Volume 121

Number 5

the cardiac arrest (exercise-induced ventricular fibrilla- tion), we thought that coronary bypass surgery was indi- cated. We decided to use the internal mammary artery for this purpose, since it is a live conduit capable of adapting to a growing organism and ensures a longer patency of the graft.

With improvements in transport and resuscitation of critically ill patients, coronary artery aneurysms with sud- den death in adults after Kawasaki disease may be ob- served more frequently in the future and should be consid- ered within the natural history of the chronic evolution of the disease.

REFERENCES

1.

2.

3.

4.

5.

6.

Kato H, Jchinose E, Yoshioka F, et al. Fate of coronary aneu- rysms in Kawasaki disease: serial coronary angiography and long-term follow-up study. Am J Cardiol 1982;49:1758-66. Brecker SJD, Gray HH, Olddershaw PJ. Coronary artery an- eurysms and myocardial infarction: adult sequelae of Ka- wasaki disease? Br Heart J 1988;59:509-12. Maroto E, Rodriguez JC, Garcia-Dorado D, et al. Evaluation cardiologica de la enfermedad de Kawasaki: protocolo de es- tudio. Rev Esp Cardiol 1987;40:327-32. Pounder DJ. Coronary artery aneurysms presenting as sudden death 14 years after Kawasaki disease in infancy. Arch Path01 Lab Med 1985;109:874-6. Kohr R. Progressive asymptomatic coronary artery disease as a late fatal sequela of Kawasaki disease. J Pediatr 1986;108: 256-9. Wit AL, Bigger JT. Possible electrophysiological mechanisms for Iethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 1975;51-52(suppl 111):96-115.

Late thrombosis of a coronary artery mycotic aneurysm

Alexander Davidson, MD, Eshagh Eshaghpour, MD, Nancy Young, MD, and Gary S. Mintz, MD. Philadelphia, Pa. Mycotic aneurysm is a known complication of bacterial endocarditis developing most commonly in the cerebral vessels and usually rupturing during or shortly after the active infection. We describe an unusual case of a coronary artery mycotic aneurysm, which was complicated by fatal thrombosis 2 years after the active endocarditis.

A 14year-old black girl underwent bilateral bunionec- tomy. Results of cardiac examination at that time were normal. Two weeks later she was seen with fever, stupor, hemiplegia, petechiae, and splinter hemorrhages. She was found to have acute bacterial endocarditis; the organism was methicillin-resistant Staphylococcus aureus. She had severe mitral regurgitation and heart failure, and echocar-

From the Departments of Pediatrics, Pathology, and Medicine, Hahnemann University Hospital. Reprint requests: Alex Davidson. MD, Dept. of Pediatric Cardiology, St. Christopher’s Hospital for Children Front & Erie Streets, Philadelphia, PA 19134.

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Brief Communications 1549

diography showed large vegetations on the mitral valve. In spite of appropriate antibiotic therapy (ampicillin and gentamicin, and later vancomycin), she remained febrile and blood cultures remained positive. At surgery the mitral valve was found to have a large perforation of the anterior leaflet, vegetations on both leaflets, and rupture of the an- terior papillary muscle. The valve was replaced with a 25 mm St. Jude prosthesis. There was no underlying patho- logic condition in the mitral valve. Cardiac catheterization was not performed before valve replacement, and at the time of surgery the coronary arteries were not noted to be abnormal. She did well for the ensuing 2 years but did not comply with anticoagulation therapy. One day after a routine and unremarkable outpatient visit, she collapsed suddenly. She was found to be agitated, confused and combative, but she could move all extremities. Results of emergency computed tomography of the head were normal. Cardiac examination findings were unremarkable. An acute inferolateral wall infarction was seen on ECG. Echocardio- graphy showed normal prosthetic valve function and ex- tremely poor left ventricular systolic contraction. She then went into cardiac arrest. After she was resuscitated an emergency catheterization was performed. Results of an- giography showed a large aneurysm in the proximal left circumflex coronary artery with a filling defect (Fig. 1). The patient died in the catheterization laboratory. At autopsy there was an aneurysmal dilatation in the proximal left circumflex coronary artery measuring 12 mm in diameter. The arterial wall was abnormal. The intima and most of the media were replaced by fibroblasts, and the elastic lamina was destroyed. The vessel was occluded by a thrombus. There was recanalization of the artery at the periphery of the thrombus, indicating that at least part of it was old (Fig. 2).

Mycotic aneurysms account for approximately 2.6 %, of all aneurysms.’ Bacterial invasion of the vasa vasorum or intima progresses to necrotic destruction of the vascular wall producing aneurysmal dilation; there is a high pro- pensity for rupture during or shortly after the acute endocardial infection.* The term “mycotic” aneurysm was coined by Osler3 in 1885. Mycotic aneurysms appear early in the course of endocarditis, even if their clinical evidence may be delayed. 4-6 However, aneurysm of the coronary ar- teries is only rarely mycotic.7

Our patient had fatal thrombosis of a coronary artery mycotic aneurysm 2 years after the episode of endocardi- tis. It is likely that the coronary mycotic aneurysm was formed during the initial staphylococcal endocarditis and that it thrombosed acutely 2 years later. In the presence of a prosthetic mitral valve, the possibility exists of an embo- lit event. The angiogram in our patient shows that the thrombus filling the mycotic aneurysm is much larger that the proximal segment of the circumflex coronary artery. Therefore it formed in situ. This fatal complication may have been preventable had the patient complied with the anticoagulation therapy. To our knowledge this is the first description of a mycotic aneurysm thrombosis occurring years after the original episode of bacterial endocarditis.

May 1991 1550 Brief Communications

REF ERENCES

2.

9 I

American Heart Journal

Fig. 1. Coronary arteriogram showing irregular shaped aneurysm on proximal circumflex artery (arroug

with filling defect.

Fig. 2. Histology of mycotic aneurysm showing replacement of normal arterial wall by fibroblastic ingrowth, thrombus (7’) in arterial lumen, and recanalization (arrow) in arterial wall.

docarditis and their management. Arch Intern Me 146:953-i.

Parkhurst GF, Decker JP. Bacterial aortitis and mycotic an- eurysm of the aorta. A report of twelve cases. Am J Path01 1955;31:821-35. Siegel MJ, McAlister WH. Aortic aneurysms in children. Ra- diology 1979;132:615-17. Osler W. Gulstonion lectures on malignant endocarditis. Br Med J 1885;1:467-70. Weinstein I. Life-threatening complications of infective en-

5. Bergsland .J. Kawaguchi A, Roland .JM, Peironi DR, manian S. Mycotic aortic aneurysms in children. Ann Surg 1984;37:314-18.

6. Pellet& LL, Petersdorf RG. Infective endocarditis: e of 125 cases from the University of Washington Hc 1963-72. Medicine 1977;56:287-313.

7. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneur the coronary artery. Am .J Cardiol 1963;2:228-37.

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