Reiji Hattori

Redirection of Hepatic Venous Drainage After Total Cavopulmonary Shunt in Left Isomerism

BACKGROUND Conversion from total cavopulmonary shunt (TCPS) to the Fontan circulation can improve cyanosis in patients with potential risks of development of pulmonary arteriovenous fistula (PAVF). METHODS Inclusion of the hepatic veins in the pulmonary circulation was employed using an intra-atrial tube graft in 5 patients with left isomerism previously undergoing TCPS. Prior to the conversion, abnormal communication was identified between the azygos vein and either the hepatic or the portal vein in all. PAVF was seen in 3. RESULTS All patients survived the procedure. Postoperative catheterization showed 13 +/- 2 mm Hg of superior caval venous pressure, and 2.3 +/- 0.4 L/min/m2 of cardiac index. Pulmonary arteriovenous fistula progressed markedly in the right lung even after the conversion in 2 patients, in whom the hepatic veins had been exclusively diverted to the left lung. Arterial oxygen saturation became below 65%, with exercise capacity reduced, in these 2 patients. The other patients remain asymptomatic. CONCLUSIONS Total cavopulmonary shunt can be efficiently converted to the Fontan circulation by appropriately redirecting hepatic venous drainage to perfuse both lungs in a balanced fashion.

Enhanced mesenchymal cell engraftment by IGF-1 improves left ventricular function in rats undergoing myocardial infarction

BACKGROUND We hypothesized that enhanced mesenchymal cell (MC) engraftment with insulin-like growth factor-1 (IGF-1) improves left ventricular (LV) function and survival. METHODS AND RESULTS IGF-1 (10 microg/ml) increased adhesion and inhibited apoptosis under hypoxia in vitro through activation of phosphatidylinositol 3-kinase (PI3K) in bone marrow-derived MCs obtained from transgenic rats expressing green fluorescence protein. Myocardial infarction (MI) in rats was produced by ligature of the left coronary artery. One month after MI, rat hearts were injected with MCs in the presence or absence of 10 microg/ml IGF-1 with or without PI3K inhibitor, 5 microM LY294002. IGF-1 significantly increased engraftment of MCs between 6 h and 3 days after transplantation associated with the increase in stromal cell-derived factor-1alpha in the infracted LV. The transplanted MCs had disappeared 1 month after transplantation in all groups. MC transplantation with IGF-1 significantly increased neovascularization and inhibited cardiomyocyte apoptosis 3 days and 1 month after MC transplantation. This was associated with improved LV function 1 month after MC transplantation and eventually survival. LY294002 abrogated all of the beneficial effects of MC transplantation with IGF-1. IGF-1 alone had no effect on neovascularization and did not improve LV function and/or survival. CONCLUSIONS These results suggest that IGF-1 improves engraftment of MCs at the time of transplantation via activation of PI3K and this improved engraftment of MCs may be attributed to an increased neovascularization and inhibition of cardiomyocyte death, leading to improvement of LV function and prolongation of survival despite the eventual loss of the transplanted MCs.

Fate of fibrin sealant in pericardial space

BACKGROUND Although fibrin sealant (Beriplast, Aventis Behring, Marburg, Germany) has been widely used as a supplementary measure for hemostasis during cardiac surgery in Europe and is becoming popular in the United States, the pharmocokinetics of fibrin sealant applied in pericardial space has not been elucidated. METHODS A small incision was made on the epicardial surface of the left ventricle of a rat, and the incision was sutured. Total 0.2 ml of fibrin sealant containing iodine 125 (125I)-labeled fibrinogen, aprotinin, blood coagulation factor XIII and thrombin was applied to the area around the suture line. RESULTS Distributions of 125I-labeled fibrinogen in the heart on postoperative days 1, 3, 7, and 14 were 48.2% +/- 1.8%, 20.7% +/- 2.2%, 0.15% +/- 0.02%, and 0.01% +/- 0.02%, respectively. The radioactivity was negligible in the blood, liver, spleen, and kidney except for the thyroid in which the radioactivity increased to 7.9% +/- 0.7% and 4.3% +/- 0.4%, respectively, on postoperative days 7 and 14. Iodine 125-labeled fibrinogen concentrations of the heart and other organs showed a similar change in the time course of distribution. Dense and thick fibrin network, observed on postoperative day 1, had dissipated and was thinner with collagen formation by postoperative day 7. CONCLUSIONS Fibrin sealant applied to the pericardial cavity regresses rapidly and plays an important role in wound healing.

Effects Of The Na+/H+ Exchange Inhibitor Cariporide (HOE 642) On Cardiac Function And Cardiomyocyte Cell Death In Rat Ischaemic–Reperfused Heart

1. Na+/H+ exchange has been implicated in the mechanism of reperfusion injury. We examined the effects of the cardiac‐specific Na+/H+ exchange inhibitor cariporide (HOE 642) on postischaemic recovery of cardiac function and cardiomyocyte cell death (i.e. necrosis and apoptosis).

