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Not another case of endocarditis: Recurrent prosthetic valve dehiscense in a Chinese man
312 Not another case of endocarditis: Recurrent prosthetic valve dehiscense in a Chinese man
Dear Sir In a majority of cases, prosthetic valve (PV) dehiscence is caused by infective endocarditis (IE) with culture negative rates of less than 5%. These usually occur in patients who have received antibiotics prior to blood cultures. Therefore, in patients with atypical clinical and/or pathological features, inflammatory conditions involving the aortic root (eg. ankylosing spondylitis and giant cell arteritis) should be considered as a cause of valve dehiscence. A 53-year-old previously well Chinese man presented to our institution (Sydney, Australia) in January 2005 with symptoms of congestive cardiac failure secondary to aortic regurgitation (AR). The aortic valve was replaced in February with histopathology of the native valve revealing myxomatous degeneration. The patient made an uneventful recovery. However, he represented in April with fevers and night sweats. Transesophageal echocardiogram (TEE) revealed valve dehiscence with regurgitation and mobile echodensities on the valve ring and antibiotics were commenced for prosthetic valve endocarditis (PVE). Extensive inflammatory adhesions with circumferential annular destruction were noted intra-operatively. In addition, an abscess cavity and a soft edematous aortic wall were seen. All cultures (blood, intra-operative swabs, aortic tissue and prosthetic valve) were negative. Serology for Coxiella burnetti, syphilis, Bartonella and Legionella species were within normal limits while 16S PCR was negative for bacterial DNA. A vasculitic screen was negative. The patient completed 6 weeks of antibiotic therapy for PVE and was discharged in June with trivial central AR on TEE. Three months later, the patient represented with symptoms of congestive cardiac failure, fevers and night sweats. Antibiotics were recommenced for PVE as the TEE confirmed severe AR secondary to prosthetic valve dehiscence. Surgery revealed no evidence of PVE but a thickened, inflamed aortic root with an anteriorly free-floating valve. All cultures, serology and 16S PCR did not reveal a cause. Histology revealed features of idiopathic aortitis (Takayasu-like syndrome). The patient was commenced on immunosuppression and has been well since. Takayasu’s disease is an uncommon arteritis of the aorta and its main branches. It predominantly occurs in patients from Japan, South-East Asia and India.1 Aortic valve involvement occurs in 25% of the patients. However, isolated aortic root involvement is uncommon.2 Strictly speaking, a patient can only be classified as
Letters to the Editor having Takayasu arteritis if symptoms develop before the age of 40.3 As our patient was 53 he was classified as having a Takayasu-like syndrome. Three similar cases have been documented before, all occurring in Chinese males.4 Treatment is as for arteritis with immuno-suppression. The timing of therapy should ideally start prior to valve replacement to prevent relapses and post-operative complications.5 However, in the absence of other specific symptoms infective endocarditis remains the most likely diagnosis and the diagnosis is usually determined on histopathology (as in our case). In conclusion, in patients who present with atypical features, clinicians should remember inflammatory conditions as part of the differential diagnosis.
References 1. Johnston SL, Lock RJ, Gompels MM. Takayasu arteritis: a review. J Clin Pathol 2002;55:481e6. 2. Kerr GS, Hallahan CW, Giordano J, et al. Takayasu arteritis. Ann Intern Med 1994;120:919e29. 3. Arend WP, Ba Michael, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990;33:1129e34. 4. Chau EMC, Cheung KL, Fu KH, Lee JWT. Recurrent aortic valve prosthesis dehiscence secondary to aortoarteritis: three case reports and literature review. Int J Card 1996;56:113e8. 5. Aoyagi S, Fukunaga S, Tayama E, Hayahida N, Akashi H, Kawara T. Aortic valve replacement for aortic regurgitation caused by aortitis. Jpn Circ J 1999;63:885e8.
