Pulmonary valve endocarditis caused by right ventricular outflow obstruction in association with sinus of valsalva aneurysm: a case report
© Nishida et al; licensee BioMed Central Ltd. 2008
Received: 13 November 2007
Accepted: 16 July 2008
Published: 16 July 2008
Right-sided infective endocarditis is uncommon. This is primarily seen in patients with intravenous drug use, pacemaker or central venous lines, or congenital heart disease. The vast majority of cases involve the tricuspid valve. Isolated pulmonary valve endocarditis is extremely rare. We report the first case of a pulmonary valve nonbacterial thrombotic endocarditis caused by right ventricular outlflow tract (RVOT) obstruction in association with a large sinus of Valsalva aneurysm.
A 60-year-old man with a six-week history of fever, initially treated as pneumonia and sinusitis with levofloxacin, was admitted to the hospital with a new onset of a heart murmur. An echocardiogram showed thickening of the pulmonary valve suggestive of valve vegetation. A dilated aortic root and sinus of Valsalva aneurysm measuring at least 6.4 cm were also identified. The patient was empirically treated for infective endocarditis with vancomycin and gentamycin for 28 days. Four months later, the patient underwent resection of a large aortic root aneurysm and exploration of the pulmonary valve. During the surgery, vegetation of the pulmonary valve was confirmed. Microscopic pathological examination revealed fibrinous debris with acute inflammation and organizing fibrosis with chronic inflammation, compatible with a vegetation. Special stains were negative for bacteria and fungi.
This is the first case report of a pulmonary valve nonbacterial endocarditis caused by RVOT obstruction in association with a sinus of Valsalva aneurysm. We speculate that jets created by the RVOT obstruction and large sinus of Valsalva aneurysm hitting against endothelium of the pulmonary valve is the etiology of this rare nonbacterial thrombotic endocarditis.
In the United States and Western Europe, the incidence of community-acquired native-valve endocarditis in recent studies is 1.7 to 6.2 cases per 100,000 person-years [1, 2]. Right-sided endocarditis is uncommon, comprising only 5–10% of all cases of infective endocarditis . This is primarily seen in patients with intravenous drug use, pacemaker or central venous lines, or congenital heart disease . The majority of cases involve the tricuspid valve. Isolated pulmonary valve endocarditis is rare, with fewer than 90 cases of pulmonary valve endocarditis being previously reported . The literature from 1960 to 2005 identified only 45 reported cases of pulmonary valve endocarditis in structurally normal hearts .
An aneurysm of the sinus of Valsalva is usually asymptomatic unless rupture occurs. However, there have been a few reported cases of unruptured sinus of Valsalva aneurysms that have presented with conduction disturbances, myocardial ischemia, and symptomatic cardiac dysfunction . One of the signs of cardiac dysfunction due to sinus of Valsalva aneurysm is right ventricular outflow tract (RVOT) obstruction . When it becomes large enough to cause significant outflow obstruction, symptoms such as exertional dyspnea, palpitations, and angina-like chest pain are typically observed . However, cardiac structural abnormalities acquired secondary to a sinus of Valsalva aneurysm have never been reported to cause pulmonary valve endocarditis. We present the case of a 60-year-old man with nonbacterial thrombotic pulmonary valve endocarditis in association with a sinus of Valsalva aneurysm and RVOT obstruction.
The pulmonary valve vegetation was sent for pathological examination. Gross appearance consisted of multiple tan-white soft tissue fragments, measuring 1.0 × 0.8 × 0.3 cm in aggregate, the largest piece measuring 0.4 × 0.4 × 0.3 cm. Microscopic examination revealed fibrinous debris with acute inflammation and organizing fibrosis with chronic inflammation, compatible with a vegetation. Special stains were negative for bacteria and fungi.
Pulmonary valve infective endocarditis is uncommon. It comprises less than 2% of hospital admissions for endocarditis . The low incidence of pulmonary valve infective endocarditis compared with other cardiac valves may relate to different hemodynamic pressure gradients across the valves, different frequencies of underlying congenital or acquired valvular abnormalities, lower right-sided blood oxygen content, and differences in the vascularity and endothelial lining of the valves . Ramadan et al. reported that from 1960 to 1999, only 81 cases of isolated pulmonary valve endocarditis were identified. The majority of these cases (55%) occurred in patients with congenital heart disease with 36 patients (44%) having isolated pulmonary valve infective endocarditis in a normal heart . In cases of right-sided endocarditis in non-drug users, 55% to 65% are caused by S. Viridans whereas S. aureus predominates in drug users . Other organisms include Neisseria, Pseudomonas, Enterococcus, and Haemophilus species.
In our case, this rare nonbacterial endocarditis involving the pulmonary valve was thought to be initiated by the jet in the sub-pulmonary obstruction caused by a massively dilated aortic root that was pushing against the RVOT. We speculate that thrombus had formed on the injured endocardial surface and subsequently became infected by bacteria which had been likely irradicated by antibiotic therapy prior to pathologic examination of the vegetation. Theoretically, any acquired heart disease that causes turbulent blood flow can predispose to infective endocarditis. The case of deep sternal wires traversing the lumen of the RVOT and vegetations in the RVOT and on the pulmonary valve was reported . It was also possible that a very small infundibular ventricular septal defect (VSD) could have created the jet hitting against the pulmonary valve (left-to-right shunt) resulting in the pulmonary valve endocarditis in our patient. However, the absence of a VSD as noted during surgery rules against this possibility.
Isolated pulmonary valve endocarditis is difficult to recognize due to its rarity, minimal cardiac manifestations, and predominance of pulmonary infections secondary to embolization of the vegetations. This is the first case report of a pulmonary valve endocarditis caused by RVOT obstruction in association with a sinus of Valsalva aneurysm. We speculate that jets created by RVOT obstruction and large sinus of Valsalva aneurysm hitting against endothelium of the pulmonary valve is the etiology of this rare nonbacterial thrombotic endocarditis.
Written consent for publication was obtained from the patient.
The authors would like to thank the staff at the Dr. Fukuyama's clinic, Honolulu, Hawaii for their assistance.
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