Upright tilt test alone [1, 2] or in conjunction with the administration of exogenous catecholamines [3] has been used to provoke neurocardiogenic syncope in patients for whom ß-adrenergic blockers have been recommended as first-line treatment. We describe a patient with neurocardiogenic syncope in whom ß-adrenergic blockade increased the frequency of syncope and caused prolonged asystole on repeat head-up tilt test.

A 37-year-old white man had a 30-year history of recurrent presyncope and syncope that occurred once or twice a year. After 20 minutes of head-up tilt at a 60-degree angle, the patient developed nausea, started yawning, and lost consciousness. The heart rate dropped to 60 beats/min, and his blood pressure was barely palpable (Figure 1). These abnormalities resolved immediately after supine position was restored.

View larger version (27K): [in this window] [in a new window]   Figure 1.

The patient took atenolol, 100 mg/d and had five episodes of syncope in the next 4 weeks. He underwent a repeat upright tilt test while receiving atenolol. After 2 minutes of tilt, the patient became nauseated and lost consciousness. The heart rate had decreased to 15 beats/min followed by complete asystole lasting 31 seconds (Figure 1). During this time, no blood pressure was palpable and he had no spontaneous respiration. The patient regained consciousness spontaneously after being restored to the supine position. Atenolol therapy was discontinued, and disopyramide, 750 mg daily, was started. A repeat tilt test during disopyramide therapy did not show any abnormality. He has had no recurrent symptoms in 6 months of follow-up.

The patient had neurocardiogenic syncope with a paradoxical response to ß-blocker therapy. Dangovian and colleagues [4] also described a patient with neurocardiogenic syncope in whom a 25-second asystole occurred during follow-up tilt on metoprolol, 100 mg/d. However, metoprolol did not increase the frequency of spontaneous syncope. The mechanism by which ß-blocker therapy may worsen the neurocardiogenic syncope is unknown. Conceivably, episodes of neurocardiogenic syncope are not always triggered by transient adrenergic surges, and a relative central hypovolemia may be of greater pathophysiologic significance in some patients. In such instances, pretreatment with ß-blockers may blunt an otherwise protective reflex sinus tachycardia; thus, the cardioinhibitory and vasodepressor reflex worsens.