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Hepatic abscesses are divided into bacterial and amoebic types. Although the prognosis of bacterial liver abscesses has improved owing to progress in drainage techniques and antimicrobial agents, poor outcomes remain common. While there have been some reports of amoebic liver abscesses complicated by thrombosis, bacterial liver abscesses and subsequent thrombus in the right atrium are very rare. We herein report the case of an 82-year-old man. He had suffered acute obstructive suppurative cholangitis 10 months previously, and bile culture yielded Enterococcus faecalis. In the present case, a right atrial thrombus caused by a bacterial liver abscess was observed and the causative organism was thought to be Enterococcus faecalis, for which was detected in a blood culture was positive. The patient was successfully treated with hepatic abscess drainage and surgical right atrial thrombectomy under cardiopulmonary bypass with a beating heart.

Congenital protein C (PC) deficiency is one type of hereditary thrombosis. Patients with hereditary thrombosis are at high risk for thrombosis in the perioperative period, but a standard management strategy has not been established. Here we report a case of perioperative management of a fracture in a child with homozygous congenital PC deficiency. The patient was a 3-year-old boy who was diagnosed with congenital PC deficiency at birth. He sustained a traumatic supracondylar fracture of the right humerus and underwent emergency surgery. To prepare for open surgery for fixation of the fracture, warfarin was discontinued, and an activated PC (APC) concentrate was used in combination with vitamin K antagonism. However, warfarin was administered during the scheduled nail extraction because the operation was minimally invasive. No thrombotic or bleeding complications occurred in either operation. In emergency surgery in patients with congenital PC deficiency, the combination of vitamin K and APC concentrate is considered a maintenance option for PC deficiency. Postoperative PT-INR control was difficult in our patient due to the administration of vitamin K and withdrawal of warfarin, and this issue must be addressed in the future. Further case experience is desirable to standardize perioperative management.

Ascending aorta thrombosis unaccompanied by an aneurysm or a primary hypercoagulable state is rare. We report a surgical case of ascending aorta thrombosis with multiple emboli. A 44-year-old woman visited the hospital for evaluation of dysarthria and was diagnosed with multiple cerebral infarcts. Contrast-enhanced computed tomography (CT) revealed a mass in the ascending aorta and the brachiocephalic artery. We performed emergency removal of the masses and endarterectomy with cardiopulmonary bypass under hypothermic circulatory arrest. Histopathological examination of the resected specimen showed thrombi. The patient had an uneventful recovery and was discharged 12 days postoperatively. No recurrent thrombus or hypercoagulable state was observed for 3 years postoperatively.

Hematologic malignancies, particularly acute myeloid leukemia, are associated with thrombocytopenia as well as hyperfibrinolytic disseminated intravascular coagulation, which increases the risk of death due to bleeding. Conversely, thromboembolism is known to complicate certain proportions of patients and lead to a poor prognosis; however, prophylaxis and treatment with anticoagulants received little attention. This article discusses the risk factors for thromboembolism in hematologic malignancies, such as acute leukemia, malignant lymphoma, and multiple myeloma, as well as thromboembolism prevention and treatment. Meta-analyses have revealed that second- and third-generation BCR-ABL tyrosine kinase inhibitors increase the risk of cardiovascular events in patients with chronic myeloid leukemia, and this article discusses strategies to prevent these events, which are regarded as a major clinical issue.

Autoimmune hemolytic anemia (AIHA) is a type of anemia caused by the destruction of red blood cells due to autoantibodies targeting membrane proteins. AIHA is divided into two types based on the thermal amplitude: warm AIHA (at 37°C) and cold AIHA (at <37°C). Anemia and jaundice are the major symptoms of AIHA, and in cold agglutinin disease the peripheral circulation disturbance deteriorates patients' quality of life. Cumulative evidence has revealed that both types of AIHA increase the risk of thrombosis and intravascular hemolysis appears to be the most critical factor in the pathogenesis. Complement activation plays an important role in the intravascular hemolysis of AIHA, though the coagulation and hemostatic systems and the crosstalk between these systems also contributes significantly to the pathogenesis of thrombosis. Future treatment of AIHA should be targeted at not only alleviating anemia but also reducing thrombotic risk.

