Kenneth A. Ellenbogen

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebsteins anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p less than 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.

Accessory Nodoventricular (Mahaim) Fibers: A Clinical Review

In 1937, Mahaim described the existence of islands of conducting tissue extending from the atrioventricular [AV) node into the ventricular myocardium. Subsequent anatomical studies have shown that true continuity between these extensions of conducting tissue and ventricular myocardium is uncommon.^^ On the basis of pathological studies, Mahaim fibers have been classified according to their site of origin into nodoventricular fibers originating from the AV node and fasciculoventricular fibers which connect the specialized conducting system of the heart to ventricular myocardium. In 1971, Wellens reported the results of a detailed electrophysiologic study in a patient with such a connection.* Since the first description of these connections, a substantial body of data has accumulated, implicating participation of these fibers in cardiac arrhythmias. A variety of arrhythmias have been described in patients with nodoventricular (NV) fibers. The fiber may participate as a necessary link or as a component of the tachycardia circuit as in Mabaim reentrant tachycardia (RT), where antegrade conduction occurs over the NV fiber and retrograde conduction occurs via the His-Purkinje system. Alternatively, the fiber may function as an innocent bystander during AV node reentry, atrial flutter, atrial fibrillation, or otber atrial arrhythmias. Tbese wide QRS tachycardias may be difficult to differentiate from ventricular tacbycardia.

Characterization of retrograde conduction by direct endocardial recording from an accessory atrioventricular pathway

Accessory pathway electrograms are rarely recorded in patients with Wolff-Parkinson-White syndrome. In one patient, during electrophysiologic study, simultaneous local ventricular (V) accessory pathway (AP) and atrial (A) deflections were recorded during bipolar catheter endocardial mapping over the pathway. Analysis of changes in electrographic intervals during performance of the ventricular extrastimulus technique allowed characterization of the retrograde conduction properties of the pathway. As coupling intervals were decreased, an initial increase was seen in the AP2A2 interval with subsequent ventriculoatrial block between the accessory pathway and atrium. When coupling intervals were further decreased, the V2AP2 interval lengthened with ultimate block between the ventricle and accessory pathway. These findings support the concept of impedance mismatch as the cause of conduction block in accessory pathways with the distal junction of the accessory pathway being the most vulnerable.

Cardiac function in patients on chronic amiodarone therapy

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Few data are available describing the chronic effects of amiodarone on myocardial function. To assess the effects of amiodarone on cardiac function, we studied 41 consecutive patients with first-pass or equilibrium radionuclide angiography prior to and 3 months after drug therapy was initiated. The mean heart rate, systolic blood pressure (BP), and diastolic BP were not significantly altered by treatment. The mean ejection fraction was 36% +/- 19 (mean +/- 1 SD) at the time of drug initiation and 36% +/- 17 3 months later (p less than 0.05). Nineteen patients had an ejection fraction greater than 30% and 16 had an ejection fraction less than 30%. The mean change in ejection fraction for these two subgroups showed no statistically significant difference, although a decrease in EF greater than 10% was seen in three patients (symptomatic in two), necessitating an increase in diuretic dose. No correlation between amiodarone dose and change in ejection fraction (r = -0.12, p greater than 0.05) was noted. There was no correlation between baseline ejection fraction and change in ejection fraction over this 3-month period (r = -0.36, p greater than 0.05). In summary, amiodarone does not depress left ventricular function and as a result can be used safely in patients with mild to moderate impairment of left ventricular function. In patients with stable left ventricular function, serial tests of left ventricular function may not be necessary.

Catheter atrioventricular junction ablation for recurrent supraventricular tachycardia with nodoventricular fibers

Abstract Patients with nodoventricular (Mahaim) fibers are predisposed to the development of a variety of arrhythmias, which are usually amenable to pharmacologic management. 1 Closed-chest catheter atrioventricular (AV) junction albation, which has been shown to be an effective treatment for supraventricular tachycardia, 2,3 has recently been applied in a patient with tachycardia involving a Mahaim fiber. 5 We report observations in 2 cases in which tachycardia was effectively controlled using this technique, including 3-year follow-up of nodoventricular fiber conduction in 1 patient and absence of retrograde conduction in both patients. The inability of the nodoventricular fibers to conduct retrogradely has not been previously described.

Pharmacodynamics and pharmacokinetics of oral pirmenol

The efficacy, pharmacokinetics, and pharmacodynamics of pirmenol, a class Ia antiarrhythmic agent, were studied in patients with frequent symptomatic premature ventricular complexes (PVCs). Pirmenol was given every 12 hours to eight patients in a dose‐ranging protocol, and median PVC suppression of 94% (range 72% to 100%) was achieved. The median effective pirmenol dose was 300 mg/day (range 200 to 500 mg/day), and mean (± SD) trough plasma pirmenol concentration at the effective dose was 0.98 ± 0.29 µg/ml. The mean half‐life of elimination was 10.5 ± 2 hours. There was considerable overlap among patients with respect to plasma pirmenol concentration and times at which PVC frequency returned to 25%, 50%, and 75% of baseline during drug washout trials. Altering pirmenols dose interval (while maintaining a constant daily dose) from 12 to 6 hours did not improve drug efficacy. Pirmenol was given to seven patients for long‐term therapy (24 to 44 months). Median PVC suppression at 24 months was 70%. Pirmenol is safe and well tolerated, and it can be administered twice daily for PVC suppresssion.

