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scintigraphic evidence of cardiac dysfunction. Chest 1990; 97:1478-80. Yarom R, Yallon S, Notowitz F, Braun K. Reversible myocardial damage by scorpion venom in perfused rat hearts. Toxicon 1974;12:347-51. Bawaskar HS, Bawaskar PH. Prazosin for vasodilator treatment of acute pulmonary oedema due to scorpion sting. Ann Trop Med Parasitol 1987:81:719-23. Safer S, Gueron M. Vasodilators and hypertensive encephalopathy following scorpion envenomation in children. Chest 1990;97:118-20. Gueron M, Ovsyshcher I. What is t,he treatment for the cardiovascular manifestations of scorpion envenomation? Toxicon 1987;25:121-4. Bawaskar HS, Bawaskar PH. Prazosin in management of cardiovascular manifestations of scorpion sting. Lancet 1986; 1:510-11. Radha Krishna Murthy K, Vakil AE. Elevation of plasma angiotensin levels in dogs by Indian red scorpion (Buthus tamulus) venom & its reversal by administration 01’ insulin + tolazoline. Indian J Med Res 1988;88:376-9. Radha Krishna Murthy K, Vakil AE, Yeolekar ME, Vakil YE. Reversal of metabolic and electrocardiographic changes induced by Indian red scorpion (Buthus tam&s) venom by administration of insulin, alpha blocker & sodium bicarbonate. Indian J Med Res 1988;88:450-7. Gueron M, Sofer S. Vasodilators and calcium blocking agents as treatment of cardiovascular manifestations of human scorpion envenomation. Toxicon 1990;28:127-8.
4/8/45837
SINGLE-VESSEL
PTCA
To the Editor: In our article’ on long-term follow-up after single-vessel percutaneous transluminal coronary balloon angioplasty (PTCA), four changes should be made to Table I (page 1160). In the fifth row (“MI before PTCA”), the second column should indicate 232/496 patients; in the fifteenth row (“Repeat angiograms performed”), the second column should indicate 582/648 patients. In the fourth (“Age”) and eighth (“Coronary score”) rows, the numbers in the third column should be deleted. Finally, the last sentence of the Results section (page 1165), should be as follows: “Younger patients, those who had no history of myocardial infarction before PTCA, those with LAD disease, and those who were free of anginal symptoms at follow-up were more likely to be working than other patients (Table IV).” Christoph Kadel, MD Abteilung fiir Kardiologie Universittitsklinik Frankfurt Theodor-Stern-Kai 7 D-6000 Frankfurt/Main German) REFERENCE
1. Kadel C, Vallbracht C, Buss F, Kober G, Kaltenbach M. Long-term follow-up after percutaneous transluminal coronary angioplasty in patients with single-vessel disease. AM HEART J 1992;124:1159-69. 4/8/4tw59
Q FEVER-INDUCED
EMF
To the Editor: We report an exceptional case of Q fever complicated by endomyocardial fibrosis. A -IO-year-old man was referred to the hospi-
American
June 1993 Heart Journal
tal for investigation of embolic heart disease 3 weeks al&r a trite sient cerebrovascular accident. He had no known medical or su: gical history. Asthenia and exercise dyspnea (New York Heart Association grade II) were the only functional symptoms. Physlcal examination on admission showed no abnormalities. The patient was apyretic. The chest radiograph was normal, and the electrocardiogram showed sinus rhythm with symmetric negative T wave in all derivations. No intlammatory biologic syndrome or hypereosinophilia were found. Results of the investigation of the complement system and the circulating immune complexes and electrophoresis of serum proteins were normal. Echocardiography showed bivent,ricular endomyocardial fibrosis with typical biventricular apical obliteration predominantly in the right cavity, sep tal thickening, and thrombi on contact, with strong echoes emanating from the endocardial surface, one of which was 1 cm across, rounded, and mobile: there were no valvular vegetations. Right cardiac catheterization was found to be normal. Endomyocardial biopsy 01’ the right vent,ricle showed patches of fibroelastosis overlaid by thick bands of collagenous fibrous tissue. Q-fever infection was diagnosed because I’osiella burnetil was isolated from three blood samples. Results of serodiagnosis of Q fever pointed towards a chronic fortn of the infection (antiphase I: immunoglobulin (lg) G 1600, IgM 50, and IgA 800; antiphase II: lg(; 1600, IgM 50, and IgA 800). Because of the increase in phase I 1gA. it was very likely that the heart was affected.’ Positive immunolluorescence with anti-C. burnetii serum was obtained on section of myocardial biopsy. Treatment with doxycycline at a dose of 2(10 mg per day associated with hydroxychloroquine at a dose of 600 mg per day was started. Thirteen months later the patient was asymptomatic. Echocardiography showed that only the two apexes were filled; there was calcification of t,he endocardium at the I ip of’ the left ventricle. The thrombi had disappeared, and cardiac function was normal. The biologic examination results were normal. C. burnetii is frequently reported as an agent of chronic endocarditi&“; however, to our knowledge this observation is the first description of endomyocardial fibrosis (EMF) resulting from C. burnetii. Many agents have been implicated in the cause of EMF”; however, none has been conclusively demonstrated to be consistently associated with the development of massive endocardial fibrosis. Our report provides evidence of a direct manifestation of the infection of the heart. It suggests that in cases of temperate EMF serologic studies be carried out. P. Chevalirr, Ml) E. Moncnda, MD C. Kirkorian, MD P. Touboul, MD J. E3’tirnrw, MD 1). Rnoult. MI) iinitij 51 Hbpital Cardiologiquc 59 Boulevard Piwl 69394 Lyon. Cedex O.‘l Frnnw REFERENCES
1. Peacock MG, Philip RN, Williams JC, Faulkner RS. Serological evaluation of Q fever in humans: enhanced phase I titers of immunoglobulins G and A are diagnosis for Q fever endocarditis. Infect Immun 1983:41:1089-98. 2. Palmer SR, Young SEJ. Q-fever endocarditis in England and Wales, 1975-1981. Lancet 1982;2:1448-9. 3. Raoult D, Etienne J, Massip P, Iacono S, Prince SA, Beaurain P, Benichou S, Auvergnat JC, Mathiew P, Bachet P. Q-fever endocarditis in the South of France. .J Infect Dis 1987: 155:570-X