George J. Klein

The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways.

In this study we sought to determine whether characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia could help differentiate atrioventricular (AV) nodal reentry from orthodromic AV reentry using an accessory pathway and to identify the site of accessory pathways in patients with Wolff-Parkinson-White syndrome. Fifty-five patients with orthodromic AV reciprocating tachycardia and 22 patients with AV nodal reentrant tachycardia were studied with standard electrophysiologic techniques. There were 24 left free wall, 23 posterior septal, seven anterior septal, and one right free wall accessory pathways. Progressively premature right ventricular complexes (V2) were introduced during reciprocating tachycardia (V1V1). The V1V1 interval during tachycardia minus the longest V1V2 at which atrial preexcitation occurred defined a preexcitation index (PI). Atrial preexcitation occurred in 49 of 55 (89%) patients with AV reentry compared with only three of 22 (14%) patients with AV nodal reentry (p less than .001). In the three patients with AV nodal reentry who demonstrated atrial preexcitation, the PI was distinct from that of the septal pathways and was in the upper range of values for left free wall pathways. The percentage of tachycardias demonstrating atrial preexcitation was not different between the free wall and septal pathways, but His bundle activation was visible at the time of atrial preexcitation in only six of 17 (35%) left free wall compared with 13 of 16 (81%) posterior septal and seven of seven (100%) anterior septal pathways (p less than .05 free wall vs posterior or anterior septal).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical efficacy and electrophysiologic effects of encainide in patients with Wolff-Parkinson-White syndrome.

We performed electrophysiologic studies in 19 patients with accessory pathways before and during encainide therapy with a mean daily dose of 197 mg. Fourteen patients had manifest accessory atrioventricular connections, and five patients had concealed accessory atrioventricular connections. The patients had recurrent atrioventricular reentrant tachycardia for a mean of 15.8 years and had received a mean of 3.6 drug trials without successful suppression of recurrent arrhythmias. Encainide caused complete antegrade conduction block in the accessory pathway in eight of 14 patients with manifest accessory atrioventricular connections. The shortest atrial pacing cycle length maintaining 1:1 conduction over the accessory pathway at control study w3as 328 +/- 66 msec in patients in whom antegrade conduction block occurred, and it was 247 +/- 21 msec (p less than .01) in patients in whom conduction remained during encainide therapy. Retrograde conduction over accessory atrioventricular connections could be evaluated in 14 patients, and complete block occurred in seven patients during encainide therapy. There was no correlation between control retrograde effective refractory period or conduction of the accessory pathway and subsequent development of conduction block with encainide therapy. It should be noted that five patients who developed drug-related retrograde block over the accessory pathway had initial retrograde effective refractory periods for the accessory pathway less than 270 msec. Nineteen patients had atrioventricular reentrant tachycardia initiated at control electrophysiologic study. Encainide prevented induction of tachycardia in 10 patients, and in the other nine patients, cycle length of tachycardia increased during drug treatment from 313.9 +/- 53.1 to 418.3 +/- 80.9 msec (p less than .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 +/- 43.8 to 238.3 +/- 87.9 msec (p less than .01). Fifteen patients continued encainide treatment for a mean of 18 months (range 7 to 38), and all but one patient remain asymptomatic. Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively.

Comparison of the electrophysiologic effects of intravenous and oral verapamil in patients with paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous verapamil (a bolus dose of 0.15 mg/kg body weight followed by infusion of 0.005 mg/kg per min) were compared with those of oral verapamil (80 mg every 6 hours for 48 hours) in eight patients who had paroxysmal supraventricular tachycardia. The mechanism of tachycardia was atrioventricular (A-V) nodal reentry in four patients and A-V reentry utilizing an accessory pathway for retrograde conduction in the remaining four. The electrophysiologic effects of oral and intravenous verapamil were similar. Both preparations significantly prolonged anterograde effective and functional refractory periods of the A-V node (p less than 0.001). Both significantly increased the shortest pacing cycle length maintaining 1:1 anterograde conduction over the A-V node (p less than 0.001). Retrograde conduction over the A-V node was greatly prolonged with verapamil in one patient but was unaffected in the others. There was no significant effect on sinoatrial conduction time, sinus nodal recovery time or atrial or ventricular refractoriness. Both preparations prevented induction of tachycardia in six patients none of whom had recurrence of sustained tachycardia while receiving long-term oral therapy (5 to 10 months). Neither preparation had a significant effect in two patients and this predicted failure of long-term oral therapy in one of these patients. The results of acute drug testing with intravenous verapamil can be extrapolated to predict the electrophysiologic results and response to long-term therapy with oral verapamil.

Atrioventricular dissociation during paroxysmal junctional tachycardia.

