Volume 104 Number 6 Brief Communications 1385 Fig. 1. Sequential ECGs of the patient described (lead V,). A, Normal sinusrhythm prior to incident. 6, Severesinus bradycardia 25 minutes after lidocaine injection. C and D, Sinus arrest. E, Supraventricular rhythm after atropine and isoproterenol administration. of 1.2 mg/L according to Nattel et al.,’ which is believed to be the minimum clinically effective plasmaconcentration. According to their findings, the peak concentration occurs 30 to 60 minutes after drug administration. In our patient, the sinoatrial arrest appeared 25 minutes after lidocaine wasinjected. We hypothesize that the interaction between lidocaine and amiodarone, both agents which may depress the sinus node especially in patients with the sick sinus syndrome, caused the severe sinoatrial arrest. Such an interaction of these two drugs has not been reported previously. In view of the danger of sinus arrest in patients with the sick sinus syndrome undergoing permanent pacemaker implantation, a temporary pacemaker should be considered and the minimum amount of lidocaine necessary for the procedure should be used. REFERENCES 1. Nattel S, Rinkenberger RL, Lehrman LL, Zipes DP: Thera- peutic blood lidocaine concentrations after local anesthesia for cardiac electrophysiologic studies. N Engl J Med 301:418, 1979. 2. Lippestad CT, Forfang K: Production of sinus arrest by lignocaine. Br Med J 1x537, 1971. 3. Wood RA: Sinoatrial arrest: An interaction between pheny- toin and lignocaine. Br Med J 1:645, 1971. 4. Jeresaty RM, Kahn AH, Landry AB: Sinoatrial arrest due to lidocaine in a patient receiving quinidine. Chest 61:683, 1972. 5. Dhingra RC, Deedwania PC, Cummings JM, Amat-y-Leon F, Wu D, Denes P, Rosen KM Electrophysiologic effects of lidocaine on sinus node and atrium in patients with and without sinoatrial dysfunction. Circulation 57~448, 1978. 6. Brown AK, Primhak RA, Newton P: Use of amiodarone in bradycardia-tachycardia syndrome. Br Heart J 4Oz1149, 1978. 7. Touboul P, Atallah G, Gressard A, Kirkorian G: Effects of amiodarone on sinus node in man. Br Med J 42:573, 1979. Myocardiaf damage in viral hemorrhagic fevers* Jose Milei, M.D., and Narciso J. Bolomo, M.D. Buenos Aires, Argentina, and Washington, D.C. Cardiovascular alterations are not rare in Argentine hem- orrhagic fever (AHF). This disease is caused by the Junin virus, a member of the arenavirus group. AHF affects mainly young rural workers from an agricultural region known as the humid pampa. Vascular lesions such as diffuse endothelial cell swelling and arterial and arteriolar hyalinization in different organs,especially in the central nervous system, have been described.‘*2 In one series,an interstitial myocarditis was reported in 26.6% of cases2 The systemic ultrastructural lesions in AHF are charac- terized by changes of the rough-surfaced endoplasmic reticulum with tortuosity and convoluted appearanceof cisternae; intracisternal virus-like particles also occur.3 These alterations are coincident with the presence of Junin virus antigenic determinants as shownby immuno- histochemical techniques.3 In addition, myocardial involvement in AHF has been suggested,4s5 with ECG From the Section of Pathology, Hospital Instituto de Cardioiogis; and the Division of Cardiovascular Pathology, Armed Forces Institute of Patholo- gy. Received for publication June 29, 1981; revision received Sept. 11, 1981; accepted Nov. 6, 1981. Reprint requests: Dr. Jo& Milei, Hospital Institute de Cardiologia, Coronel Diaz 2423; 1425 Buenos Aires, Argentina. *The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.