We present a surgical case of mycotic aneurysm of the ulnar artery occurring 2 months after surgical treatment for infective endocarditis (IE). A 59-year-old man was referred to our hospital because of dyspnea and fever. An echocardiogram showed severe mitral regurgitation with vegetations. Blood culture disclosed Methicillin-resistant Coagulase Negative Staphylococcus (MRCNS), and brain computed tomography (CT) demonstrated an intracranial hemorrhage in the right posterior lobe. After one month of antibiotic treatment, mitral valve replacement (MVR) was performed successfully. Antibiotic treatment was continued postoperatively for 4 weeks; the C-reactive protein (CRP) level and peripheral white blood cell count were reduced to the normal range. Two months after MVR, a pulsatile mass rapidly increasing in size was seen in his right forearm. Contrast-enhanced CT showed aneurysm formation in his right ulnar artery. The aneurysm was managed by excision, and the brachial artery was reconstructed with a reversed saphenous vein graft. It is essential when observing the course of IE patients to bear in mind at all times that a healed mycotic aneurysm might increase in size.

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 Streptococcus pneumoniae 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^® 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.

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.

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 Candida 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.

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.

A 64-year-old man was transferred to our hospital because of acute heart failure associated with myocardial infarction. Echocardiography revealed severe mitral regurgitation due to total rupture of the posterior papillary muscle. Following the diagnosis of papillary muscle rupture, intraaortic balloon pumping support was started, and surgery was performed without coronary angiography because of cardiogenic shock and renal dysfunction. The posterior papillary muscle was completely ruptured, and the anterior leaflet of the mitral valve was severely prolapsed. Without resecting the posterior leaflet, mitral valve replacement was successfully performed using a St. Jude Medical^® prosthetic valve. The postoperative course was uneventful except for ventricular tachyarrhythmia which occurred during the acute phase postoperatively. Postoperative coronary angiography demonstrated no significant coronary arterial stenosis. In a patient with cardiogenic shock due to papillary muscle rupture, immediate surgical intervention is recommended as soon as the diagnosis has been established by echocardiography.

We report a 25-year-old man with ventricular septal perforation due to blunt chest trauma. He was transferred by ambulance to our hospital following a traffic accident. On admission, he had no cardiac murmur. Two days later, a pansystolic murmur appeared over the left lower sternal border. Doppler echocardiogram revealed a large left-to-right shunt through a ventricular septal perforation. We postponed surgical treatment as long as possible because he also exhibited bronchial bleeding due to a lung contusion. Surgical repair of the ruptured ventricular septum was performed 8 days after the chest trauma, because the pulmonary to systemic flow ratio was elevated to 4.6 and cardiac function had deteriorated. During the operation, the site of the septal perforation was easily detected by epicardial echocardiography. A 4-cm tear in the muscular septum was closed through a right ventriculotomy using a pericardial patch reinforced with a Dacron patch. Postoperative recovery was uneventful with the exception of transient right ventricular failure. There was no residual shunt.

Essential thrombocythemia is considered one of the chronic myeloproliferative disorders resulting in arterial thromboembolism, venous thrombosis, and bleeding tendency. We report a case of left ventricular aneurysm with successful treatment of the complications of this disease. A 66-year-old man who suddenly experienced right upper limb paralysis was carried to a nearby hospital. Computed tomography revealed multiple cerebral infarctions. An electrocardiogram confirmed findings of old myocardial infarctions in the anteroseptal wall. Echocardiography indicated a left ventricular aneurysm with mobile thrombus. The blood tests showed an abnormally high platelet count of 120×104/μl. His left ventricular thrombus showed an increasing tendency regardless of heparin administration ; thus, he was transferred to our hospital. The resection of the aneurysm and left ventricular restoration was performed emergently to avoid re-embolism. There was a soft thrombus inside the aneurysm at its apex. During cardiopulmonary bypass, the activated clotting time was not prolonged easily. We gave additional heparin and antithrombin III. The patient had no problem with hemostasis or postoperative bleeding. We started low-molecular-weight heparin from the second postoperative day and he was diagnosed with essential thrombocythemia by bone marrow biopsy. We started warfarin and aspirin on the fifth day after surgery. The number of platelets increased to 183×104/μl on the 8th day ; thus, oral administration of hydroxycarbamide was started. His platelet count fell to less than 100×104/μl around 3 weeks after surgery and he was discharged on the 34th day without new embolisms.