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Article in Japanese | WPRIM | ID: wpr-374583


Studies have shown that postoperative disseminated intravascular coagulopathy (DIC) occurs in some patients with cardiac disease, acute aortic dissection, and ruptured abdominal aortic aneurysm. The specific pathophysiology of DIC in these settings are related to low cardiac function, shock, infection and sepsis as well as activation of coagulation cascade in the aneurysm sac or dissected aorta. A soluble form of recombinant human thrombomodulin (rhsTM) was approved in 2008 for the treatment of DIC. This report describes the safety and efficacy of rhsTM for the treatment of DIC in patients with cardiovascular disease operated in our department. Between October 2010 and March 2012, 35 patients with postoperative DIC were treated with rhsTM. Diagnosis of DIC was based on the diagnostic criteria for DIC of the Japanese Association for Acute Medicine (JAAM). During the first 6 months of the study period, after a diagnosis of DIC was made, the patients were treated with gabexate mesilate and antithrombin III, and if patients showed no improvement with conventional treatment, they received rhsTM for 6 days. During the last 10 months of the study period, patients received rhsTM soon after a diagnosis of DIC was made. Twenty seven patients survived for 28 days after rhsTM treatment, and the mortality rate was 22.9% (8/35). Patients who survived showed improvement in acute phase DIC scores, FDP levels, D-Dimer, fibrinogen and platelet counts during rhsTM treatment, but no improvement was observed in patients who died. No serious adverse events were found up to 28 days after the start of rhsTM administration. In conclusion, this study showed no adverse events of rhsTM, and further studies are needed to confirm that rhsTM administration is an effective therapeutic modality in the management of DIC after cardiovascular surgery.

Article in Japanese | WPRIM | ID: wpr-362001


Neointimal hyperplasia is the principal mechanism of graft failure in coronary artery bypass surgery. Systemic administration of cilostazol has been reported to suppress neointimal hyperplasia in some vascular injury models. We sought to deliver cilostazol locally in an attempt to augment its beneficial effect to inhibit neointimal hyperplasia at an anastomotic site. We examined whether the external application of a novel cilostazol-eluting film can inhibit neointimal hyperplasia in a vascular anastomosis model. Canine femoral artery graft interposition was performed in 20 beagle dogs, assigned to 4 groups of 5 dogs each : a graft interposition without copolymer of L-lactide and ε-caprolactone (P (LA/CL) ) film (control group) and groups with P (LA/CL) film containing cilostazol of either 10 mg, 40 mg, or 80 mg doses. All the cilostazol-eluting film with 10 mg, 40 mg, and 80 mg dose groups had a reduced intima/media ratio compared to the control group (0.15±0.03, 0.11±0.03, and 0.12±0.03, vs. 0.31±0.03, <i>p</i><0.05). Immunohistochemical analyses for proliferating cell nuclear antigens revealed reduced cellular proliferating activity associated with decreased α-actin positive cells in the cilostazol-eluting film groups compared to the control group. External application of cilostazol-eluting film can inhibit neointimal hyperplasia, at least in part, by inhibiting smooth muscle cell proliferation in the intima.

Article in Japanese | WPRIM | ID: wpr-366177


In the past 13 years, 17 patients underwent reoperation after intracardiac repair, including reconstruction of the right ventricular outflow tract. Primary diagnoses of the cardic anomalies were tetralogy of Fallot (TOF) (8 patients), extreme type (TOF) (4 patients), TOF with absent pulmonary valve (1 patient), double outlet right ventricle (DORV) (2 patients), truncus arteriosus (1 patient) and transposition of the great arteries (TGA) (1 patient). Patients were divided into 4 groups based on the surgical procedures for reconstruction of the right ventricular outflow tract as follows: Group A, porcine valved conduit; Group B, autologous pericardial valve bearing tube graft; Group C, transannular patch; Group D, outflow patch with pulmomary valvotomy. The main reason for reoperation in groups A and B was pulmonary stenosis due to calcification of the porcine valve or shrinkage of the pericardial tube graft. Average periods between corrective surgery and reoperation were 7 and 13 years in groups A and B, respectively. Reoperation was performed for massive tricuspid regurgitation and residual shunt, 15 and 24 years after previous operations in groups C and D, respectively. Low cardiac output syndrome, proconged right heart and respiratory failure were major postoperative complications in groups A, B and C. Furthermore, one patient in group A and one other in group C died in the long-term period after reoperation. Both patients had had markedly dilated hearts associated with frequent PVCs. In conclusion, earlier reoperation for progressive and/or residual lesions should be performed to obtain better surgical outcome and quality of life of the patients.