Vascular diseases are a feature of myeloproliferative neoplasms (MPNs) with a driver mutation, such as JAK2V617F. There is growing evidence that clonal hematopoiesis with JAK2V617F (JAK2V617F-CH) is often complicated with vascular diseases, even in the absence of MPN onset. Such vascular diseases associated with the MPN driver mutation include arterial/venous thrombosis, atherosclerotic coronary artery disease and aortic aneurysm, and pulmonary hypertension. Murine studies have recently revealed mechanisms by which hematopoietic cells activated by the MPN driver mutation may promote thrombosis and vascular remodeling in deep vein stenosis, atherosclerosis, and pulmonary hypertension models. Furthermore, MPN driver mutations mediate various downstream molecules of JAK-STAT activation in neutrophils and macrophages, such as inflammatory cytokines, which may be candidates for preventing and treating vascular diseases in MPNs and JAK2V617F-CH.

An 86-year-old female on dialysis experienced a decrease in blood pressure and worsening of her respiratory condition during dialysis, for which she visited our emergency unit. She was admitted to our Department of Cardiology with a diagnosis of acute myocardial infarction complicated with heart failure because of anterior wall of left ventricular dysfunction, positive troponin T levels and negative T wave on a precordial lead electrocardiogram. On the same day, she underwent coronary angiography and stenting at left anterior descending artery #7 with 99% stenosis. She also showed an elevated D-dimer level on admission, and contrast-enhanced computed tomography (CT) was performed the day after admission, considering the likelihood of respiratory failure due to pulmonary thromboembolism. However, the findings were negative. On the 4th day of hospitalization, she showed marked hypoxemia. Her D-dimer level was further elevated, and when she underwent enhanced CT again, there was no evidence of deep vein thrombosis, but thrombus in the pulmonary artery and apex of right ventricle was noted. She was therefore diagnosed with acute pulmonary embolism due to thrombosis from the right ventricle rather than from a deep vein. She rapidly received anticoagulant therapy and non-invasive positive pressure ventilation therapy for respiratory failure, but she entered cardiopulmonary arrest and quickly died. She was suspected to have been complicated with a right ventricular infarction and an acute anterior wall myocardial infarction, resulting in a large thrombus along the apex of the right ventricle. This case of both myocardial infarction and pulmonary embolism is very rare, and we report it here with consideration.

A 55-year-old man presented with recurrent brain infarction which had increased multifocally mainly in the cerebral white matter over the course of one year. Antibodies associated with antiphospholipid syndrome (APS) were initially negative. The patient was admitted to our department because of the thickened meninges shown on gadolinium enhanced brain MRI, mimicking hypertrophic pachymeningitis. However, blood and cerebrospinal fluid analysis revealed no significant inflammatory changes. On histopathological examination of the biopsied meninges, the arachnoid membrane was thickened with fibrosis, and arachnoidal microvessels were enlarged without significant inflammatory changes. The dura mater was not thickened, and no inflammation or microvessel enlargement were revealed. Finally, serum IgG anticardiolipin antibody testing was positive twice at an interval of more than 12 weeks, confirming the diagnosis of APS. Since initiating antithrombotic therapy with warfarin, brain infarction has not recurred. Without inflammation in the arachnoid membrane, the congestion of blood flow caused by thrombosis of microvessels in the arachnoid membrane might have increased the thickness of the arachnoid membrane.

A 63-year-old man was referred to our hospital for detailed examinations and treatment of a hepatic tumor. Abdominal contrast-enhanced CT examination showed a huge mass measuring 12 cm in diameter with ring enhancement in the left liver lobe. The liver tumor was accompanied by a macroscopic tumor thrombus in the left portal branch. Under preoperative diagnosis of intrahepatic cholangiocarcinoma with portal vein tumor thrombus, left liver lobectomy, removal of the tumor thrombus, extrahepatic bile duct excision, and lymph node dissection were performed. Histopathological examination of the resected specimens revealed moderately differentiated adenocarcinoma concomitant with tumor thrombus in the left portal branch. Adjuvant chemotherapy with S-1 was administered. However, 3 months after the surgery, CT examination revealed postoperative recurrences in the liver, lung, and bone. Systemic chemotherapy with gemcitabine and cisplatin was administered with radiotherapy for the bone metastasis. However, the chemotherapy was not effective, and 6 months after surgery, he died of the cancer. There have been few reports of cases with ICC accompanied by a macroscopic portal vein tumor thrombus. Based on the reported cases and the present case, prognosis of the disease seems very poor.

