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, p<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.

A 57-year-old man was admitted with high fever and chest discomfort associated with aortic valve infective endocarditis. An echocardiogram showed severe aortic valve regurgitation. An emergent operation was performed. The aortic valve was destroyed and an annulus abscess was observed. Aortic valve replacement was performed. There was a large amount of pleural effusion in both chest cavities. Bilateral chest drainage was performed. Cardiopulmonary bypass weaning was performed uneventfully. The operation was finished without any mechanical support required. However, respiratory failure was observed to progress rapidly immediately after the operation. A postoperative X-ray showed bilateral pulmonary edema. Re-expansion pulmonary edema was diagnosed. Because oxygenation was not improved in ventilator settings, venovenous extracorporeal membrane oxygenation (V-V ECMO) was installed. Respiratory support with V-V ECMO was needed for 17 days postoperatively. It took 36 days before the patient was removed from the ventilator. V-V ECMO successfully managed bilateral re-expansion pulmonary edema.

A 57-year-old man presented with a one-month history of dyspnea. Computed tomography revealed a pulmonary embolism, and echocardiography revealed multiple linear floating thrombi in the right atrium. An urgent surgical thrombectomy was performed, and most of the thrombi in the right atrium and bilateral pulmonary arteries were removed under cardiopulmonary bypass. The thrombi in the right atrium adhered to the linear Chiari networks. The patient was treated with rivaroxaban uneventfully and subsequently discharged on postoperative day 26. Herein, we report a case of right atrial thrombi and pulmonary embolism likely augmented by the Chiari network, which was successfully treated with surgical thrombectomy.