Syncope Mediated by Posturally Induced Ventricular Tachycardia

Case Report

A 66-year-old woman with no previous history of cardiac disease or symptomatic arrhythmia began having dyspnea on exertion. Three weeks later, she sought medical attention when she developed severe substernal chest pressure, postural syncope, and near-syncope.

In the emergency department, the patient's supine blood pressure, measured using an arm cuff, was 142/78 mm Hg. Monitoring documented sinus rhythm at 82 beats per minute with episodes of ventricular bigeminy, unifocal couplets, and 10- to 14-beat runs of nonsustained monomorphic ventricular tachycardia. This tachycardia had a right bundle-branch heart block morphology, left-axis deviation, and a cycle length of 280 ms. The electrocardiogram was otherwise normal, with a QT_c interval of 410 ms. Electrolyte levels were within normal limits. The patient was treated with lidocaine, heparin, and aspirin. During the subsequent 24 hours, she continued to have short episodes of nonsustained ventricular tachycardia elicited by upright posture. Her systolic blood pressure remained greater than 90 mm Hg during ventricular tachycardia. Creatinine kinase plasma concentrations were not elevated, and no serial changes were seen on electrocardiogram.

The day after admission, while supine, the patient had isolated, unifocal premature ventricular complexes and bigeminy. She had a Bruce protocol thallium exercise test. After 1 minute of exercise, she developed episodes of nonsustained monomorphic ventricular tachycardia associated with near-syncope that were identical to her previous episodes of nonsustained ventricular tachycardia. The ventricular tachycardia resolved after the patient lay down.

Coronary angiography showed normal coronary arteries. The left ventricular ejection fraction was normal, and there were no wall-motion abnormalities on the biplane left ventriculogram. The left ventricular end-diastolic pressure was 11 mm Hg. The episodes of ventricular tachycardia began to increase in frequency and became more easily provoked with simple activity, such as rising from bed. The patient was transferred to the University of Michigan for further management.

On the evening of hospital admission, the patient continued to have bouts of nonsustained and sustained ventricular tachycardia with any activity. To prevent the tachycardia, she refused to move from a supine position. Her electrocardiogram and electrolyte level remained normal. Her vital signs while supine and the results of her physical examination were normal except for an S₄ gallop.

During a continuous 12-lead electrocardiogram recording, the head of the patient's bed was gradually raised while the patient's feet dangled over the side of the bed. As the angle of the head of the bed approached 90 degrees, the ventricular ectopy progressed from bigeminy, to couplets and triplets, to nonsustained monomorphic ventricular tachycardia, and finally to sustained ventricular tachycardia (Figure 1). During the tachycardia, the patient's symptoms were reproduced. The patient became lightheaded and developed chest pressure; her blood pressure was 88/56 mm Hg. As the head of the bed was lowered to the supine position, the severity of the tachycardia progressively diminished from sustained ventricular tachycardia to bigeminy and unifocal premature ventricular contractions. This phenomenon of postural ventricular tachycardia was reproducibly induced by changes in the position of the head of the bed. The morphology of the ventricular tachycardia was identical to that of the previous bouts of sustained and nonsustained ventricular tachycardia and was a right bundle-branch heart block pattern with left-axis deviation. The QRS duration was 130 ms, and the cycle length was 280 ms. Although the ventricular tachycardia prohibited assessment of the upright sinus rate, no physical findings suggested hypovolemia. The patient remained in bed, and an electrophysiology test was done.

When the patient arrived in the electrophysiology laboratory, her rhythm was ventricular bigeminy. After informed consent was obtained, three 6-Fr diagnostic quadripolar electrode catheters (Mansfield EP, Watertown, Massachusetts) were inserted into a femoral vein and positioned in the high right atrium, the His bundle position, and the right ventricular apex. Ventricular tachycardia was not inducible by programmed atrial or ventricular stimulation. During an infusion of isoproterenol (2 µg/min), spontaneous episodes of nonsustained ventricular tachycardia occurred. The morphology of the ventricular tachycardia was identical to that of the clinical ventricular tachycardia.

A 7-Fr quadripolar electrode catheter with a 4-mm tip electrode (Mansfield EP) was placed in the right femoral artery, intravenous heparin was administered in a bolus of 5000 U, and the catheter was advanced into the left ventricle. Pace mapping showed the site of origin of the ventricular tachycardia to be along the septal aspect of the inferobasal left ventricle. Two applications of radiofrequency energy at this site successfully eliminated all ventricular ectopy. No ectopy occurred during a 6 µg/min infusion of isoproterenol or during upright posture.

The patient remained on a telemetry unit for 48 hours and had no recurrence of ventricular arrhythmia. A treadmill test was done, and the patient exercised for 8 minutes of a Bruce protocol and had no ventricular ectopy during or after exercise. At 1 year of follow-up, the patient had no recurrence of dyspnea, chest pain, or syncope, and no recurrence of the clinical ventricular ectopy on a 24-hour ambulatory monitor.

Discussion

In patients without structural heart disease, repeated episodes of syncope related to upright posture are often caused by hypovolemia, autonomic insufficiency, or vasodepressor syncope. However, we describe an example of recurrent syncope caused by postural idiopathic left ventricular tachycardia. The only other reported case of orthostatic ventricular tachycardia occurred in 1945 and had a left bundle-branch heart block pattern with an inferior axis, consistent with a site of origin in the right ventricular outflow tract [1]. Each of these tachycardias was exquisitely sensitive to increases in adrenergic tone, which may account for the marked exacerbation seen with postural changes. Although it is unusual, postural idiopathic ventricular tachycardia should be considered in the differential diagnosis of recurrent orthostatic syncope, even in patients without structural heart disease.

Idiopathic left ventricular tachycardia may originate in the left posterior fascicle and is often successfully ablated with radiofrequency current [2, 3]. The mechanism of idiopathic left ventricular tachycardia may be either reentry, triggered activity, or abnormal automaticity. In the case described here, the inability to induce ventricular tachycardia by pacing and the induction by isoproterenol infusion suggest that the ventricular tachycardia was caused by abnormal automaticity.

Dr. Dimitrijevic: 43421 Garfield, Mt. Clemens, MI 48044.

@copy; 1995 American College of Physicians