We report cerebral embolism in 2 patients with Duchenne muscular dystrophy (DMD) after respiratory tract infection. A 31-year-old man (Case 1) was admitted to the hospital because of an upper respiratory tract infection, then suddenly developed left-sided hemiparesis. Transthoracic echocardiography revealed an intracardiac thrombus in the left ventricle, and, under assumption of cardioembolic stroke, oral anticoagulation was initiated. Case 2 was a 36-year-old man who developed dysphasia after increasing sputum. Based on brain CT scan findings, we confirmed a diagnosis of cerebral infarction. There was no recurrence in either case. Both cases developed cerebral infarction due to embolism after mild upper respiratory tract infections. DMD patients have various risk factors for thrombus and embolus, while physicians should also be aware of possible cerebral infarction and other coagulation disorders irrespective of respiratory and cardiac therapy.

A 80-years-old woman suddenly presented with aphasia, right hemiparesis, and dysesthesia. MRA showed the left middle cerebral artery occlusion. She was diagnosed as hyperacute ischemic stroke. She was treated with intravenous recombinant tissue plasminogen activator and underwent endovascular thrombectomy. On admission, she had a fever and high C reactive protein, and was treated with antibiotic therapy. The pathological diagnosis of the retrieved thrombus revealed the cluster of the gram positive cocci. The blood culture was negative and thransthoracic echocardiogram did not detect the vegetation. She was finally diagnosed as cardioembolic stroke due to infective endocarditis based on the pathological diagnosis of the retrieved thrombus. The pathological diagnosis of the retrieved thrombus was quite important to clarify the cause of ischemic stroke.

Reportedly, patients with cancer have an increased risk (four- to seven-fold) of developing thrombotic events (TEs) compared with healthy volunteers. Multiple myeloma (MM) is one of the neoplasms that exhibit a high incidence of TEs, and approximately 10% patients with MM develop TEs during their clinical courses. The underlying risk factors of TEs are classified into patient-, disease-, and treatment-related factors. Specific treatment-related risk factors comprise the use of immunomodulatory drugs combined with dexamethasone. As the occurrence of TE in patients hampers the treatment for MM itself, which results in unfavorable outcomes, elucidating TE pathogenesis and adequate prophylaxis for each patient are essential to prevent MM-related TEs.

Among all types of myeloproliferative neoplasms (MPNs), polycythemia vera (PV) and essential thrombocythemia (ET) require careful management of both thrombosis and hemostasis. One recent concern associated with MPNs is the JAK2 mutation (V617F). This mutation is essential for MPN pathology, but it has also garnered attention for its association with thrombosis. Several studies have reported the mechanisms underlying the onset of thrombosis in both PV and ET and have also discussed the association between JAK2 mutations and thrombotic tendencies. Arterial thrombosis is a common clinical symptom that is associated with the diagnosis and course of both PV and ET. Particularly, cerebral infarction has been identified as the leading cause of death in patients with untreated PV. Notably, PV and ET are also associated with a high incidence of venous thromboembolism (VTE). The occurrence of this type of thrombosis at atypical sites, such as cerebral venous sinus thrombosis and splanchnic vein thrombosis (SVT), is not uncommon. Generally, patients with PV and ET have good life expectancy; their treatment essentially focuses on dealing with thrombosis and bleeding. Phlebotomy may be used for treating patients with PV; however, low-dose aspirin is used to prevent the onset of arterial thrombosis. For patients with a history of VTE, oral anticoagulants are commonly prescribed to prevent recurrence.

A 67-year-old woman developed weakness of the entire left side of the body and disturbance of consciousness, and was admitted to our hospital. She had atrial fibrillation (AF) on arrival at the hospital. Diffusion weighted magnetic resonance imaging showed high intensity area in the right basal ganglia, and magnetic resonance angiography showed occlusion of the right internal carotid artery (ICA). Thrombolytic therapy with intravenous tissue plasminogen activator (IV tPA) was administered 225 minutes after onset, and endovascular procedure also performed. After endovascular therapy, the patient had successful recanalization of the right ICA. Transesophageal echocardiography (TEE) showed a mass in the left atrium. Cardiac surgery for the excision of a left atrial mass and the maze procedure for atrial fibrillation were performed on the 29th hospital day. The mass was pathologically confirmed as thrombus. Follow up TEE after cardiac surgery revealed recurrence of thrombus at the both origin of pulmonary vein in the left atrium. Finally, the thrombus was disappeared at 6-month after onset with taking warfarin. She had no stroke events during the clinical course.

