Copyright © Italian Federation of Cardiology. Unauthorized reproduction of this article is prohibited. Aorto-right atrial fistula secondary to infective endocarditis presenting with cardiogenic shock Ozkan Candan, Cetin Gecmen, Ahmet Guler, Can Yucel Karabay, Soe M. Aung, Hicaz Z. Agus and Kenan Sonmez J Cardiovasc Med 2012, 13:65–67 Keywords: aorto-right atrial fistula, cardiogenic shock, infective endocarditis Kartal Kosuyolu Heart and Research Hospital, Istanbul, Turkey Correspondence to Dr Can Yucel Karabay, MD, Kartal Kosuyolu Heart and Research Hospital, Istanbul, Turkey Received 20 April 2010 Revised 10 July 2010 Accepted 26 July 2010 To the editor A 55-year-old female patient who had a previous history of three mitral valve operations presented to our clinic with fever and fatigue. Four years ago, she underwent mitral valve replacement (MVR) with a 29 St Jude mechanical valve for severe rheumatic mitral insuffi- ciency. One year later, she had dehiscence secondary to culture-negative infective endocarditis and a redo MVR was performed. Unfortunately, 3 years after the operation, she again underwent mitral valve repair due to a severe paravalvular leak secondary to infective endo- carditis, and Staphlococcus epidermidis was cultured. At the time of her current presentation, which was 1 month after the last operation, the patient had fever and her heart rate was 130 bpm; blood pressure, 80/35 mmHg; body temperature, 38.58C; and a 2–3/6 holosystolic murmur was heard on the aortic area. An electrocardiogram showed atrial fibrillation with rapid ventricular response and nonspecific ST-segment changes on lateral deri- vations. Laboratory findings demonstrated leukocytosis (19.0 Â 10 3 /ml), moderate anemia, elevated erythrocyte sedimentation rate (120 mm/h), and high C-reactive protein level (120 mg/dl). Transthoracic echocardiogram (TTE) revealed normal left ventricular function, normal mitral mechanic prosthetic valve function [(mitral valve area: 2.5 cm 2 (by pressure halftime method) and gradient: 11/6 mmHg], moderate aortic insufficiency, severe tricus- pid insufficiency (systolic pulmonary arterial pressure: 35 mmHg), and a significant shunt from noncoronary sinus to right atrium (Fig. 1a). Transesophageal echocar- diogram (TEE) demonstrated several vegetations on the mitral prosthetic valve (Fig. 1b) and paravalvular leak causing mild mitral insufficiency. There was an echolu- cent area (approximately 1 cm 2 ) between the noncoron- ary sinus and right atrium (Fig. 2a). Color and continuous Doppler imaging showed a jet flow between aorta and right atrium and a 60 mmHg gradient was measured (Fig. 2b). While the patient was prepared for emergency open-heart surgery, empirical antibiotherapy with vanco- mycin, gentamycin and rifampicin was started after blood samples were drawn for cultures. The patient, who had been in cardiogenic shock, developed electromechanical dissociation and immediate cardiopulmonary resuscitation was started. After about 10 min of successful resuscitation, she was transferred to the operative theater under inotropic support. Right and left atriotomy and aortotomy were performed. Surgical findings correlated well with the preoperative TEE findings. Except for tissue destruction at the noncoronary sinus and vegetations on the mitral prosthetic valve, surgical exploration did not reveal any vegetation or abscess formation around the fistula, peri- valvular area, and aortic leaflets. Fistula repair with a patch and mechanical aortic valve replacement due to the aortic insufficiency were performed, and vegetation on the mitral prosthetic valve was cleaned, but the patient died during the early postoperative period. Later, the culture was reported to be positive for S. epidermidis. Comment Despite recent advances in pharmacological and micro- biological fields, the mortality rate of infective endocar- ditis is still relatively high. In the presence of major complications such as cardiogenic shock, severe valvular insufficiency or stenosis, paravalvular abscess, and fistula, surgical therapy should be applied in addition to aggres- sive antibiotherapy. The spread of infection to annulus and abscess formation are more commonly seen in infec- tive endocarditis of the aortic valve than the mitral valve. 1 The rate of perivalvular abscess secondary to infective endocarditis in autopsy and surgical studies was reported to be 30–40%. 1–6 Aortocavitary ruptures and fistulae are generally seen secondary to aortic arch aneurysms. How- ever, they can also be caused by previous cardiac surgery, autoimmune vasculitis, or infective endocarditis without aortic root dilatation. 7–9 Fistulous intracardiac shunts, such as aortoatrial and aortoventricular fistulae, secondary to infective endocarditis usually occur as a result of fistulization of previously formed perivalvular abscess into cardiac chambers, and 6–9% of perivalvular abscesses have been reported to form fistula cases. 10,11 Fistulae can also be formed by progression of valvular infection to the relatively avascular perivalvular tissue, causing local tissue destruction. Research letter 1558-2027 ß 2011 Italian Federation of Cardiology DOI:10.2459/JCM.0b013e328340370c