A 30-year-old man was admitted to our hospital because of high grade of fever. Two weeks before admission he developed general fatigue and fever. He visited a local clinic and received antibiotics, but his symptoms worsened.
On admission, his height was 187 cm and his weight was 75 kg. The blood pressure was 110/60 mmHg. The first and second heart sounds were normal. A pansystolic Levine 3/6 murmur at apex was detected on physical examination. The transthoracic echocardiography showed destructive, ruptured aneurysmal anterior mitral leaflet and severe eccentric mitral regurgitation, bicuspid aortic valve and mild aortic regurgitation. With the transesophageal echocardiograhy, destructive anterior mitral leaflet and oscillating rims of rupture site into left atrium were seen more clearly.
To enlighten the source of infection, including the dental examination a systemic examination was performed and a dental abscess was detected. The dental abscess culture and blood cultures were taken. IV peniciline and gentamycin therapy was administered. Non-hemolytic group G streptococcus was detected from both dental abscess and 12 hours separately taken blood cultures.
The abscess related tooth was extracted during antibioteraphy. With the proceeding echocardiography examinations, the increases in cardiac dimensions and pulmonary artery systolic pressure were observed. Subsequently, mitral valve replacement procedure with the heart port access method was performed on the 27th hospital day.
A specimen of the resected mitral valve confirmed a ruptured mitral anterior leaflet due to endocarditis. Discussion Aneurysm of the mitral valve is most commonly associated with infective endocarditis of the aortic valve. The destruction of the aortic valve results in a regurgitant jet that strikes the anterior leaflet of the mitral valve, creating a secondary site of infection leading to the development of an aneurysm.
These aneurysms may perforate and result in mitral regurgitation and pulmonary edema especially in patients with left ventricular volume overloading from aortic regurgitation (1). The incidence of mitral valve aneurysm was found as 9.6% in a group of patients with left-sided infective endocarditis. Mitral valve aneurysm without a history of endocarditis is very rare and usually associated with connective tissue disorders, myxomatous valvular degeneration, Marfan syndrome, pseudoxanthoma elasticum, or physical stress due to severe aortic regurgitation (2).
In our patient, in spite of mild aortic valve degeneration and regurgitation, there was no definitive echocardiographic evidence of aortic valve infective endocarditis according to the Duke criteria (3). We considered that the endocarditis could have started from aortic valve and spread to mitral valve. In the other hand, because of no definitive evidence of aortic valve endocarditis, we assumed that mild aortic regurgitation causing by bicuspid aortic valve could have affected mitral anterior leaflet and caused tissue damage and the infective endocarditis might have started at that affected point and caused aneurysmal formation and eventually rupture. With transesophageal echocardiography, it was clearly seen that the aneurysmal rupture site was just at the aortic regurgitan jet strike site. The transesophageal echocardiography is superior to the transthoracic echocardiograhy in the diagnosis of infective endocarditis.
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Notes to editor
Submited by Oya Yuksel (Istanbul, Turkey) and Alper Yuksel (Tekirdag, Turkey)