A 64-year-old man with flank pain was diagnosed with right renal angiomyolipoma (AML) with tumor thrombus invading the inferior vena cava (IVC). Computed tomography showed a 55 mm IVC tumor thrombus with fat density. The patient underwent radical nephrectomy and IVC thrombcetomy with uneventful postoperative recovery. Pathological diagnosis was AML without malignancy. No recurrence has been observed for 18 months after surgery. We reviewed 60 case reports of AML with venous involvement. Furthermore, we discussed differential diagnosis between AML and other renal tumors mimicking AML with caval involvement.

We describe a 35-year-old woman with Down's syndrome who was admitted to a clinic with anorexia and vomiting. Since laboratory findings showed anemia (Hb 7.4 g/dl) and thrombocytopenia (0.5 × 10⁴/μl), she was transferred to our hospital for treatment. Further laboratory examinations revealed schistocytes, LDH elevation, and a negative Coombs' test. Thrombotic thrombocytopenic purpura (TTP) was suspected. Plasma exchange (PEX) and prednisolone administration were thus immediately initiated. Prior to these treatments, ADAMTS13 activity was less than 5% and inhibitors were detected at a level of 0.8 Bethesda U/ml. Although her platelet count had risen to 13.0 × 10⁴/μl by day 6 (post 4 sessions of PEX), it had decreased to 1.8 × 10⁴/μl on day 7. Despite ongoing PEX, thrombocytopenia persisted. On day 21, she suddenly died. Autopsy findings revealed no evidence of myocardial necrosis or coronary artery thrombosis. Extensive microthrombi were, however, detected in precapillary arterioles, capillaries, and post-capillary venules of the heart. Therefore, this patient's sudden death was clinically suspected to have been caused by cardiomyopathy, which had produced cardiogenic shock.

A 74-year-old man was incidentally discovered during treatment of prostate cancer to have a pelvic tumor, measuring 8 cm in diameter. Enhanced abdominal computed tomography (CT) showed a roundish-shaped hypovascular solid tumor compressing the left internal iliac artery to the inner back side. Values on endocrinological examination were within normal ranges. The tumor was suspected to be chronic abscess, angiosarcoma, or gastrointestinal stromal tumor (GIST) or neurogenic tumor, but no definitive diagnosis was able to be established before operation. During laparotomy, given its location relative to the internal iliac artery wall, the tumor was extracted by sacrificing periphery of the artery. The pathological diagnosis was an internal artery aneurysm with complete thrombotic occlusion. Isolated internal iliac aneurysm is rare, and this is the first case which resulted in complete thrombotic occlusion.

Left atrial free ball thrombus (LABT) after mitral valve replacement (MVR) is very rare, and sudden death may occur by thrombus impaction to the mitral valve orifice. A 81-year-old woman who underwent MVR and tricuspid annuloplasty ten years ago presented with syncope. She was admitted to a hospital, and echocardiography revealed a LABT. When she took sitting position, she fainted. The free ball thrombus possibly impacted mitral valve orifice. She was transferred to our hospital and an emergent operation was performed. There was a LABT of 4 cm in diameter, which was removed. Postoperative course was uneventful. There are 12case reports which described LABT after MVR, and anticoagulant therapy was insufficient in most of those cases. Strict anticoagulant therapy is important to prevent left atrial thrombus after MVR.

The patient was a 69-year-old male who had had percutaneous transvenous mitral commissurotomy (PTMC) 15 years ago, and had stopped taking warfarin after PTMC. He was transferred to our emergency room( ER) because of sudden severe pain in his both lower legs. We recognized pulselessness in his both femoral arteries, and pallor, paresthesia and poikilothermia in his lower extremities. Electorocardiogram(ECG) showed arterial fibrillation, and computed tomography( CT) showed occlusion of the abdominal aorta just below inferior mesenteric artery( IMA) and both common iliac arteries. By echocardiography, a giant thrombus was detected in the left atrium with severe mitral stenosis. Thrombectomy and angioplasty were performed at about 5 hours after the onset of occlusion, and revascularization was successful. Three days after the operation, we excised the giant thrombus in the left atrium and performed mitral valve replacement because we considered that myonephropathic metabolic syndrome (MNMS) had been prevented. The postoperative course was uneventful and he was discharged on the 27th postoperative day.

