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J Thorac Cardiovasc Surg 1995;110:545-546
© 1995 Mosby, Inc.
BRIEF COMMUNICATIONS |
Leicester, England
From the Department of Cardiothoracic Surgery, Glenfield NHS Trust Hospital, Groby Rd., Leicester, LE3 9QP, United Kingdom.
In 1975, Chusid and colleagues
1 defined hypereosinophilic syndrome as an unexplained eosinophilia lasting more than 6 months in the presence of end-organ involvement. Cardiac involvement occurs in more than 75% of patients with the hypereosinophilic syndrome. We report a case of prosthetic valve thrombosis caused by eosinophilic endocarditis.
CASE REPORT
A 23-year-old girl of Ghanan origin was referred to us for mitral regurgitation suspected to be of rheumatic origin. She was admitted in an acute condition with pulmonary edema, and an urgent mitral valve replacement with a 29 mm St. Jude Medical prosthesis (St. Jude Medical, Inc., St. Paul, Minn.) was performed. At operation, the gross appearance of the valve suggested a rheumatic origin. Incompetence was caused by lack of leaflet mobility and was not thought suitable for repair. Preoperative echocardiography did not reveal any significant findings apart from gross mitral regurgitation.
On postoperative day 2, she had pyrexia of 38 ° C. Her leukocyte count was 41.1 x 106 cells/ml with 81% eosinophilia. She also had diarrhea. Results of blood cultures, urine culture, and stool examination and cultures did not suggest any cause. Early morning on day 4, the patient became acutely breathless and was transferred to the intensive treatment unit. A diagnosis of mitral valve prosthetic obstruction was made. She was taken to the operating room and cardiopulmonary bypass was quickly established. At operation, there was heavy pannus formation over a previously placed prosthetic valve. This obstructed both leaflets. The valve was excised and replaced with a further 27 mm St. Jude Medical mechanical prosthesis. During attempts to wean the patient from cardiopulmonary bypass, there was gross right ventricular dysfunction. The lungs looked and felt granular and were extremely difficult to inflate. Because ours is an active extracorporeal membrane oxygenation (ECMO) center, the patient was given ECMO. She continued to receive ECMO for a period of 10 days. Her eosinophil count remained high. Meanwhile, all serologic tests for various parasites were done, with negative results. Steroid treatment were ultimately commenced. Because of bleeding complications and failure to respond to ECMO, ECMO was removed, and the patient died on postoperative day 12.
Histologic examination of the native valve showed thickening of the valve cusp by dense, hyalinized, fibrous tissue. There was an increase in small-caliber blood vessels within the valve cusp. These vessels contained abundant eosinophils. At autopsy, the left ventricle showed apical endomyocardial fibrosis and marked fibrosis and thickening of the posterior mitral valve anulus. The histologic findings in the lungs were grossly masked by the ECMO and could not be commented on. The overall finding fits well with the diagnosis of eosinophilic endocarditis.
DISCUSSION
Patients with idiopathic hypereosinophilic syndrome have a variety of clinical presentations. The most common is a systemic disorder in which cardiac disease is one component. High serum levels of eosinophilic cationic proteins, with potential hypercoagulable effects, contribute to the increased prevalence of thromboembolic episodes among these patients.
We had diagnostic difficulty with our patient. Hypereosinophilic syndrome is typically seen in men in their fourth decade who live in a temperate climate. Our patient was a young girl from a tropical country who had symptoms highly suggestive of rheumatic heart disease. Echocardiography did not reveal any evidence of endomyocardial fibrosis. The only positive finding was eosinophilia. Mild eosinophilia was recorded once 3 months before her operation, when the patient was seen with tenosynovitis of her wrist joint. In retrospect, all her symptoms could have been caused by eosinophilic endocarditis, as suggested by the histologic characteristics of her valve.
Review of the literature reveals that nine patients to date have undergone operation for hypereosinophilic syndrome involving the cardiac valves. Eight underwent mitral valve replacement and one underwent annuloplasty repair. Most of the authors reported using a xenograft in their patients. Harley and coworkers 2 in 1982 used a Björk-Shiley valve in their first patient and had to replace it as a result of thrombotic obstruction by a porcine Hancock valve. Davies and colleagues 3 reported two cases, one of which involved mitral valve replacement with a Starr-Edwards valve, with no complications. The choice of valve prosthesis for this group of patients is difficult. Because of the rarity of the disease and the difficulty of diagnosis, as in our case, there are no data to evaluate the thrombotic potential and long-term structural integrity of available prosthetic valves in these patients. Mechanical valves are thrombogenic and mural thrombi are characteristic of hypereosinophilic endocarditis, so it would appear that a porcine heterograft prosthesis with additional anticoagulation would be beneficial. However, the toxic effects of eosinophilic granules on the xenograft remain to be evaluated. At autopsy in one such patient (Harley and colleagues 2), although there were no mural thrombi, small thrombi were present on the bioprostheses despite treatment with warfarin.
Review of the literature 4 further suggests that the exacerbations of symptoms in these patients, as in ours, should be treated with prednisolone 1 mg/kg and hydroxy urea 500 mg daily Once the endocarditis is under control and remission of systemic symptoms has occurred, operation should be planned for relief of cardiac symptoms.
Footnotes
J THORAC CARDIOVASC SURG 1995; 110:545-6 
References
This article has been cited by other articles:
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  N. Chaudhuri, M. St.J. Hickey, and T. J. Spyt An unexplained cluster of thrombosed bileaflet mechanical heart valve prostheses Ann. Thorac. Surg., May 1, 1999; 67(5): 1542 - 1543. [Full Text] [PDF]
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