European Journal of Echocardiography 2008 9(1):58-59; doi:10.1016/j.euje.2006.08.016
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2006. For permissions please email: journals.permissions@oxfordjournals.org.
Spontaneous chordae rupture of tricuspid valve in patient with chronic renal failure
Hyungseop Kim*,
Yun-Kyeong Cho,
Chang-Wook Nam,
Seong-Wook Han,
Seung-Ho Hur,
Yoon-Nyun Kim and
Kwon-Bae Kim
Division of Cardiology, Department of Internal Medicine, Keimyung University, Dongsan Medical Center, Junggu Dongsandong 194, Daegu, Republic of Korea
Received 13 July 2006; accepted after revision 29 August 2006; online publish-ahead-of-print 10 October 2006.
* Corresponding author. Tel: +82 53 250 7998; fax: +82 53 250 7034. E-mail address: khyungseop{at}dsmc.or.kr
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Abstract
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Spontaneous chordae rupture of the tricuspid valve is relatively
rare, unlike the mitral valve. We present a 27-year-old male
with chronic renal failure on hemodialysis therapy for treatment
of parathyroid adenoma. The echocardiography showed the severe
tricuspid regurgitation with chordae rupture which was not noted
1 year ago. In addition, the papillary muscle of both mitral
and tricuspid valve was shortened and calcified extensively.
However, in his clinical history, the specific causes for chordae
rupture, such as chest trauma or endocarditis, were not disclosed.
It was presumed that dilated right ventricle with volume or
pressure overloading and secondary hyperparathyroidism are probably
responsible for the chordae rupture of tricuspid valve.
Keywords: Tricuspid valve; Chordae rupture; Hyperparathyroidism; Echocardiography
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Case report
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A 27-year-old male, diagnosed as chronic renal failure with
IgA nephropathy, presented to our hospital for operation of
parathyroid adenoma. He was being treated with hemodialysis
and also, hypertension was accompanied with hemodialysis. One
year ago, the echocardiography showed that papillary muscles
of both mitral and tricuspid valve were severely calcified with
shortened and calcified chordae of tricuspid valve (
Figure 1),
with decreased systolic function and dilated chambers. On this
admission, the follow-up studies showed isolated severe tricuspid
regurgitation with chordae rupture, calcified papillary muscle
and limited motion of both leaflets (
Figure 2). We excluded
the infective endocarditis through the transesophageal echocardiography
(TEE) and more detailed clinical history for trauma or physical
injury. In his serologic test, the values of parathyroid hormone
(1882 pg/mL), calcium (11.0 mg/dL) and phosphate (8.6 mg/dL)
were all increased, respectively, and the product of calcium
by phosphate was more over 70.
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Discussion
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The most common cause of tricuspid regurgitation is secondary
form due to annular dilation and malcoaptation of the leaflet
from underlying disorders such as pulmonary hypertension, primary
left heart disease, or disease of the right ventricular myocardium.
In addition, the etiology of isolated tricuspid valve regurgitation,
especially rupture of chordae tendineae, was congenital, chest
trauma or infective endocarditis. However, spontaneous chordae
rupture of the tricuspid valve has been rare and the effects
of chronic renal failure with long-term hemodialysis on the
cardiac valve are not clear.
1 In 1982, the report by Abrahams
et al.
2 which was based on examination of the heart at autopsy
in patients with secondary hyperparathyroidism and long-term
hemodialysis, showed the fibrosis, thickening and extensive
calcification in the mitral valve apparatus. For these valvular
changes, other potential explanations would be the increased
cardiac output and mechanical stress on the valve apparatus.
Besides valvular calcification, Kunhali et al.3 reported the case of tricuspid papillary muscle rupture, which was associated with primary pulmonary hypertension. In that study, one explanation for papillary muscle rupture would be the increased wall tension in a dilated ventricle leading to the increased tension with predisposing to rupture.
In the present case, it is tempting to speculate that this is a consequence of long-standing progression of hyperparathyroidism and increased wall tension resulting from the hemodialysis, which would be the etiology of isolated spontaneous rupture of tricuspid valve apparatus in selected patients.
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Notes
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No grant support.
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References
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- Maher ER, Young G, Smyth-Walsh B, Pugh S, Curtis JR. Aortic and mitral valve calcification in patients with end-stage renal disease. Lancet (1987) 2:875–7.[Web of Science][Medline]
- Abrahams C, D'Cruz I, Kathpalia S. Abnormalities in the mitral valve apparatus in patients undergoing long-term hemodialysis. Arch Intern Med (1982) 142:1796–800.[Abstract/Free Full Text]
- Kunhali K, Cherian G, Bakthaviziam A, Abraham MT, Krishnaswami S. Rupture of a papillary muscle of the tricuspid valve in primary pulmonary hypertension. Am Heart J (1980) 99:225–9.[CrossRef][Web of Science][Medline]
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