Osamu Namura

Therapeutic Role of Pericardiocentesis for Acute Necrotizing Eosinophilic Myocarditis With Cardiac Tamponade

We describe a patient with acute necrotizing eosinophilic myocarditis who recovered rapidly after pericardial drainage and without corticosteroid therapy. The 25-year- old man was referred to our hospital with suspected acute myocardial infarction on the basis of severe epigastralgia, abnormal Q waves and ST elevation on electrocardiography, and an increase in cardiac enzymes. Echocardiography disclosed pericardial effusion that compressed the right ventricle, left ventricular dysfunction in conjunction with posterolateral hypokinesis, and a thickened ventricular wall but no mural thrombus. The eosinophil count in the peripheral blood was slightly increased. Coronary angiography showed normal arteries and thus prompted an endomyocardial biopsy. The patient was transferred to the intensive care unit with a clinical diagnosis of myocarditis associated with cardiac tamponade. Emergency pericardiocentesis relieved symptoms immediately. The cells in the pericardial effusion were mainly eosinophils; interleukin 5 and interleukin 13 levels were predominantly elevated, and the effusion was drained for 5 days. The biopsy specimen revealed necrotizing eosinophilic myocarditis. Left ventricular function recovered within a week without corticosteroid therapy. No relapse was observed as of 8 months after diagnosis.

Successful surgical treatment of a ruptured abdominal aortic aneurysm without homologous blood transfusion in a Jehovah's Witness: report of a case.

Abstract We report herein the case of a 47-year-old woman of the Jehovahs Witness faith in whom Y-grafting for a ruptured abdominal aortic aneurysm was successfully performed without a homologous blood transfusion. We used a Cell Saver (Haemonetics, Braintree, MA, USA) red cell salvaging device and an aortic occlusion balloon catheter, and performed gentle and minimal dissection during the operation. Postoperatively, the patient was kept heavily sedated and required hypothermic therapy for only 14 h. We treated her severe anemia using conventional drugs, including iron and folic acid, and her hemoglobin increased smoothly. Although her hemoglobin level decreased to 2.8 g/dl during the operation, her postoperative course was uneventful.

The effect of fibrin glue on inhibition of pericardial adhesions

The effect of fibrin glue on inhibition of pericardial adhesions was tested using 26 beagle dogs. Dacron patches were sutured to the heart and tincture of iodine was applied to promote adhesions. Fibrin glue (3 ml) was sprayed over the patches in 15 dogs (test group), and was not separated in the remaining 11 dogs (control group). All animals in the test group had minimal adhesions between the pericardium and the epicardium or patched region, and an accumulation of gelatinous material was found in the subpericardial space. Marked fibrosis and a poor demarcation of the subpericardial space were found in the control group. The adhesion score and the visibility of coronary anatomy in the test group were significantly better than in the control group. The tension strength in the test group was significantly less than in the control group. We concluded, therefore, that fibrin glue may also be useful as an adhesion inhibitor.

Floating thrombus originating from an almost normal thoracic aorta

We present a case of floating thrombus originating from an almost normal thoracic aorta in a 54-year-old man who presented with acute arterial occlusion of his left leg. Transesophageal echocardiography (TEE), computed tomography, and magnetic resonance imaging showed two masses in an almost normal aorta after embolectomy for the acute arterial occlusion. Although the embolus was thrombus histologically, malignant tumors could not be ruled out. The masses did not decrease in size after 7 days of anticoagulant therapy, so they were extirpated under cardiopulmonary bypass (CPB) and TEE guidance. Frozen section examination during CPB indicated that there was no evidence of malignancy in the removed mass. TEE played an important role in the diagnosis and surgery of this condition, and it was useful when deciding on a surgical strategy. Because the treatment strategy for this disease remains controversial, further studies are needed.

Deterioration of body oxygen metabolism by vasodilator and/or vasoconstrictor administration during cardiopulmonary bypass.

During cardiopulmonary bypass (CPB), tissue perfusion injury occurs even if perfusion pressure is maintained. Although a vasodilator and a vasoconstrictor are clinically administered if bypass flow is maintained, they may restore perfusion pressure without improving tissue perfusion. We evaluated the influence of vasodilators and vasoconstrictors on the whole body during CPB. Fifty-six patients with valvular disease who received moderately hypothermic CPB without blood transfusion were divided into four groups, depending upon whether a vasodilator and/or a vasoconstrictor was administered, and postoperative data were compared. Bypass flow and aortic pressure were maintained at 2.4 l/min/m2 and 5090 mm Hg. Body weight, dilution, hematocrit level, CPB, and aortic clamp duration, blood temperature, bypass flow, perfusion pressure, base excess levels during CPB, cardiac index, arterial and mixed venous oxygen pressure, and alveolar-arterial oxygen distribution after CPB were comparable among the four groups. However, the time to extubation was significantly longer. Blood lactate levels, measured for patients returned to the ward, were significantly higher in the agent-administered groups than in the no-agent group, whereas blood lactate levels on extubation and blood creatinine levels on postoperative day 1 were comparable among the groups. Vasodilator and/or vasoconstrictor administration during CPB may deteriorate the body oxygen metabolism, which might imply tissue perfusion and worsen the complications induced by hypoperfusion during CPB.

