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W E Gaum

Publications and source records attributed to W E Gaum.

11 recordsLinked to original sources

Age-related changes in electromechanical properties of canine ventricular muscle: effect of ouabain.

In this report, alterations between the electrical and mechanical responses of isolated neonatal and adult canine ventricular muscle preparations before and after ouabain exposure are described. No significant differences were observed between the two age groups in the concentration-dependent effects of ouabain on increasing contractile force or decreasing maximum diastolic transmembrane potential. The action potential plateau duration was decreased by high concentrations of ouabain (0.3-1 microM) in both neonatal and adult ventricular muscle. In addition, more adult preparations developed delayed afterdepolarizations associated with aftercontractions after exposure to ouabain than did neonatal preparations. These results suggest that the higher glycoside tolerance in neonatal dogs as compared with adults may be due in part to differences in the mechanisms responsible for development of abnormal ventricular automaticity. The results may also indicate that immature animals do not require higher glycoside levels to produce augmentation of cardiac contractility.

Aging

Accelerated ventricular rhythm in childhood.

Four patients, aged 6 to 14 years, with accelerated ventricular rhythm were studied from June 1976 to June 1978. Three were asymptomatic and had no evidence of cardiac disease. One patient had equivocal evidence of myocarditis. All four patients are well without therapy. The benign nature of this rhythm and the importance of its differentiation from ventricular tachycardia is stressed.

Adolescent

Influence of excitability on the ventricular fibrillation threshold in dogs.

The influence of the excitability threshold on the ventricular fibrillation threshold was studied in dogs during myocardial ischemia and potassium and aprindine infusion. Interventions that influenced excitability threshold were associated with similar changes in ventricular fibrillation threshold although the percent change in both values differed. Although it is possible that the interventions studied caused parallel but independent changes in excitability threshold and ventricular fibrillation threshold, it is likely that the excitability threshold influences the ventricular fibrillation threshold. An increase in excitability threshold could result in an increase in ventricular fibrillation threshold in spite of an increase in the actual tendency of the heart to fibrillate spontaneously. Such discordance between the "electrical stability of the heart" and the ventricular fibrillation threshold was found during myocardial ischemia.

Animals

Effect of drugs on conduction delay and incidence of ventricular arrhythmias induced by acute coronary occlusion in dogs.

The effects of various drugs on delayed activation of the ischemic myocardium and the incidence of ventricular arrhythmias were studied in 34 open-chest anesthetized dogs. The left anterior descending coronary artery was occluded for 6 minutes before and 42 minutes after administration of aprindine (2.85 mg/kg body weight), quinidine (8 mg/kg) and verapamil (0.2 mg/kg) and during infusion of isoproterenol (0.2 microng/min). The time intervals from the onset of the QRS complex to the major deflection of the bipolar electrograms recorded within the normal and ischemic zones were measured at cycle lengths of 500, 400 and 300 msec and were correlated with the development of ventricular arrhythmias. At a cycle length of 500 msec, aprindine increased by 19.5 msec the delay in activation time produced by coronary ligation alone (P less than 0.05), whereas verapamil reduced by 10 msec the extent of ischemia-induced conduction delay (P less than 0.05). The delay in activation time in the ischemic zone was not significantly altered by quinidine or isoproterenol. The incidence of ventricular arrhythmias was increased by aprindine (from 1 in 11 to 8 in 11 dogs), decresed by verapamil (from 3 in 7 to 0 in 7 dogs) and was not changes by quinidine or isoproterenol. Thus, delayed activation of the ischemic myocardium appears to play an important role in the genesis of early arrhythmias due to myocardial ischemia, and drugs that significantly depress conduction in the ischemic myocardium may predispose to the development of ventricular arrhythmia whereas those that improve conduction may be protective. Contrary to their effects on slow channel-dependent conduction, verapamil improved and isoproterenol worsened conduction during ischaemia.

Animals

Atrial tachycardia without P waves masquerading as an A-V junctional tachycardia.

Two patients who presented by scalar ECG with an A-V junctional tachycardia were demonstrated during an electrophysiologic evaluation to have an atrial tachycardia without P waves in the surface ECG. Case 1 had an atrial tachycardia that conducted through the A-V node with a Wenckebach block. Atrial activity was recorded only from the proximal portion of the coronary sinus and from right atrial areas near the tricuspid valve. Case 2 had an atrial tachycardia that abruptly began and terminated following carotid sinus massage. Atrial activity was recorded only in the coronary sinusos, and pacing at that site resulted in atrial capture, with Wenckebach conduction to the ventricles. These observations demonstrate that an atrial tachycardia without P waves can simulate A-V junctional tachycardia with or without Weckebach block. Such findings may have a bearing on some important electrophysiologic concepts such as the origin of A-V junctional rhythms and the need for atrial participation in A-V nodal re-entry.

