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a Department of Cardiothoracic Surgery, Appalachian Regional Healthcare System, 260 Hospital Dr, South Williamson, KY 41503
b Department of Surgery, Department of Cardiothoracic Surgery, The University of Tennessee HSC, 6029 Walnut Grove, Ste 401, Memphis, TN 38120
(Email: egarrettmd{at}cvsclinic.com).
The comments by Marchiori and colleagues [1] regarding our case report [2] are worthy of consideration, given the frequency of tricuspid valve endocarditis associated with intravenous drug abuse. To resolve this question, additional information is provided.
Shortly after the patient's initial presentation to the hospital, a computed tomographic angiogram with pulmonary embolism protocol was performed with thin slices of 0.65 mms. No evidence of pulmonary embolism was identified on this study. In addition, no micro-thromboembolism was identified in the microscopic pathologic evaluation. Neither blood cultures nor an erythrocyte sedimentation rate were obtained. An echocardiogram was also not performed on the initial admission. However, in response to the questions raised by Marchiori and colleagues [1], the patient has been contacted and re-evaluated. An echocardiogram appeared completely normal. Specifically, there was no evidence of vegetation or more than a trace regurgitation affecting any of the four cardiac valves.
Although the radiologic evidence of septic embolization could be transient, and tricuspid valve vegetations could have resolved with antibiotic therapy, no evidence of septic embolization was identified, whereas talc induced granulomatosis was identified in the pathologic specimen.
Marchiori and colleagues [1] present an important consideration in the differential diagnosis of pulmonary pathology in patients using intravenous drugs. However, there is no evidence that septic embolization or tricuspid valve endocarditis was involved in this case.
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