Supplementation of C1-esterase inhibitor concentrates for a patient suffering from hereditary angioedema undergoing complex open-heart surgery

Hereditary angioedema (HAE) is an autosomal dominantly inherited deficiency of C1-inhibitor, and it is an extremely rare condition. During surgery, oedema can be induced by a variety of stresses, and a high mortality rate has been reported. Since open-heart surgery involves cardiopulmonary bypass, the inflammatory response and complement activity are increased, meaning that an even greater risk can be anticipated. Perhaps for this reason, the only reports to date of cases of open-heart surgery have been cases of short-term cardiopulmonary bypass or off-pump coronary artery bypass grafting (CABG). We provide the first report of long-term cardiopulmonary bypass (longer than 5h) for open-heart surgery in a patient with HAE that did not result in any postoperative decline in respiratory function, systemic oedema, laryngeal oedema or similar complications, and a favourable outcome was obtained.

Marked Decrease of Plasma VEGF After Implantation of Autologous Bone Marrow Mononuclear Cells in a Patient with Critical Limb Ischemia A Case Report

The authors performed autologous bone marrow mononuclear cells implantation (BMI) in a 79-year-old man with critical limb ischemia. After BMI, the resting pain of the ischemic leg improved gradually. They measured the plasma concentrations of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and serum hepatocyte growth factor (HGF) in the blood from bilateral femoral veins. Before BMI, the plasma VEGF and bFGF concentrations were much greater in the ischemic leg than in the other lower limb, but decreased to the same concentrations as those in the contralateral lower extremity after BMI. The large concentrations of the angiogenic factors VEGF and bFGF in plasma indicate the severity and extent of the leg ischemia. BMI resulted in lower levels of VEGF and bFGF, and this fall is the hallmark of the effectiveness of BMI in the treatment of peripheral artery disease.

Thrombus on the intraluminal felt strip. A possible cause of postoperative stroke.

We report a case of a 60-year-old woman who received an operation for acute aortic dissection and who had a postoperative complication of multiple cerebral infarction. Through aggressive investigation using transesophageal echocardiography, a mobile thrombus on the intraluminal felt strip used for the enforcement of the dissecting aortic wall was detected as the possible source of the cerebral thromboembolism. After anticoagulation therapy was started, the mobile thrombus growing on the intraluminal felt strip disappeared, and no new lesions of cerebral thromboembolism occurred.

MYCOTIC ABDOMINAL AORTIC ANEURYSM ASSOCIATED WITH MYELODYSPLASTIC SYNDROME(MDS) : REPORT OF A CASE

A 59-year-old man, who manifested lower back pain, was admitted with sepsis and disseminated intravascular coagulation (DIC). A computed tomographic scan showed a slight thickening of the abdominal aortic wall. A blood examination revealed pancytopenia. Myelodysplastic syndrome was diagnosed after bone marrow aspiration and a chromosome analysis. Sepsis due to a Staphylococcus aureus infection and DIC subsided after medical treatment; however, an aortobifemoral bypass was performed upon the detection of a localized rupture of a mycotic abdominal aortic aneurysm 1 month later. The patient is still alive 2 years after operation despite the presence of a hematological disorder.

Improvement of anemia with decreasing hepcidin levels following valve replacement for severe tricuspid regurgitation

To the Editor: Severe right heart failure is occasionally accompanied by anemia (1, 2), but the underlying mechanisms for this association remain unknown. Hepcidin, a circulating hormone that is synthesized mainly by the liver, has emerged as a key regulator of systemic iron homeostasis (3). Hepcidin suppresses the expression of the iron transporter, ferroportin-1, thereby inhibiting the absorption of iron from the duodenum and the release of iron from the reticuloendothelial system. Therefore, the excessive production of hepcidin decreases serum iron levels, consequently causing and consequently causes anemia (3). Here, we report on a sixty-two-year-old woman of severe tricuspid regurgitation with refractory anemia in a patient with a very high serum hepcidin level who recovered from anemia after valve replacement, which was accompanied by a decrease in the hepcidin level. She had undergone mitral valve replacement for mitral stenosis 24 yrs before this episode. An echocardiogram revealed severe tricuspid regurgitation and dilatation of the right atrium. Right heart catheterization was performed after admission. Her right atrial pressure (RAP) was high (mean RAP, 15 mmHg; prominent V wave, 21 mmHg). Abdominal CT revealed hepatic vein dilatation and massive ascites. She received drug therapy for right heart failure, but this failed to reduce the massive ascites. She also had normocytic, normochromic anemia, but fecal occult blood tests were negative, and no bleeding source was found. She received oral iron preparation and red blood cell transfusions; however, her anemia did not resolve. As the massive ascites and progressive abdominal distension were believed to be life threatening, we decided to perform valve replacement surgery. The patient’s preoperative hemoglobin (Hb) level was 7.9 g ⁄dL, red blood cell (RBC) count was 271 million ⁄L, hematocrit (Ht) was 25.0%, serum iron level was low (26 lg ⁄dL), and serum ferritin level was high (724 ng ⁄mL; Table 1). Moreover, using a hepcidin EIA kit (Bachem Americans Inc., San Carlos, CA, USA), we found that her serum hepcidin levels (828 ng ⁄mL) were very high compared with the normal range (normal range, 1.8– 48.7 ng ⁄mL). Her preoperative serum C-reactive protein (CRP) level (15.91 mg ⁄dL) and interleukin-6 (IL-6) level (695 pg ⁄mL) were very high, but infectious disease was not found in any region of her body. Tricuspid valve replacement for severe tricuspid valve regurgitation and mitral valve replacement for the old ball valve were performed on July 1, 2010. Three months after the operation, the massive ascites completely disappeared. Postoperative right heart catheterization showed a decrease in RAP (mean RAP, 7 mmHg; V wave, 9 mmHg). Serum