulnerability in a patient with the Wolff-Parkinson-White syndrome.

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter. The atrial and ventricular effective refractory periods were 180 ms and less than 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atrial or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal by-pass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.

Adult↗
PubMed1981

Mechanisms of spontaneous tachycardia termination in a patient with the Wolff-Parkinson-White syndrome and dual atrioventricular nodal pathways.

A patient with the Wolff-Parkinson-White syndrome and recurrent bouts of paroxysmal supraventricular tachycardia under-went electrophysiologic studies. These studies revealed evidence of dual atrioventricular nodal pathways and a septal accessory pathway. The tachycardia circuit involved anterograde conduction over a slow atrioventricular nodal pathway and retrograde conduction over the accessory pathway. Spontaneous tachycardia termination was frequently observed, was almost always abrupt, and was associated with a beat-to-beat decrease in the A-H interval. In this patient, the mechanism for spontaneous tachycardia termination appeared to be an abrupt shift in anterograde conduction from the slow to the fast pathway, advancing the tachycardia so that the block occurred in the accessory pathway (or atrium). To our knowledge, this mechanism of spontaneous tachycardia termination has not been described previously. Use of agents to facilitate fast atrioventricular nodal conduction (i.e., atropine) may be effective in tachycardia termination for these patients.

Atrioventricular Node↗
PubMed1981

Electrophysiologic effects on combined autonomic blockade in patients with sinus node disease.

Thirty-two patients were studied before and after i.v. administration of 0.15-0.20 mg/kg of propranolol. Twenty-one of the 32 underwent combined autonomic blockade with the additional infusion of 0.04 mg of atropine. Twenty other patients with sinus node disease underwent electrophysiologic studies both before and after i.v. administration of 0.04 mg of atropine alone. Spontaneous cycle length, maximal corrected sinus node recovery time, sinoatrial conduction time, secondary pauses and intrinsic heart rate were measured. Secondary pauses were more common in those with abnormal intrinsic heart rates, and they did not correlate with changes in maximal corrected sinus node recovery time or sinoatrial conduction time. In patients with normal intrinsic heart rate, abnormal test measurements usually returned to normal after combined blockade (hypervagotonia); however, some patients showed a new abnormality after propranolol that was not reversible with atropine (catecholamine-dependent). Abnormal test responses in patients with abnormal intrinsic heart rate persisted or increased after combined blockade. We conclude that patients with sinus node disease may be categorized as (1) those with intrinsic sinus node disease; (2) those with normal intrinsic sinus node function but either relative hypervagotonia or catecholamine dependency; and (3) those with abnormal intrinsic sinus node function affected by vagal or catecholamine factors.

Adult↗
PubMed1981

His-ventricular dissociation in a patient with reciprocating tachycardia and a nodoventricular bypass tract.

A patient with recurrent bouts of atrial fibrillation and wide-complex regular tachycardia underwent electrophysiologic studies. Premature atrial stimulation or atrial pacing during sinus rhythm resulted in gradual lengthening of the PR and AH intervals, narrowing of the HV interval and progressive preexcitation with a left bundle branch block and left-axis contour. Induction of tachycardia was dependent on critical delay in the atrioventricular interval and was associated with attainment of a maximal preexcitation pattern. During tachycardia, the ventriculoatrial interval was constant, whereas the interval from His bundle deflection to the ventricular complex was variable. We postulate that the tachycardia circuit involved reciprocation within the atrioventricular node and that a nodoventricular bypass tract was present in close anatomic or functional association with the slow atrioventricular nodal pathway. Our data suggest that both the nodoventricular bypass tract and the His-Purkinje system may be passive "bystanders" rather than essential components of the tachycardia circuit. In addition, although HV dissociation usually implies ventricular tachycardia, this case demonstrates that HV dissociation during wide-complex regular tachyarrhythmia is not diagnostic of ventricular tachycardia.

Adult↗
PubMed1981

Primary oxalosis with pan-conduction cardiac disease: electrophysiologic and anatomic correlation.

A 27-year-old man with primary oxalosis and extensive visceral involvement was maintained on long-term chronic hemodialysis. He had an episode of presyncope associated with electrocardiographic findings of an erratic atrial rhythm, atrioventricular dissociation due to an accelerated junctional rhythm and right bundle branch block. Electrophysiologic studies showed irregular atrial depolarizations probably associated with multiple atrial pacemakers, atrial inexcitability, atrioventricular dissociation and infranodal conduction delay. These findings correlated well with extensive oxalate infiltration of the sinoatrial node and its approaches, the atrial preferential pathways, the approaches to the atrioventricular node, the atrioventricular node, and the His bundle and bundle branches. This is the first reported case of cardiac electrophysiologic abnormalities due to oxalate infiltration in a patient with primary oxalosis.

Adult↗
PubMed1981

Cardiovascular collapse associated with disopyramide therapy.

Five patients with severe left ventricular failure, renal insufficiency, and recurrent ventricular tachycardia had cardiovascular collapse and died eight hours to 23 days after initiation of the usual doses of disopyramide. Three patients had recent myocardial infarction (12 to 33 days), and one had severe congestive cardiomyopathy. ECG changes antedated appearance of cardiovascular collapse and consisted of lengthening of the QRS (0.10 plus or minus 0.02 to 0.22 plus or minus 0.09; P less than 0.025) and the QTc duration (0.44 plus or minus 0.04 to 0.56 plus or minus 0.09; P less than 0.05). Sinus bradycardia or varying degrees of atrioventricular block or both occurred in all patients. Terminal disopyramide blood concentration (4.9 and 8.1 micrograms/ml) were available in two patients. A syndrome of progressive lengthening of ventricular depolarization and repolarization terminating in cardiovascular collapse and death associated with disopyramide is described. In addition, a high incidence of sinus bradycardia, atrioventricular conduction disturbances, or both was also noted. Disopyramide is contraindicated in patients with severe heart failure and renal insufficiency. Progressive widening of the QRS complex or the QT interval may presage appearance of severe myocardial dysfunction.

