ABSTRACT
<p>A 41-year-old man had undergone mitral valve replacement (On-X 27/29 mm) and tricuspid valve replacement (TVR) (On-X 31/33 mm) for infectious endocarditis of the mitral valve and severe tricuspid regurgitation 6 years ago. Postoperative echocardiography showed aortic regurgitation and perivalvular leakage of the prosthetic mitral valve and left ventricular (LV) septal perforation. He therefore underwent aortic valve replacement (On-X 25 mm), patch closure of a leak around the prosthetic mitral valve, direct closure of the LV septal perforation, and re-TVR (On-X 31/33 mm). After discharge, he was placed on anticoagulant therapy with warfarin (international normalized ratio of prothrombin time target : 2.0-2.5). Transthoracic echocardiography three and -a half years after the operation revealed an increased mean tricuspid valvular pressure gradient (14 mmHg) compared with that seen on an echocardiograph of previous year. Cine-fluoroscopy showed almost no movement of the leaflets of the mechanical tricuspid valve. Tricuspid valve thrombosis or pannus formation was suspected. He was placed on thrombolytic therapy using tissue plasminogen activator (monteplase 1.6 million units). Five days later, cine-fluoroscopy showed movement of the mechanical tricuspid valve leaflets, and echocardiography revealed recovery of the mean tricuspid valve pressure gradient (4 mmHg). Valvular thrombosis was diagnosed as the cause of the non-moving valve. Hemorrhagic and embolic complications were not observed. Thrombolytic therapy was extremely useful.</p>
ABSTRACT
A 72-year-old man, in whom hypertrophic cardiomyopathy (HCM) had been treated with medication for 4 years, complained of general fatigue and mild dyspnea on effort. Transthoracic and transesophageal echocardiography revealed diffuse left ventricular (LV) hypertrophy and LV obstruction from the mid-portion to the outflow tract with a peak pressure gradient of 94 mmHg. Additionally, anterior displacement of the abnormal, hypertrophied anterior papillary muscle (PM) and restricted motion of the anterior mitral leaflet, caused by the shortened chordae arising from the abnormal PM, were found. Furthermore, during the systolic phase, the abnormal, hypertrophied anterior PM was shifted to the septal side, causing LV obstruction with systolic anterior motion of the mitral leaflet. The diagnosis was HCM with LV obstruction due to abnormal PM. Mitral valve replacement (MVR) using a mechanical valve and excision of the abnormal PM was performed. His postoperative course was uneventful, and he was discharged on the 14th postoperative day. Postoperative echocardiography revealed no residual obstruction and no pressure gradient in the LV, indicating that complete release of the LV obstruction had been accomplished. In cases of HCM with LV obstruction due to an abnormal mitral subvalvular apparatus, transaortic septal myectomy may not always be an effective procedure. Therefore, we propose that MVR with excision of the PM should be considered one of the useful surgical procedures for such cases.
ABSTRACT
A 62-year-old man with a history of insulin-dependent diabetes mellitus was admitted to our hospital because of a high-grade fever and general fatigue. Laboratory data showed evidence of inflammation and <i>Streptococcus pneumoniae </i>was identified in the blood cultures. Transthoracic echocardiography revealed vegetations on the right coronary cusp of the aortic valve and septal leaflet of the tricuspid valve, and an aorto-right ventricular fistula secondary to abscess formation in the aortic annulus. We diagnosed active infective endocarditis with an aorto-cavity fistula and performed an emergency operation. The infected tissue was curetted as much as possible and the fistulous openings in the right ventricle and aortic root were closed using bovine pericardial patches. We subsequently performed aortic annular reconstruction and aortic full-root replacement using a Freestyle<sup>®</sup> stentless valve. Although a permanent pacemaker was implanted to treat a complete atrioventricular block, the postoperative course was uneventful and the C-reactive protein level normalized. He was discharged on the 46th postoperative day. Postoperative echocardiography revealed no signs of valve dysfunction, recurrent endocarditis, or residual abscess cavity and shunt. Infective endocarditis with abscess formation complicated by a fistula formation between the cardiac chambers is rare, and surgical treatment for this is challenging. In such cases, both radical debridement of the infected tissue and precise closure of the fistulous tract are essential.
ABSTRACT
Nonocclusive mesenteric ischemia (NOMI) after cardiac surgery is a rare and fatal complication. Although there are a few reports of successful treatment of NOMI, progress after treatment is not known. This case report describes the postoperative course of a 79-year-old male patient who underwent successful treatment of NOMI after aortic valve replacement (AVR). Plain abdominal computed tomography revealed gas in the small intestinal wall 14 days after AVR. Emergency massive small bowel resection was performed because wide and discontinuous necrotic changes of the small intestine were confirmed. Although the patient temporarily returned to normal life after discharge, sepsis due to urinary tract infection or acute cholecystitis and central venous route infection occurred repeatedly. The patient was intermittently admitted for a total of 14 of 25 months after the first discharge. The patient died of sepsis due to <i>Candida </i>infection and liver failure 52 months after AVR. Even if treatment for NOMI is successful, there is an unfavorable prognosis in terms of immunity and nutrition for short bowel syndrome. Because there are no symptoms or laboratory data specific to NOMI, it is considered important to immediately and adequately diagnose and treat NOMI without overlooking abnormalities after cardiac surgery.
ABSTRACT
A 38-year-old woman was admitted due to an abnormal ECG and dyspnea on effort. Transoesophageal echocardiography and cardiac computed tomography (CT) showed severe aortic regurgitation (AR) due to pentacuspid aortic valve, which consisted of 4 relatively equal cusps and 1 larger cusp. Mild mitral regurgitation, atrial septal defect (ASD) and coronary-pulmonary artery fistula were complicated for her. She underwent aortic valve replacement, mitral valve annuloplasty, direct closures of ASD and coronary-pulmonary artery fistula. The pathophysiology of the resected aortic valve showed 4 equal size cusps and a large one with mild myxomatous change. Aortic valve regurgitation due to pentacuspid aortic valve is extremely rare and there was little report concerning it in the literature. We reported the surgical repair of this rare case of severe AR due to pentacusupid aortic valve.