cells, and cultures and fungal staining reactions were nega- tive. The specimens for biopsy revealed portions of normal pulmonary vein, bronchial mucosa, and normal alveoli, with a few chronic inflammatory cells. Unfortunately, the etiology of the lesion remains un- known, as the patient declined further investigations. Six months later, the patient remains asymptomatic, and the mass has remained unchanged in size. DISCUSSION Cerebral embolization following the endobronchial instillation of particulate contrast material has not been previously reported. One would expect this complication to be exceedingly rare, but the incidence might be ex- pected to increase if simultaneous fiberoptic transbron- chial biopsy and selective bronchography studies are performed. Propyliodone (Dionosil), one of the most common bronchography agents, is extremely viscous, whether suspensions in oil or aqueous suspensions are used. If injected via the bronchoscope through a tube with a small bore, considerable pressures are generated. Brisk bleeding is not a rare complication following trans- bronchial biopsy, 4 and inadvertent biopsy of a pul- monary vessel is usually the cause. If the contrast ma- terial is injected near the site of the bleeding and if there is a free communication between the pulmonary vessel and the bronchus, the high pressures required to inject the dye could conceivably lead to an "angio- graphic" injection. Presumably, this is what occurred in our patient, resulting in the microembolization of particulate contrast material to the cerebral cortex and the immediate grand mal seizure and subsequent tran- sient neurologic defects. The direct visualization of sys- temic embolization, the time course and the prolonged period of recovery make it unlikely that the patient had an idiosyncratic reaction to either the contrast material or the local anesthesia with lidocaine; however, the possibility of a simultaneously occurring air embolus, caused by clearing of the dead space of the poly- urethane catheter prior to injection of the contrast ma- terial, cannot be ruled out. As a result of this compli- cation, we have abandoned the use of selective trans- bronchoscopic bronchography studies where bleeding has occurred following bronchial biopsy. REFERENCES  1 Levin DC, Wicks AB, Ellis JH Jr: Transbronchial lung biopsy via the fiberoptic bronchoscope. Am Rev Respir Dis 110:4-12, 1974 2 Zavala DC: Diagnostic fiberoptic bronchoscopy: Tech- nique and results of biopsy in 600 patients. Chest 68:12-19, . 1975 3 Sackner M: Bronchofiberoscopy: The state of the art. Am Rev Respir Dis 111:62-88,1975 4 Zavala DC: Pulmonary hemorrhage in fiberoptic trans- bronchial biopsy. Chest 70:584-588,1976 CHEST, 73: 6, JUNE, 1978 Propranolol-lnduced Dysfunction of the Sinus Node in Wolff-Parkinson- White Syndrome Elliot M. Berry, M.B., and Yonathan Hasin, M.D. We report thefindingsin a patient with Wolff-Parkinson- White syndrome (type A) who initially had recurrent fainting episodes. It appeared that they were caused by prolonged posttachycardiac depression of the sinus node, which was induced by treatment with propranolol. The possibility of covert dysfunction of the sinus node in pa- tients with Wolff-Parkinson-White syndrome should be considered before commencing therapy with ^-adrener- gic blocking agents. S yncopal attacks in patients with Wolff-Parkinson- White syndrome are rare, but when such attacks occur, they may be attributed either to paroxysmal tachycardia 1 or to extreme bradycardia. 2 We describe a patient who initially had syncopal episodes that only commenced after he had been receiving therapy with propranolol. CASE REPORT A 21-year-old man was admitted because of repeated episodes of fainting and palpitations. Six months before this admission, his condition had been diagnosed as Wolff-Parkin- son-White syndrome, and treatment with propranolol (10 mg three times daily) had been started. Thereafter, the palpita- tions became less frequent, but they were followed by episodes of fainting. The findings from physical and labora- tory investigations, including an electroencephalogram, were normal. A resting electrocardiogram was typical of Wolff- Parkinson-White syndrome, type A. In an attempt to provoke a reentrant tachycardia, direct atrial pacing was performed. Figure 1 shows the patient's 12- lead ECC. Alongside the limb leads, Vi and V2, are seen the widened QRS complexes induced by atrial pacing at 120 impulses per minute. Reentrant tachycardia could not be produced by programmed stimulation of die right atrium or bundle of His; however, after one minute of atrial stimula- tion, asystole occurred consistently and reached 5.0 seconds (Fig 2, top). Treatment with propranolol was then stopped, and the examination was repeated ten days later. Figure 2, bottom (A), shows a reentrant tachycardia of 150 beats per minute, with retrograde conduction (presum- ably via the bypass tract) induced by stimulation of the His bundle. After the spontaneous cessation of the reentrant tachycardia (Fig 2, bottom [B]), there was no significant sinus arrest. Pacing of the atrium and His bundle at different rates disclosed a slightly prolonged recovery time for the sinus node. It was thus assumed that the posttachycardiac depression of the sinus node was apparently not produced by a mecha- From Internal Medicine Department B and the Intensive Cardiac Care Unit, Hadassah Medical Center, Jerusalem, Israel. Reprint requests: Dr. Hasin, Hadassah Medical Organiza- tion, PO Box 499, Jerusalem, Israel PROPRANOLONNDUCED DYSFUNCTION OF SINUS NODE 873