We describe the rare occurrence of atrioventriculor dissociation in three patients during paroxysmal functional tachycardia. The mechanism of tachycardia was atrioventricular nodal reentry in two patients. The third patient had reentrant tachycardia that utilized the A V node for at least part of the reentrant circuit. This patient also had a nodoventricular pathway that may have participated in the reentrant circuit. In two patients, ventricular tachycardia was diagnosed prior to electrophysiologic assessment and medication to prevent tachycardia was not successful. After electrophysiological studies, treatment directed at suppressing AV nodel reentry prevented recurrent tachycardia. These case studies demonstrate the importance of detailed electrophysiological assessment of tachycardia in patients whose arrhythmia does not respond to empirical antiarrhythmic therapy. (PACE, Vol. 4, November‐December, 1981)

Stress myocardial imaging in mitral leaflet prolapse syndrome

Mitral leaflet prolapse syndrome has been associated with anginal chest pain, atypical chest pain, electrocardiographic abnormalities and positive stress electrocardiograms. These features overlap those of ischemic heart disease. Furthermore, coronary artery disease is frequently associated with mitral leaflet prolapse. This study evaluated the usefulness of stress myocardial scintigraphy in distinguishing these two disorders. Thirty-two patients with an angiographic diagnosis of mitral leaflet prolapse were studied. Of the 22 patients (8 men and 14 women, mean age 48 years) with a normal coronary arteriogram, 5 had typical angina pectoris, 6 had resting electrocardiographic abnormalities and 6 had a positive stress electrocardiogram; all 22 patients had a normal stress myocardial scintigram. Of the 10 patients (7 men and 3 women, mean age 55 years) with at least 70 percent stenosis of one coronary artery, 6 had typical angina pectoris, 1 had resting electrocardiographic abnormalities and 7 had a positive stress electrocardiogram. Nine of these 10 patients had one or more demonstrable perfusion defects on stress myocardial scintigrams. It is concluded that mitral leaflet prolapse syndrome is not associated with regional myocardial ischemia as demonstrated with stress scintigraphy, and that stress scintigraphy, a noninvasive technique, is useful in distinguishing the mitral prolapse syndrome from mitral prolapse associated with coronary artery disease.

Chapter 85 – The Use of Implantable Loop Recorders

The ideal diagnostic test for unexplained syncope would obtain comprehensive physiologic information during spontaneous symptoms without risk of harm to the patient. It would be accessible and inexpensive and would not rely on interpretation vagaries applied in a probabilistic manner. Clearly this test does not exist, although the implantable loop recorder represents an initial step in long-term physiologic monitoring to determine patient status during spontaneous symptoms. The periodic and unpredictable nature of events and the high spontaneous remission rate are the major obstacles to diagnosis in most patients. Other forms of testing in unexplained syncope include patient profiling such as echocardiography or an electroencephalogram. These usually provide a context for bedside formulation of a differential diagnosis and prognosis but rarely provide a specific diagnosis. Provocative testing with tilt and electrophysiologic testing are meant to uncover or provoke abnormalities that are potentially related to the cause of syncope. Considerable clinical judgment is required to interpret the results of provocative testing, as reflected by the poor predictive value of both tests. The obvious limitations of these established tests turn our attention to long-term monitoring as a step toward the gold standard of comprehensive physiologic assessment during spontaneous symptoms.

Chapter 94 – Wolff-Parkinson-White Syndrome

In 1930, Wolff, Parkinson, and White 1 described 12 otherwise healthy young people who presented with “functional bundle branch block” pattern and a short PR interval on the electrocardiogram (ECG) during sinus rhythm and had repeated paroxysms of tachycardia. It is now appreciated that this is a congenital disorder whose anatomic substrate in most patients is an accessory atrioventricular (AV) pathway, although anatomic variants exist and can give rise to a similar clinical picture. Investigations in small numbers of patients have identified genetic defects associated with ventricular pre-excitation, often but not always accompanied by cardiac hypertrophy. 2 3 4 5 The electrophysiologic characteristics of accessory pathways in four of these patients were similar to those in patients with isolated Wolff-Parkinson-White (WPW) syndrome. 5 Why these genetic defects cause ventricular pre-excitation requires further study.

Arrhythmias in Chronic Lung Disease

Patients who have pulmonary disorders, especially those with chronic obstructive pulmonary disease, often have atrial and ventricular arrhythmias. However, the pathogenesis of these arrhythmias is complex and may involve many factors. For example, these individuals often have anatomic cardiac abnormalities, such as right ventricular hypertrophy, with or without associated congestive heart failure. Cigarette smoking is protean in patients with chronic obstructive pulmonary disease, and, consequently, atherosclerotic heart disease may be present with its attendant complications. Hypoxia and hypercapnia occur in these patients and, under appropriate circumstances, can be arrhythmogenic. Patients may receive drugs that can cause arrhythmias. For example, diuretics may lead to hypokalemia, and aminophylline and adrenergic bronchodilator drugs may create the environment necessary for arrhythmias to emerge. Finally, patients with pulmonary disease are prone to any arrhythmias that occur in other people, for example, atrioventricular nodal reentry and Wolff-Parkinson-White reentry.