S.J. van Hal* B.J. Hudson Infectious diseases, Royal North Shore Hospital, St Leonards, Sydney NSW 2039, Australia *Corresponding author. Tel.: þ610299268480. E-mail address: [email protected] (S.J. van Hal) Accepted 13 February 2006 Available online 3 April 2006
0163-4453/$30 ª 2006 The British Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jinf.2006.02.009
Dear Sir In a majority of cases, prosthetic valve (PV) dehiscence is caused by infective endocarditis (IE) with culture negative rates of less than 5%. These usually occur in patients who have received antibiotics prior to blood cultures. Therefore, in patients with atypical clinical and/or pathological features, inflammatory conditions involving the aortic root (eg. ankylosing spondylitis and giant cell arteritis) should be considered as a cause of valve dehiscence. A 53-year-old previously well Chinese man presented to our institution (Sydney, Australia) in January 2005 with symptoms of congestive cardiac failure secondary to aortic regurgitation (AR). The aortic valve was replaced in February with histopathology of the native valve revealing myxomatous degeneration. The patient made an uneventful recovery. However, he represented in April with fevers and night sweats. Transesophageal echocardiogram (TEE) revealed valve dehiscence with regurgitation and mobile echodensities on the valve ring and antibiotics were commenced for prosthetic valve endocarditis (PVE). Extensive inflammatory adhesions with circumferential annular destruction were noted intra-operatively. In addition, an abscess cavity and a soft edematous aortic wall were seen. All cultures (blood, intra-operative swabs, aortic tissue and prosthetic valve) were negative. Serology for Coxiella burnetti, syphilis, Bartonella and Legionella species were within normal limits while 16S PCR was negative for bacterial DNA. A vasculitic screen was negative. The patient completed 6 weeks of antibiotic therapy for PVE and was discharged in June with trivial central AR on TEE. Three months later, the patient represented with symptoms of congestive cardiac failure, fevers and night sweats. Antibiotics were recommenced for PVE as the TEE confirmed severe AR secondary to prosthetic valve dehiscence. Surgery revealed no evidence of PVE but a thickened, inflamed aortic root with an anteriorly free-floating valve. All cultures, serology and 16S PCR did not reveal a cause. Histology revealed features of idiopathic aortitis (Takayasu-like syndrome). The patient was commenced on immunosuppression and has been well since. Takayasu’s disease is an uncommon arteritis of the aorta and its main branches. It predominantly occurs in patients from Japan, South-East Asia and India.1 Aortic valve involvement occurs in 25% of the patients. However, isolated aortic root involvement is uncommon.2 Strictly speaking, a patient can only be classified as
Letters to the Editor having Takayasu arteritis if symptoms develop before the age of 40.3 As our patient was 53 he was classified as having a Takayasu-like syndrome. Three similar cases have been documented before, all occurring in Chinese males.4 Treatment is as for arteritis with immuno-suppression. The timing of therapy should ideally start prior to valve replacement to prevent relapses and post-operative complications.5 However, in the absence of other specific symptoms infective endocarditis remains the most likely diagnosis and the diagnosis is usually determined on histopathology (as in our case). In conclusion, in patients who present with atypical features, clinicians should remember inflammatory conditions as part of the differential diagnosis.
References 1. Johnston SL, Lock RJ, Gompels MM. Takayasu arteritis: a review. J Clin Pathol 2002;55:481e6. 2. Kerr GS, Hallahan CW, Giordano J, et al. Takayasu arteritis. Ann Intern Med 1994;120:919e29. 3. Arend WP, Ba Michael, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990;33:1129e34. 4. Chau EMC, Cheung KL, Fu KH, Lee JWT. Recurrent aortic valve prosthesis dehiscence secondary to aortoarteritis: three case reports and literature review. Int J Card 1996;56:113e8. 5. Aoyagi S, Fukunaga S, Tayama E, Hayahida N, Akashi H, Kawara T. Aortic valve replacement for aortic regurgitation caused by aortitis. Jpn Circ J 1999;63:885e8.
S.J. van Hal* B.J. Hudson Infectious diseases, Royal North Shore Hospital, St Leonards, Sydney NSW 2039, Australia *Corresponding author. Tel.: þ610299268480. E-mail address: [email protected] (S.J. van Hal) Accepted 13 February 2006 Available online 3 April 2006
0163-4453/$30 ª 2006 The British Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jinf.2006.02.009