Antiphospholipid syndrome (APS) is a clinical condition characterized by recurrent thrombotic events and/or pregnancy morbidity associated with the persistence of antiphospholipid antibodies (aPLs). It is the one of the most common diseases in acquired thrombophilia. In approximately 50 % of APS patients, systemic lupus erythematosus coexist. APS is diagnosed by the 2006 Sydney revised Sapporo criteria. The pathogenic processes of APS have not been fully elucidated. Multiple mechanisms have been proposed, including interference with hemostatic reactions, activation of endothelial cells and complement activation. The treatment of APS is virtually the preventive therapy such as long-term anticoagulation and the role of corticosteroid or immunosuppressive agents is limited.

Meta-analysis of randomized controlled studies and case-control studies showed that the risk of low-dose aspirin for upper gastrointestinal bleeding was 1.6-8.2. Some reports showed that the risk of upper gastrointestinal bleeding (UGIB) was high in patients receiving ticlopidine or clopidogrel. A meta-analysis study reported that data regarding the risk for GI bleeding of new direct oral anticoagulants (apixaban, dabigatran and rivaroxaban) were inconclusive. Proton-pump inhibitor and histamine 2-recetor antagonist were effective for prevention of upper GI mucosal injury in patients receiving low-dose aspirin. Some case-control studies showed that PPI use significantly reduced the risk of UGIB in patients with receiving clopidogrel, but not in those with receiving warfarin.

This report describes a case of successful recanalization of intracranial internal carotid artery occlusion by rapidly changing from the Penumbra System® to the Merci® Retrieval System for the retrieval of a predicted white thrombus. A 72-year-old man was consulted to our department with a consciousness disturbance. The patient had undergone graft placement for the management of a thoracic aortic aneurysm 14 days prior. Neurological examination revealed left-sided severe motor weakness and dysarthria. Magnetic resonance(MR)imaging showed a cerebral infarction in the territory of the right internal carotid artery(ICA), while MR angiography revealed occlusion of the right ICA. The systemic intravenous injection of recombinant tissue plasminogen activator was contraindicated, so a mechanical thrombectomy was performed. The use of the Penumbra System® failed to achieve recanalization of the right ICA;therefore, revascularization using the Merci® Retrieval System was performed. As a result, complete recanalization was achieved approximately 2 hours and 45 minutes after symptom onset. The retrieved specimen was elastic and hard, and histological examination revealed a white thrombus without endovascular organization. Postoperatively, the patient was restless for 1 day but did not show any neurological abnormalities. His postoperative course was uneventful, and he was discharged 7 days later without any neurological deficits.

We report 2 cases of ruptured type B aortic dissection with thrombosed pseudolumen presenting hemodynamic deterioration which is a life-threatening condition. In such cases, surgical treatment often resulted in high mortality rates. We underwent total arch replacement via median sternotomy. In both cases, postoperative courses were uneventful. This approach ensured us wider operative field to establish cardiopulmonary bypass quickly, and to perform distal anastomosis without much difficulty.

We reported a case of peripheral embolization arising from diffuse thoracoabdominal aortic thrombi with minimal evidence for atherosclerosis or other aortic pathology. After the patient was treated with anticoagulation therapy, surgical removal of peripheral embolus was performed.

A 70 year old woman had a right renal tumor with vena cava thrombus up to right atrium. We started medical treatment with sunitinib at a dose of 50 mg as neoadjuvant therapy. In 2 months, the vena cava thrombus shrank to the same level of the diaphragm. After stopping sunitinib for 2 weeks, a nephrectomy and thrombectomy was performed with extracorporeal circulation. Pathological diagnosis was clear cell carcinoma, G2. The TNM stage was pT3bN0M0. There were no viable cells at the tip of the thrombus. There is no recurrence during 9 months after the operation. Although we had to stop medication due to thrombocytopenia, it was possible to continue to take sunitinib for 3 months and achieved the operation. Because of down-staging of the tumor thrombus, we didn't have to do thoracic surgery. These results suggest that neoadjuvant therapy with molecular target drug may reduce surgical invasion.

A 59-year-old woman, who was given a diagnosis of portal vein aneurysm at another hospital 2 years previously, visited our institution complaining of abdominal pain in November 2005. Abdominal imaging including computed tomography and ultrasonography demonstrated that the portal vasculature had dilated to 5 cm in maximum dimension and its center was at the junction of the superior mesenteric vein and the splenic vein. Moreover, a large thrombus was seen in the portal vein, the superior mesenteric vein and the splenic vein. She was conservatively followed-up with warfarin. After 6 months, angiography revealed cavernous transformation around the portal vein was found with collateral flow toward the liver. At the time of writing the patient's condition is stable with neither extension of the thrombus nor constriction of the esophageal varices.

