We set out to assess our treatment strategy of acute aortic dissection associated with atherosclerotic aortic aneurysm, and to assess its results. A total of 228 patients with acute aortic dissection were admitted to our hospital between 1994 and 2009. Among these, 30 cases were associated with atherosclerotic aortic aneurysm and we retrospectively analyzed their patient data. Of these, 5 patients received diagnoses of Stanford A dissection and 25 patients demonstrated Stanford B. Coexisting aneurysms consisted of postabdominal aortic replacement in 9 patients, ascending aortic aneurysm in 1, arch aortic aneurysm in 6, descending aortic aneurysm in 2, thoracoabdominal aortic aneurysm in 3, and abdominal aortic aneurysm in 9. Patients were divided into 3 groups based on the relationship between aneurysm and dissection : acute aortic dissection occurred after graft replacement of an aortic aneurysm (Group 1, n=9), dissection coexisted with aneurysm in a different segment of the aorta (Group 2, n=8), and dissection extended to or involved the aneurysm (Group 3, n=13). Our treatment strategy for all patients excluding those with aortic rupture or malperfusion is described below. In the cases of Stanford A dissection, emergency ascending aortic replacement or total arch replacement was performed. In cases of Stanford B, patients were treated conservatively in the acute phase. Surgery for the coexisting aortic aneurysm was then performed in the chronic phase, if the aneurysm was large. We think that the interval between dissection onset and aneurysm surgery should be extended to at least 1 month, because the aortic wall was too fragile to perform anastomosis in the acute phase in the present cases. As a result, there were 2 hospital deaths in Group 3, but there was no aortic rupture during treatment in the acute phase in any of these 3 groups. There were no vascular-related deaths during follow up. Our treatment strategy obtained favorable outcomes.

Swelling and pain appear when blood flow is delayed in states of “oketsu.” Until now “oketsu” as a circulatory disturbance has been studied from profiles of vascular resistance characteristics and blood fluidity. Blood fluidity is influenced by blood cell function, plasma ingredients and reactive oxygen. In this study, we administered the various Chinese herbal medicines, tokishakuyakusan, saikokaryukotsuboreito, tokakujokito, keishibukuryogan and juzentaihoto to determine the effect of these medicines on “oketsu” by observing reactive oxygen dynamics and blood fluidity in rats.SPF male Wistar rats weighing 200 g were used. Each experimental group was given feed containing 3% extract of one Chinese herbal medicine for1week. Blood samples were mixed with heparin, EDTA-2K or sodium citrate to block coagulation. Blood fluidity was measured with a Micro Channel Array Flow Analyzer (MC-FAN). A PA-20 examined platelet aggregation by the reaction to ADP, which activates platelet aggregation. Reactive oxygen dynamics were measured with a Free Radical Elective Evaluator (FREE).As a result, anti-oxidative ability and blood fluidity increased in all Chinese herbal medicine-administered groups. Furthermore, an inverse correlation between the fluidity of erythrocyte suspensions and anti-oxidative ability was shown. We speculate that an anti-oxidative influence of Chinese herbal medicines affected erythroid deformability or stickiness. In addition, tokishakuyakusan, tokakujokito and keishibukuryogan decreased platelet aggregation ability.This study shows that “oketsu” improves blood properties and suggests that Chinese herbal medicine improves decrease in blood fluidity, the causes of conditions such as thrombosis or embolism.

Lung hemorrhage associated with pulmonary reperfusion injury is a rare but lethal condition. We presented a case salvaged by non-heparinized extracorporeal life support for massive lung hemorrhage after pulmonary thromboembolectomy. Sub-acute pulmonary thromboembolism with a floating right atrial thrombus was diagnosed in 63-year-old woman by computed tomography and echocardiography. An emergency pulmonary thromboembolectomy was performed using cardiopulmonary bypass and moderate hypothermia. Immediately after reperfusion, extraordinary lung hemorrhage occurred and continued. We decided to take over the standard cardiopulmonary bypass with a non-heparinized extracorporeal life support system. Fortunately, hemostasis of the lung hemorrhage was completely secured within 12h, and the extracorporeal life support was terminated at 20h after the surgery. The patient was extubated at 48h after the surgery, and was discharged after the insertion of an inferior vena cava filter for a floating deep venous thrombus. Although the necessity, efficacy and risk of the non-heparinized extracorporeal life support should be clarified, we conclude that it could be the treatment of choice for life threatening lung hemorrhage associated with pulmonary reperfusion injury.

Supravalvular aortic stenosis is a rare obstructive lesion of the left ventricular outflow tract localized at the level of sinotubular junction. It has been recognized that supravalvular stenosis may occur as a part of Williams syndrome and is sometimes complicated by obstruction of the left main coronary artery. We successfully performed single patch augmentation for supravalvular aortic stenosis and left coronary ostial stenosis with concomitant aortic valvotomy in a child without Williams syndrome. The patient had been followed as congenital bicuspid aortic valvular and supravalvular stenosis. At the age of 3 years, cardiac catheterization revealed an increased pressure gradient of 90mmHg at the left ventricular outflow and newly developed ostial stenosis of the left coronary artery. An oblique incision on the ascending aorta was made above the sinotubular junction and extended leftward onto the left main coronary artery, and this incision opened the fibrous ridge at the left coronary artery. After commissurotomy for the bicuspid valve, both the supravalvular and ostial stenosis were augmented with a single autologous pericardial patch treated by glutaraldehyde. The pressure gradient was significantly reduced and the ischemic left ventricular dysfunction was eliminated.