Multiple papillary fibroelastoma with quadricuspid aortic valve.

had chronic rheumatoid arthritis; 9 patients (30%) had other underlying risk factors, such as congenital or degenerative heart valve disease or coagulation problem; and 3 patients (10%) had no risk factors. The majority of their patients underwent surgery for valve dysfunction. When patients can tolerate cardiac surgery with cardiopulmonary bypass, indications for surgery are valve dysfunction, recurrent embolic events, and mobile vegetation. Removal of vegetation and repair of the valve seem to be feasible if the vegetation is small and localized. Prognosis after valve replacement or repair for nonbacterial thrombotic endocarditis is unknown but depends on the underlying cause. Even if the previous femoropopliteal bypass was performed with the working diagnosis of Burger disease, it is unlikely because there was no arterial disease in the other leg. Because of the large size of the vegetation plus the possible delay of time between ischemic events, the patient’s limb ischemia was thought to be arterial embolization caused by the vegetation. His noncoronary aortic leaflet was atrophic, which may be a factor in causing nonbacterial thrombotic endocarditis. Despite the patient’s young age and good general condition, he should be monitored carefully for possible occult malignant disease.

Experimental study of pulmonary artery infusion with cisplatin in a solitary pulmonary tumor model using a rat colorectal adenocarcinoma cell line

OBJECTIVES We assessed a tumor model prepared by open lung injection to study metastatic lung tumors, and evaluated the efficacy of pulmonary artery infusion. METHODS Subjects were 30 male F344 rats. In experiment 1, we evaluated chemosensitivity of a rat colorectal adenocarcinoma cell line (RCN-9) using a colorimetric [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. In experiment 2, we injected RCN-9 cells into the left lung on day 0; on day 10, we measured tumor tissue blood flow before and after pulmonary arterial occlusion. In experiment 3, we injected RCN-9 cells into the left lung and conducted no further procedures in controls. The pulmonary artery infusion group underwent pulmonary artery infusion with 0.1 mg of cisplatin on day 3 and the sham group injection with saline solution alone. On day 10, rats were sacrificed and maximum tumor cross-section measured. RESULTS In experiment 1, the drug concentration required to inhibit cell growth 50% was 2.45 x 10(-6) M. In experiment 2, tumor tissue blood flow decreased significantly after arterial occlusion (p = 0.003). In experiment 3, the maximum tumor cross-section in the pulmonary artery infusion group was significantly smaller than in shams (p = 0.0027) and controls (p = 0.0019). CONCLUSIONS The pulmonary artery supplies tumors with blood, so this model appears useful in studying metastatic lung tumors, whose size was reduced significantly by pulmonary artery infusion with cisplatin. Pulmonary artery infusion is thus a promising modality in metastatic lung tumor treatment.

Potential role of vacuolar H+–adenosine triphosphatase in neointimal formation in cultured human saphenous vein☆

OBJECTIVE Vacuolar H(+)-adenosine triphosphatase plays a pivotal role in pH regulation and molecular transport across the vacuolar membranes and is involved in cell proliferation and transformation. In the present study, possible involvement of vacuolar H(+)-adenosine triphosphatase in neointimal formation was investigated in an organ culture model of human saphenous vein. METHODS AND RESULTS Cultured saphenous vein segments developed neointimal formation and marked thickening of the media within 14 days. Neointimal formation and medial thickening were completely inhibited by 10 nmol/L bafilomycin A(1), a selective inhibitor of vacuolar H(+)-adenosine triphosphatase, although structurally related macrolide antibiotics FK-506 and erythromycin were without an effect. The neointimal cells were positive for alpha-smooth muscle actin and vimentin but negative for desmin, indicative of myofibroblasts. The emergence of myofibroblasts was inhibited, and endothelial cells were preserved in the saphenous vein segments treated with bafilomycin A(1). Uptake of bromodeoxyuridine, a proliferation marker, by myofibroblasts was abrogated in the saphenous vein segments treated with 10 nmol/L bafilomycin A(1). Detection of apoptotic cells by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling concomitant with identification of desmin-expressing smooth muscle cells demonstrated that neointimal myofibroblasts, but not medial smooth muscle cells, that expressed desmin underwent apoptosis by treatment with bafilomycin A(1). CONCLUSIONS These results suggest that vacuolar H(+)-adenosine triphosphatase may be involved in myofibroblast growth that contributes to neointimal formation and medial thickening in cultured human saphenous vein. Increased sensitivity of myofibroblasts, but not endothelial cells, and differentiated smooth muscle cells to bafilomycin A(1) may have potential therapeutic implications in the treatment for vein graft disease.

Single patch multilayer aortic annular repair for destructive infective endocarditis.

Active infective endocarditis may progress to annular abscess formation. We describe a patch annuloplasty technique to treat the fragile aortic root tissue in these patients. doi: 10.1111/jocs.12485 (J Card Surg 2015;30:424–426)

Multiple Coronary Artery-Pulmonary Artery-Bronchial Artery Fistulas

A 75-year-old male presenting with angina was found to have significant lesions in the right coronary artery (RCA) and left anterior descending artery (LAD). In addition, a three-dimensional computed tomogram (3DCT) revealed a network of fistulae between the LAD and RCA forming a plexus of dilated vessels in the anterior aspect of the pulmonary artery (Fig. 1A and B). There was also a network of vessels communicating between the right bronchial artery with multiple fistulas to the RCA and LAD (Fig. 1A and C). At the time of surgery, saphenous vein was used to bypass the RCA lesion and the left internal mammary artery was used to

Repair of a recurrent pseudoaneurysm of the ascending aorta in an atomic bomb survivor with myelodysplastic syndrome.

Abstract  The occurrence of infective aortic pseudoaneurysms tends to be intractable and difficult to treat. We experienced a very rare case of a recurrent infective pseudoaneurysm in the ascending aorta that occurred after cardiac surgery in an atomic bomb survivor with myelodysplastic syndrome. The pseudoaneurysm was successfully repaired using a femoral artery autograft with an omentopexy and the patient recovered well without any recurrence.