Acute coronary syndrome(ACS), including acute myocardial infarction and unstable angina, is a clinical state induced by the thrombus formation following the disruption of unstable atherosclerotic plaque. Recent studies have reported that activated macrophages in the vulnerable plaques destabilize the fibrous cap by the induction of protease such as matrix metalloproteinases. Also, macrophages produce tissue factor and plasminogen-activator inhibitor type 1 those activate thrombus formation following plaque rupture. On the other hand, coronary spasm plays an important role in the pathogenesis of ACS especially in Japan. In this article, we review related factors leading to plaque rupture and erosion in the basic aspect.

We report a case of emphysematous cholecystitis (EC). An 82-year-old woman was hospitalized for subarachnoidal hemorrhage. She presented with fever, vomiting, hypotension, and slight abdominal tenderness in the right upper quadrant. Abdominal computed tomography (CT) revealed the air-fluid level in the lumen of the gallbladder and gas around the wall. The patient underwent cholecystectomy. Laparotomy revealed necrotic changes in the gallbladder. A bile culture revealed Clostridium species infection. The histopathological findings were multiple arterial thromboses and gallbladder infarction. The pathogenesis of EC is controversial, but many cases of emphysematous cholecystitis were acalculous and have been reported in individuals with a history of diabetes mellitus, hypertension, cerebrovasucular accidents, or ischemic heart disease. We consider that the case presented here proves the hypothesis that ischemia and necrotic changes may occur in the gallbladder due to a primary vascular compromise, and that gas-producing bacteria grow under anaerobic conditions, resulting in the development of EC.

A 67-year-old woman was admitted to our hospital for weakness in her right hand. MRI showed multiple cerebral infarctions and ultrasonic cardiography revealed vegetation on her aortic valve, so embolic stroke was diagnosed. Though she was afebrile and her vital signs were normal, chest CT revealed several enlarged mediastinal lymph nodes and a small nodule in the left lower lobe of the lung. Stage III adenocarcinoma of the lung was diagnosed, and the cause of her cerebral infarctions was found to be nonbacterial thrombotic endocarditis (NBTE). NBTE is known as the cause of embolic stroke among patients with advanced cancer, particularly adenocarcinoma. Prompt initiation of continuous heparin administration is required to interrupt the progress of cerebral thromboembolism in NBTE. In cases of coexisting cancer and embolic stroke, we should consider the possibility of NBTE.

A 49-year-old man suddenly suffered left hemiplegia, and was brought to our hospital by ambulance at the beginning of August, 2006. He had a history of hypertension, and had received replacement of a synthetic graft in the ascending aorta and aortic arch with innominate artery for dissecting aneurysm in the aorta 2 years before. On diffusion-weighted magnetic resonance images obtained after admission, cerebral infarction was detected at the right corona radiata, and MR angiography (MRA) showed obstruction of the right middle cerebral artery. He was given intravenous tissue-plasminogen activator (t-PA) a few hours after arrival, and his hemiplegia was improved on the following day. At 11 days after onset, recanalization of the right middle cerebral artery was seen by MRA. On Doppler ultrasonographic examination, obstruction and thrombus in the innominate artery were observed. Retrograde flow of the right vertebral artery was demonstrated by both pulse-Doppler ultrasonography and velocity-coded color MRA. This patient is a rare example of innominate artery steal and ischemic cerebrovascular disease with obstruction of the innominate artery. Cerebral infarction in this patient might have developed via artery-to-artery embolism, with the thrombus in the innominate artery, rather than through a hemodynamic mechanism with innominate artery steal.

