BRIEF REPORTS the only incident occurred in a patient with sinus node Tenormine in man. Eur J Cardiol 1979,9:333-342. dysfunction. Unfortunately, many of the children with 3. Robinson C, Birkhead J, Crook B, Jennings K, Jewitt D. Clinical electrophysio- atria1 flutter are prone to developbradycardia-tachycar- logical effects of atenolol--a new cardioselective beta blocking agent. Br Heart J 1978;40:14-21. dia syndrome, limiting the usefulness of /3 blockers. 4. Pimenta J, Britto Pereira C. Effects of atenolol in patients with reciprocating Atenolol is effective, relatively free of side effectsand supraventricular tachycardia. C/in Cardiol 1986,9:191 -I 95. convenient to administer with once-daily dosing at ap- 1. Lindsay BD, Saksena S, Rothbart ST, Herman S, Barr MJ. Long term efficacy and safety of beta-adrenergic receptor antagonists for supraventricular tachycar- proximately 1 mg/kg/day. It is therefore an attractive dia. Am J Cardiol 1987,60:63D-700. alternative @ blocker for long-term suppression of supra- 6. GarsonA, Bink-Boelkens M, He&in RS, Hordof AJ, KeaneJF, Neches WH, ventricular tachycardia in children and adolescents. Porter CJ. Atria1 flutter in the young: a collaborative study of 380 cases. JACC 1985.6:871-878. 1. Gillette PC, Wampler D, Garson A, Porter CJ. Tachycardia in children. In: Josephson ME, Wellens HJ, eds. Tachycardias: Mechanisms, Diagnosis, and Treatment. Philadelphia Lea and Febiger, 1984:241-257. 2. DiBiase M, Favale S, Rizzon P. Electrophysiologic properties of intravenous 7. Gillette PC, Kugler JD, Garson A, Gutgesell HP, Duff DF, McNamara DG. Mechanisms of cardiac arrhythmias after the Mustard operation for transition of the great arteries. Am J Cardiol 1980:45:1225-l 230. 8. Serbelescu R. Atenolol in the treatment of cardiac dysrhythmias. Acfa Ther 1977:3:109-116. Increase in Plasma Atrial Natriuretic Factor During Ventriculoatrial Pacing Kenneth A. Ellenbogen, MD, Ketan Kapadia, Bs, Mary Walsh, PhD, and Prarnod K. Mohanty, MD A trial natriuretic factor (ANF) is a peptide produced by the atria in response to increases in atria1 pres- sure, volume or stimulation frequency.’ ANF has been shown to be a potent arterial vasodilator at physiologic concentrations during arterial infusions in normal sub- jects.2 Previousstudiesfrom this laboratory have shownthat ventriculoatrial (VA) pacing with a VA interval of 100to 150ms is associated with increases in right and left atria1 pressure.3 It has been suggested that increasedANF re- lease due to atria1 distensionmay play a role in the hypo- tension that occursin patients with pacemaker syndrome who have VVI pacemakers and intact (retrograde) VA conduction.4v5 We undertook this study to examine the relation betweenvascular tone measured by forearm ve- nous occlusion plethysmography and circulating ANF during VA pacing. We studied 16 adult patients referred for electro- physiologic study to evaluate symptomatic cardiac ar- rhythmias. All cardioactive medications were withheld for at least 4 half-lives. Studies were performed in the fasting, nonsedated state after written informed consent was obtained. The protocol was approved by institution- al review boards of Virginia Commonwealth University and the Veterans Administration Medical Center. Two multipolar catheters were introduced percuta- neously and positioned in the right atria1 appendage and right ventricular apex. A 7.5Fr Swan-Ganz catheter was positioned in the pulmonary artery for recording phasic and mean right atrial, pulmonary artery and pulmonary capillary wedge pressures. Cardiac output was mea- From the Division of Cardiology, 111 J, Department of Medicine, McGuire Veterans Administration Medical Center, 1201Broad Rock Boulevard, Richmond, Virginia 23249, the Medical Collegeof Virginia, Richmond, and Wayne State University School of Medicine, Detroit, Michigan. This study was supportedin part by funds from the Veterans Administration, Washington,DC. Manuscript receivedMarch 9,1989; revisedmanuscript receivedand accepted April 21, 1989. 236 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 64 sured in triplicate by the thermodilution method. An 18- gauge cannula was inserted into the right brachial artery for continuous arterial pressure monitoring. Atria1 (AAZ), ventricular (VU) and VA pacing was performed at 100 beatslmin with a programmable stimulator at 2 times diastolic threshold and a 2-ms pulse width for a 5- minute duration. Forearm blood flow was measured by venous occlu- sion plethysmography with a mercury-in-silastic strain gauge plethysmograph (EC-3 or EC-4; D. E. Hokan- son). The technique of venous occlusion plethysmogra- phy used has been described previously in detail6 ANF was measured by radioimmunoassay using techniques described previously.7 The normal range in our labora- tory is 1 to 30 fmol/ml, and sensitivity is 3 fmolltube. The detailed protocol for pacing, hemodynamic mea- surements, forearm blood flow recording, and blood samplingfor hormonal assays in our laboratory has been previously described.7 ~p<0.0001--------------1 ap<o.olF 200 -p<oo1 T " 150 E 1 5 100 (L 2 50 0 Baseline AAI VVI VA FIGURE 1. Plasma ANF lsvek (mean f stamlard emw ol the llUSll)for66dlpadnglI?6d6.