Ryoji Hatano

Duplicate origin of left vertebral artery.

SummaryA verified case of duplicate origin of the left vertebral artery in association with a large aneurysm arising from the aortic arch immediately distal to the left subclavian artery is presented. An anomalous left vertebral artery arises directly from the aortic arch between the left common carotid and subclavian arteries, and joins with the normal left vertebral artery in the transverse foramen of the fifth cervical vertebra.

Multiple aneurysms of the visceral arteries with migrating vascular bruit on postural change: A case report

Multiple aneurysms of the gastroepiploic artery and the ileocecal branch of the superior mesenteric artery were found in a 68-year-old male patient by angiography. The patient presented with one-hour postprandial epigastric pain of 10 years duration. Abdominal bruit was auscultated at the two different sites, one of which shifted downwards upon upright position. From the freely movable nature of the great omentum, this bruit, migrating upon postural change, was most likely from the gastroepiploic artery aneurysms. The aneurysms were excised and the abdominal bruit disappeared. The etiology of the aneurysms was suggested to be arterial fibrodysplasia histologically. From this experience, it was stressed that postural change should be added to a routine physical examination to rule out an aneurysm from the freely movable great omentum.

Degenerative changes of vein grafts in preparation media: preliminary studies by electron microscopy and fibrinolytic autography.

Degenerative changes of saphenous vein grafts in four preparation media (heparinized whole blood at room temperature and 4°C, and heparinized normal saline at same temperatures) were examined by scanning and transmission electron microscopy and fibrinolytic autography. Following 60–90 min. storage in heparinized normal saline at room temperature, marked morphological changes were present in the media, accompanied by swellingof the endothelial cells, however the tunica media and adventitia were well preserved even after 120 minutes in all of the four preparation media. The decrease in fibrinolytic activity was comparable to the observed morphological changes. In heparinized whole blood at 4°C, degenerative changes were slow and mostly of a slight nature.

Surgical treatment of juxtarenal aortic occlusion

From 1974 to 1976, four patients with juxtarenal aortic occlusion were operated upon with no surgical mortality. Thromboendarterectomy (TEA) of the aorta with renal revascularization was performed in one patient, and TEA with grafting in three. Intraoperative renal protection was particularly important, since suprarenal aortic clamping was often required in these cases. Possible renal embolism developed in one patient postoperatively. In order to prevent renal embolism and to minimize ischemic insult to the kidney, the value of the following procedures was stressed; (a) irrigation of aortic lumen with saline after TEA under suprarenal aortic clamping with renal arteries kept occluded, and (b) re-application of aortic clamp below the renal arteries after irrigation.Since the most distal level of occlusive process was the common femoral artery in our series, the patient with this desease entity should be treated more actively.

Simplified operative technique for the long-segment atypical coarctation of the aorta

Simplified operative technique for the long-segment atypical coarctation of the aorta was described. The main objective of this technique is to gain quick access to both thoracic and abdominal aorta with minimal blood loss, and preservation of diaphragmatic function. This procedure consists of standard thoracotomy and pararectal incision with an entry into the retroperitoneal space. Long prosthetic graft was anastomosed in an end-to-side fashion to bypass the coarctated aorta. The graft is placed through peripheral circumference of the left hemidiaphragm, where phrenic nerve injury is not likely to occur. This technique was successfully applied to two cases of long-segment atypical coarctation of the aorta due to Takayasu’s aortitis. Retroperitoncal placement of the graft prevents fatal hemorrhage due to direct contact with the graft. Contamination with transintestinal exudate can also be avoided. Results of the ten-year follow-up of the similar procedure in the literature is encouraging.

Pulmonary hemodynamics following reconstructive mitral valve surgery

The hemodynamic response in the immediate postoperative period after reconstructive mitral valve surgery was evaluated by means of cardiac output, pulmonary artery and left atrial pressures, pulmonary blood volume and pulmonary vascular resistance using indwelling catheters in the pulmonary artery and left atrium. Elevated pulmonary artery pressure returned to near-normal levels immediately after the correction of mitral stenosis by closed commissurotomy and mitral insufficiency by annuloplasty or valvuloplasty. Pulmonary artery and left atrial pressures returned to near-normal levels within 24 hours after surgery. In contrast, normalization of pulmonary artery and left atrial pressures were not conspicuous in cases of open commissurotomy. The difference could not be explained by the blood volume deficits, ischemic cardiac arrest during surgery, or residual valvular lesions. The most likely explanation appears to be due to further impairment of chronically diseased left ventricle by open heart surgery and increased water load after hemodilution perfusion which leads to interstitial pulmonary edema. Comparison between the pulmonary artery, left atrial pressures and cardiac output suggested that keeping pulmonary artery mean pressure below 35 mmHg. and left atrial mean pressure below 15 mmHg. are important to maintain optimum cardiac output without causing interstitial pulmonary edema in the immediate postoperative period after mitral valve surgery.

Successful resection of an aortic arch aneurysm using a temporary trifurcation bypass graft.

Resection of a syphilitic aortic arch aneurysm in a 62-yearold woman was accomplished using a trifurcation temporary bypass system. The bifurcation graft was sutured end-to-side to the ascending thoracic aorta, to the brachiocephalic trunk and to the left common carotid artery, respectively. The attached third limb end was anastomosed end-to-side to the infrarenal abdominal aorta. This technique enabled a larger shunt into the abdominal aorta. Occlusion of the iliac arteries proved to be effective in coping with hypotension while attending to the bypass and the volume replacement. The post-operative recovery was uneventful and the patient has remained well after 43 months.

A role of extracorporeal circuit in the post-perfusion thrombocytopenia: A scanning electronmicroscopic observation

Thrombocytopenia is one of the adverse effects of extracorporeal circulation (ECC) but the mechanism of which has not been fully understood. Blood-gas interface, mechanical agitation, rough surface of extracorporeal circuit and sequestration in the liver have been considered to be a cuase of platelet loss. Extracorporeal circuit which provides large artificial surface for contact of blood has been blamed as the site of platelet destruction during oxygenation. However, the part of the oxygenator responsible for platelet loss has not been located. This study was designed to identify the sites of extracorporeal circuit responsible for platelet loss during ECC with scanning electron microscopy (SEM) of the post-perfusion circuit. The accumulation of platelet aggregates was most pronounced at the defoaming net and blood filter where a sudden changes in velocity of blood flow take place. The aggregates were considered to be formed locally at these sites. However, there were no accumulation and/or adherence of platelet aggregates of significant degree at the other parts of the circuit, namely venous and arterial tubings, venous colum and arterial reservoir. Platelets seem to be removed from the circulation during each passage by defoaming net and blood filter. However the other parts of the circuit seem to be less blamed for the platelet loss. It was not possible to conclude whether the formation and trapping of platelet microaggregates at the defoaming net and blood filter or the destruction by oxygen bubbles is mainly responsible for the plateletloss during ECC.