Metabolic syndrome is defined as a complex of hypertriglyceride, insulin resistance, hypertension, and accumulation of visceral fat. This syndrome is often accompanied by thrombotic diseases (e.g., myocardial infarction, cerebral infarction), but the mechanism (s) of thrombotic tendency has not yet been elucidated. Plasminogen activator inhibitor-1 (PAI-1), a principal regulator of fibrinolytic system, plays a pathological role in the development of thrombosis and cardiovascular diseases. PAI-1 is regarded to be one of adipocytokines because it is produced and secreted by adipocytes. The expression of PAI-1 in adipocytes is upregulated by insulin, TNF-alpha, and TGF-beta, suggesting that it is relevant to insulin resistance. PAI-1 antigen level in plasma is elevated in obese subjects and increases in parallel with their BMI and visceral fat. It was experimentally revealed that PAI-1 expression in adipose tissue was dramatically increased in genetically obese mice and abundant expression of PAI-1 was localized to adipocytes in vivo. PAI-1 deficient mice were resistant to high fat diet-induced body weight gain, adipose accumulation, and insulin resistance in association with lack of decreased expression of adiponectin. Taken together, PAI-1 may be a key molecule to develop obesity and insulin resistance as well as thrombotic diseases. It is possible to prevent thrombotic complications and cardiovascular diseases in obese patients by controlling PAI-1 expression and function. Each pathology included in metabolic syndrome could stimulate PAI-1 expression, and thus, PAI-1 would be a good marker of progression of metabolic syndrome itself and of risk for thrombotic cardiovascular diseases as well.

A 54-year-old man with general fatigue and lumbago was admitted for further examination of hypercalcemia and leukocytosis. CT showed a huge renal tumor and extension of the tumor thrombus to the inferior vena cava (IVC). Moreover, the serum granulocyte colony-stimulating factor (G-CSF) and the C-terminal of parathyroid hormone-related protein (PTHrP) were elevated. Under the diagnosis of advanced renal tumor, we performed nephro-ureterectomy and throbectomy. Pathological examination revealed squamous cell carcinoma of the renal pelvis. To our knowledge, this is the first case in Japan that of the simultaneous production of G-CSF and PTHrP in squamous cell carcinoma of the renal pelvis accompanied with IVC thrombus.

We report, with serial angiograms, a case worsening of dural arteriovenous fistulae (DAVFs) located at the hypoplastic right cavernous sinus and draining into the left superior ophthalmic vein across the inter-cavernous sinus. The patient presented with sudden onset of external ophthalmoplegia and deterioration of visual acuity on the left. An imaging work-up at the day of admission included contrast-enhanced computed tomography and conventional catheter angiography, which demonstrated complete thrombosis of the left cavernous sinus. There was no strong evidence to suggest DAVFs other than small faint opacification of the posterior cavernous sinus on the right at the late arterial phase. For this reason a diagnosis of left cavernous sinus thrombosis was made, followed by aggressive anticoagulation therapy with intravenous administration of antibiotics. Although the patient's eye symptoms improved significantly after the anticoagulation therapy, the follow-up angiogram obtained 5 days after admission demonstrated small right cavernous sinus DAVFs, which drained into the left superior ophthalmic vein. The patient was followed up conservatively at the out-patient clinic. Three-month follow up angiograms demonstrated spontaneous cure of the DAVF. Also noted was a complete recovery of external ophthalmoplegia with significant improvement of left visual acuity. The alternation of clinical and angiographic findings in this case may help to understand the etiology of paradoxical worsening of cavernous sinus DAVF. In selected cases, anticoagulation therapy may help to improve the prognosis of paradoxical worsening.

An 82-year-old woman presented with mitral regurgitation and atrial fibrillation. She was hospitalized for further examination of cardiac thrombus detected by transthoracic echocardiography. No definitive diagnosis could be made based on computed tomography and magnetic resonance imaging. Intravenous contrast echocardiography suggested a coronary sinus thrombus. Coronary angiography showed coronary sinus ostial atresia. Multislice computed tomography confirmed the presence of thrombus in the enlarged coronary sinus with coronary sinus ostial atresia and persistent left superior vena cava. Persistent left superior vena cava is present in 3% of patients with congenital heart disease. Persistent left superior vena cava is detected by chance during cardiac catheterization for other conditions in patients without cardiac malformations. The present case was detected at an advanced age, and in the absence of prior symptoms.

A 79-year-old woman was admitted for treatment of bronchial asthma. ST-segment elevation in the precordial leads (V4-V6) and T-wave inversion in leads II, III, and aVF was recognized. Transthoracic echocardiography and emergent cardiac catheterization demonstrated two large mobile thrombi (1.2 x 1.3 cm, 0.7 x 1.0 cm) attached to the left ventricular wall. There was no organic stenosis. Left ventriculography revealed anterolateral, apical and inferior dyskinesis, and basal hyperkinesis. The clinical diagnosis was ampulla cardiomyopathy. Anticoagulant therapy was started. Prothrombin time-international normalized ratio was remained at 2.5-3 and partial thromboplastin time was controlled at 1.5-2 times compared with the normal value. Repeated echocardiography showed the mass reduced gradually and had disappeared about 2 weeks later.