Administration, Oral↗
PubMed1981

Treatment of supraventricular arrhythmias with intravenous and oral verapamil.

Verapamil or placebo was administered as a bolus infusion in a double-blind fashion to 24 patients with either atrial fibrillation or flutter and to ten patients with paroxysmal supraventricular tachycardia. Patients whose heart rate did not decrease below 100 beats/min were given a second dose. Of the 24 patients with atrial fibrillation or flutter, 11 received placebo first. Control heart rate and blood pressure were not modified by placebo; however, verapamil significantly reduced heart rate and systolic blood pressure in the 24 patients. Of the ten patients with paroxysmal supraventricular tachycardia, one reverted to sinus rhythm after administration of placebo. For the remaining nine, the heart rate was not modified by placebo but was significantly reduced by verapamil administration. Blood pressure was not modified by verapamil or placebo in these ten patients. Long-term oral verapamil treatment was maintained without interruption in 18 patients for a mean of 16 +/- 7.5 months, and 15 patients required concomitant therapy with other antiarrhythmic drugs for rhythm control. All patients reported symptomatic improvement, and the number of hospitalizations required for arrhythmia control decreased significantly. Verapamil is safe and effective for acute control of supraventricular arrhythmias. Long-term oral administration, alone or with other antiarrhythmic drugs, is an important contribution to the management of recurrent supraventricular arrhythmias.

Administration, Oral↗
PubMed1980

Unusual complications of epicardial pacemakers. Recurrent pericarditis, cardiac tamponade and pericardial constriction.

Three patients with unusual complications after insertion of an epicardial pacemaker are described. In one patient pericarditis and severe cardiac tamponade developed that required emergency pericardiocentesis 8 weeks after pacemaker insertion. No evidence of myocardial perforation was observed at operation. In another patient two unusual complications developed: (1) migration of the pulse generator from the epigastric site of implantation into the pelvis, and (2) recurrent pericarditis with occult signs of constriction. In another patient recurrent pericarditis and clinical evidence of constriction developed. All three patients required pericardiectomy. Recurrent pericarditis after insertion of an epicardial pacemaker requires careful medical follow-up because either life-threatening tamponade or chronic constrictive pericarditis may develop.

Adult↗
PubMed1980

Enhanced atrioventricular nodal conduction in a patient with dual extranodal pathways.

A patient was admitted to the hospital with wide complex tachycardia and a history of recurrent palpitations. Electrophysiologic studies showed evidence of dual atrioventricular (AV) accessory pathways. One proved to be an anteroseptal (possible right anterior) pathway probably capable of only unidirectional conduction. The other pathway was in the posterior septum and conducted only in the retrograde direction. The tachycardia circuit involved anterograde conduction via either the AV node-His axis or the anteroseptal pathway and retroconduction over the posteroseptal accessory pathway. In addition, enhanced AV nodal conduction coupled with two accessory AV nodal pathways has rarely been described in English medical literature. Previous reports have carefully described anatomic, electrocardiographic, and electrophysiologic evidence of more than one accessory pathway in patients with the Wolff-Parkinson-White syndrome. The introduction of surgical techniques for ablation of an accessory pathway demands precision in the electrophysiologic evaluation of patients with ventricular preexcitation. Reported herein is a patient with the unique finding of two extranodal accessory pathways and enhanced atrioventricular (AV) nodal conduction (or AV nodal bypass).

Atrioventricular Node↗
PubMed1980

Effects of antiarrhythmic drugs on atrioventricular conduction in patients with acute myocardial infarction.

Three hundred fifty-eight of 429 (83%) consecutive patients with acute myocardial infarction (MI) and a normal PR interval received various antiarrhythmic drugs (AD), including lidocaine and/or procainamide, quinidine, digoxin, propranolol or disopyramide. There was no significant difference in the incidence of progression to any degree of atrioventricular (AV) block or to higher degrees of AV block (Mobitz II or third-degree AV block) between those treated and not treated with AD: 38 of 358 (11%) and six of 358 (1.7%) with AD vs 11 of 71 (15%) and two of 71 (2.8%) in the untreated group, respectively. Similarly, there was no significant difference in progression between treated and untreated patients with anterior MI, 14 of 144 (10%) vs five of 32 (16%); inferior MI, 21 of 111 (19%) vs five of 26 (19%), or subendocardial MI, three of 103 (3%) vs one of 12 (8%). Bundle branch block (BBB) (without AV block) was initially present in 89 of 249 (21%). The incidence of AV block (seven of 24, 30%) was higher in treated patients with newly acquired BBB (27 patients) than in the untreated patients (none of three, p less than 0.05). The commonly used ADs did not adversely affect AV conduction in patients with acute MI with narrow QRS and either normal, first-degree, or Mobitz I AV block. Moreover, no subset of patients grouped by infarct location, specific AD used, or BBB (except perhaps for those with newly acquired BBB) appeared to be at risk of development of AV block during AD therapy.

Aged↗
PubMed1980

Bundle branch block.

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Anti-Arrhythmia Agents↗