Effects of bolus injection of esmolol in healthy exercising subjects

Esmolol is an investigational ultra‐short‐acting β‐adrenergic blocker that has potential application in many clinical cardiology settings. The purpose of this study was to investigate the effect of a bolus dose of esmolol on heart rate, blood pressure, and PR interval in healthy, exercising male subjects. We gave a single esmolol bolus over 30 seconds to 13 men who exercised to a predetermined target heart rate. Each subject performed the exercise protocol twice, receiving a different dose between 10 and 300 mg each time. An additional eight subjects received two esmolol boluses 5 minutes apart while performing the same exercise protocol. Esmolol doses of 180 mg or greater caused a 13% to 18% decrease in heart rate, an 11% to 18% decrease in blood pressure, and a 13% to 22% prolongation of the PR interval. The median time to peak esmolol effect was 1 minute for heart rate, 2 minutes for blood pressure, and 4 minutes for PR interval. The median time required to recover 50%, 75%, and 90% of the decrement in heart rate was 8, 10, and 13 minutes, respectively. The rapid onset and disappearance of esmolol effects may make it an appealing drug in acute care settings.

Utility of Introducing Ventricular Premature Complexes During Reciprocating Tachycardia in Specifying the Location of Left Free Wall Accessory Pathways

The usefulness of the response to single and double ventricular premature complexes (VPCs) introduced during reciprocating tachycardia (RT) in predicting the location of a left free wall accessory pathway was studied in 55 patients with the Wolff-Parkinson-White syndrome. One VPC introduced from the right ventricle into narrow QRS RT when the His bundle was refractory resulted in retrograde atrial preexcitation in 25 of 55 (45%) patients, while 30 (55%) showed no preexcitation. Double VPCs produced retrograde atrial preexcitation in 9 of 26 patients not responding to a single VPC. No difference in RT cycle length, AH, HV or ventriculoatrial intervals was found between those patients who did or did not show retrograde atrial preexcitation. The response to single and double VPCs during RT was related to the location of the AP. The average distance of the AP from the crux determined by intraoperative epicardial mapping in the 41 patients who underwent surgery was 2.7 +/- 0.7 mapping units (left posterolateral region) in patients showing retrograde atrial preexcitation with a single VPC, 3.6 +/- 0.7 units (at the lateral left ventricular margin) in those responding to double VPCs and 4.3 +/- 0.8 units (beyond the LV margin) in those showing no response. Left bundle--branch block (LBBB) aberrancy during RT resulted in an average 60 +/- 14 ms prolongation of the ventriculoatrial interval in 40 patients, including 5 in whom LBBB was seen only after procainamide infusion. VPCs introduced into LBBB RT resulted in significant retrograde atrial preexcitation in 6 additional patients in whom no response during normal QRS RT was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Sustained Intravenous Diltiazem Infusion in Healthy Persons

A 3-stage infusion of diltiazem was tested in 8 subjects for up to 48 hours: a bolus injection (10 mg over 3 minutes), a rapid loading infusion (20 mg over 30 minutes) and a maintenance infusion (10 mg/hour to the end of the study). This regimen produced stable median plasma diltiazem concentrations of approximately 150 ng/ml. The median half-life of elimination for diltiazem was 206 minutes (range 144 to 452) and median total clearance was 980 ml/min (range 665 to 1,907). The PR interval lengthened 10 to 18% during the maintenance infusion in 7 subjects; in 1 subject atrioventricular nodal Wenckebach conduction was recorded during the rapid loading infusion. Systolic blood pressure decreased from 124 +/- 7 mm Hg (mean +/- standard deviation) during the control period to 121 +/- 8 mm Hg during the rapid loading infusion (p = 0.03 compared with control) and to 117 +/- 7 mm Hg (p = 0.04 compared with control) during the maintenance infusion. Heart rate did not change. PR interval and blood pressure returned to control levels within 4 hours after the infusion was stopped. Loading and maintenance infusion may be an attractive method of administering diltiazem when stable drug concentrations are required for prolonged periods.

Ultrasound diagnosis of pseudoaneurysm and contiguous ventricular septal defect complicating inferior myocardial infarction.

Two patients with recent inferior myocardial infarction were found by two-dimensional and Doppler echocardiography to have both an inferior wall pseudoaneurysm and a contiguous rupture of the posterior ventricular septum. The pseudoaneurysm was not suspected clinically in either patient. In one patient, a complex or dissecting septal rupture was visualized in detail. To our knowledge, the combined defect has not previously been diagnosed during life by noninvasive methods.