Atrioventricular Node

Alterations in canine myocardial excitability during ischemia.

Changes in the ventricular diastolic excitability threshold following occlusion of the left anterior descending coronary artery (LAD) were studied in open-chest anesthetized dogs by using a new automatic threshold-following pacemaker (ATFP). The ATFP measures the diastolic excitability threshold by successively decreasing the duration of regularly occurring pacing stimuli until the ventricle fails to respond. Under control conditions, the threshold stimulus duration was 60 +/- 4 (mean +/- SEM) musec. In the first 1-3 minutes following occlusion of the LAD, the diastolic excitability threshold in the ischemic zone (IZ) decreased to 51 +/- 5 musec and then rapidly increased to 600 musec at 5 minutes. The initial decrease in excitability threshold at IZ could be abolished by elevating the serum K+ concentration prior to the LAD occlusion. These changes in excitability threshold at IZ could be prevented by infusing nonoxygenated solutions into the LAD at a site distal to the occlusion. As the excitability threshold increased in IZ during ischemia, the earliest time at which IZ could be reactivated by a stimulus with a voltage equal to twice the preligation diastolic voltage threshold was increased. In nine of 16 dogs, after 5 minutes of LAD ligation, the IZ to normal zone (NZ( activation time (when stimulating at IZ) exceeded the NZ to IZ activation time (when stimulating at NZ) by an average of 9 msec. We also found that in four dogs the NZ to IZ activation time exceeded the IZ to NZ activation time by an average of 10 msec. We conclude from these findings that a gradient of increasing excitability threshold exists as one moves from normally perfused toward more ischemic tissue, passing through a heterogenous border zone that manifests some areas which have a decreased excitability threshold and other areas which have an increased excitability threshold, and that these changes in excitability importantly influence the determination of refractory period durations and conduction times.

Animals

Dissimilar atrial rhythms in a patient with the Wolff-Parkinson-White syndrome.

In this report, we present the findings in a patient who had paroxysmal supraventricular tachycardia and atrial flutter associated with the Wolff-Parkinson-White syndrome. During atrial flutter, localized atrial fibrillation was recorded in the coronary sinus (dissimilar atrial rhythms), near the accessory pathway; and during 90 minutes of observation, ventricular activation occurred solely over the normal pathway. We postulate that localized atrial fibrillation repetitively invaded the accessory pathway and rendered it refractory to conduction by flutter impulses.

Atrial Fibrillation

When is echocardiography unreliable in patients undergoing catheterization for pediatric cardiovascular disease?

Technologic advances in echocardiography (e.g., better spatial resolution, Doppler, and color flow mapping) have improved our ability to demonstrate anatomy and physiology in previously problematic conditions, precluding catheterization and angiography in some instances. However, diagnostic catheterization remains necessary in other instances. The aims of this study were to determine whether echocardiography alone was sufficient to delineate the anatomic and flow abnormalities in patients subsequently selected to undergo catheterization and, if not, under what circumstances was echocardiography unable to establish the definitive diagnosis. Echocardiograms of 252 infants and children who underwent catheterization during a 14-month interval were analyzed retrospectively to determine whether the echographic assessment was nondiscrepant (group 1) or discrepant (group 2) with the catheterization assessment. Any deviation in the complete accurate assessment constituted a discrepancy; identification of more than one discrepancy in a single patient was possible. Independent variables included patient's age, weight, operative status, use of color flow mapping, echocardiograph operator, and interval between echocardiogram and catheterization. To determine whether the discrepancies were clinically significant, data from patients in group 2 were reviewed independently by three cardiologists to determine whether patient management would have changed given the added data provided by catheterization. Echocardiographic evaluations were discrepant in 155 instances. In 54 of 155 instances (35%), discrepancies were judged to be clinically significant (group 3). Twenty-three of 54 cases (43%) involved extracardiac lesions (i.e., aortic arch, pulmonary arterial, bronchial collateral, and pulmonary venous anomalies), 20 of 54 (37%) involved pressure gradients, 7 of 54 (13%) involved intracardiac lesions, and 4 of 54 (7%) involved coronary arterial lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent