Pulmonary valve endocarditis caused by right ventricular outflow obstruction in association with sinus of valsalva aneurysm: a case report
Journal of Cardiothoracic Surgery
Pulmonary valve endocarditis caused by right ventricular outflow obstruction in association with sinus of valsalva aneurysm: a case report
Katsufumi Nishida 1
Osamu Fukuyama 1
Dean S Nakamura 0
0 Department of Surgery, John A. Burns School of Medicine, University of Hawaii , Honolulu, HI , USA
1 Department of Medicine, John A. Burns School of Medicine, University of Hawaii , Honolulu, HI , USA
Background: 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. Case presentation: 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. Conclusion: 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.
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Background
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
510% of all cases of infective endocarditis [3]. This is
primarily seen in patients with intravenous drug use,
pacemaker or central venous lines, or congenital heart disease
[4]. 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 [5]. The literature from 1960 to 2005
identified only 45 reported cases of pulmonary valve
endocarditis in structurally normal hearts [6].
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 [7]. One of the signs of cardiac dysfunction due to
sinus of Valsalva aneurysm is right ventricular outflow
tract (RVOT) obstruction [8]. When it becomes large
enough to cause significant outflow obstruction,
symptoms such as exertional dyspnea, palpitations, and
angina-like chest pain are typically observed [9].
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.
Case presentation
A 60-year-old man with hypertension and type II diabetes
mellitus was admitted to the local community hospital for
a six-week history of low grade fever and recent
development of chills and shortness of breath on October, 2005.
Prior to this admission, the patient had been treated as an
outpatient by his primary care physician for possible
sinusitis and pneumonia with three different kinds of oral
antibiotics including levofloxacin. On admission, the
patient had a fever of 37 degrees centigrade and elevated
white cell count of 17 109/L. Physical examination was
significant for a hyperdynamic precordium, 2+
parasternal lift, grade 23 out of 6 continuous murmur best heard
at the left sternal boarder, and gallop at the apex. The chest
x-ray showed right pleural effusion and features consistent
with congestive heart failure. An echocardiogram showed
a markedly dilated sinus of Valsalva, measuring at least
6.4 cm, with turbulent blood flow in a RVOT. This was felt
to possibly represent a left-to-right shunt and the
possibility of a ruptured sinus of Valsalva was raised. The
echocardiogram also showed a vegetation on one of the
pulmonary valve leaflets (figure 1). The patient was
subsequently treated empirically for infective endocarditis with
vancomycin and gentamycin for 28 days. During cardiac
catheterization, oximetry studies showed there was no
step-up in saturation in the pulmonary valve. This made
the presence of a significant left-to-right shunt less likely.
Aortic injection revealed significant dilation of all of the
coronary sinuses. There was no jet noted from the
coronary sinus to the right side of the chamber. Minimal aortic
regurgitation was present. Pulmonary artery injection
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A transesophageal echocardiogram depicting an enlarged
right coronary sinus (medium white arrow) and identification
of the vegetation on the pulmonary valve (small white
arrow).
showed mild pulmonary insufficiency. Blood cultures did
not grow any organisms.
On May 2006, the patient underwent resection of a large
aortic root aneurysm, replacement of the aortic valve
using a 23 mm St. Jude medical valve conduit,
re-implantation of left coronary artery, coronary artery bypass
grafting using a saphenous vein graft to the right coronary
artery, and exploration of the pulmonary valve with
debridement of pulmonary valve leaflet vegetation. No
evidence of a ventricular septal defect was noted during the
surgery (figure 2 and 3).
The pulmonary valve vegetation was sent for pathological
examination. Gross appearance consisted of multiple
tanwhite 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.
Discussion
Pulmonary valve infective endocarditis is (...truncated)