A 73-year old man with multiple hepatocellular carcinomas underwent 4 transarterial chemoembolizations, but a tumor thrombus appeared in the left portal vein. The tumor sizes in segments 4 and 5 were 4.0 cm and 2.4 cm, respectively. The serum levels of AFP and PIVKA-II were 14,991 ng/ml and 15,944 mAU/ml, respectively. The tumor was 5-FU palpable in the epigastric region. Four ml of SMANCS and 4 ml of Lipiodol were injected to proper hepatic artery using the Seldinger technique. In addition, epirubicin (20 mg), MMC (4 mg) and Lipiodoi (2 ml) were injected into a proper hepatic artery via a reservoir every 3 weeks. The tumor was not palpable, and the tumor markers were markedly reduced after 2 months. The evaluation of response to the treatment was a partial response 3 months and 6 months later. Chemo-lipiodolization was very useful for advanced hepatocellular carcinoma with portal vein thrombus.

A floating ball thrombus in the left atrium is relatively a rare case. A 70 year-old female patient who showed a symptom of heart failure was admitted to our hospital. By echocardiography, the mass in the dilated left atrium was appeared to be a floating ball thrombus, and the patient was diagnosed to be mitral valve stenosis. Following the treatment of heart failure, the patient underwent mitral valve replacement and the ball thrombus was successfully removed. Because of the high risk of sudden death with strangulated ball thrombus and systemic embolization, surgical removal of the ball thrombus should be done immediately after the diagnosis was established.

An 86-year-old man with severe chest pain and shock was transferred to our hospital. Computed tomography revealed type A aortic dissection with cardiac tamponade. He needed intubation and closed chest massage preoperatively. At operation, intrapericardial space was filled with clotted blood and rupture of the ascending aorta was confirmed. He underwent a successful emergency graft replacement of the ascending aorta. Postoperative course was uneventful except for mild hemianopsia due to cerebral infarction. He had recovered to be able to walk and is doing well.

We report a rare case of free-floating ball thrombus in the left atrium with mitral stenosis. The patient was 71-year-old woman who admitted to the local hospital for transient ischemic attack. Electrocardiography showed atrial fibrillation and an echocardiogram examination revealed free-floating ball thrombus in the left atrium with mitral stenosis. She was transferred to our hospital for emergency open heart operation. After removal of the ball thrombus, mitral valve replacement and modified MAZE procedure were successfully performed. The size of the ball thrombus was 40 x 30 x 33 mm and weighed 20 g. Postoperative course was uneventful.

A 38-year-old woman was admitted to our hospital because of pulmonary thromboembolism. Thrombolysis therapy resulted in initial improvement in symptoms and laboratory data. However, 4 months later, pulmonary thromboembolism recurred despite antiplatelet and anticoagulation therapy. Contrast venography and venous ultrasonography of both upper and lower extremities revealed subtotal occlusion and venous thrombosis of the left subclavian vein with collateral vessels, but no evidence of lower extremity venous thrombosis. She had no history of subclavian venous catheterization, neoplasm, hypercoagulability or other predisposing cause of thrombus formation. Operative ligation of the left subclavian vein was performed at the junction with the internal jugular vein. White thrombus was identified within the venous lumen. She was well without recurrent pulmonary thromboembolism or venous insufficiency for 10 months after the operation. Surgical interruption of the subclavian vein may be effective to prevent recurrent pulmonary thromboembolism in patients with recurrent pulmonary thromboembolism due to venous thrombosis of the upper extremity despite therapeutic anticoagulation.

The risk and mortality of pulmonary embolism is high in patients with free-floating inferior vena cava thrombi. We present a successful surgical case of a 70-year-old male who had acute massive pulmonary embolism associated with a giant free-floating inferior vena cava thrombus extending above the renal veins. Emergent thrombectomy of the pulmonary artery and the inferior vena cava using cardiopulmonary bypass was carried out because he was considered at high risk for fatal recurrent pulmonary embolism. Prophylactical insertion of a Greenfield filter in the inferior vena cava was added. In this report, diagnosis and treatment of inferior vena cava thrombosis is also discussed.