We studied the acute and chronic biological reaction to balloon-expandable intracoronary
To overcome the problem of recurrence of stenosis after vascular balloon dilatations, we developed an expandable, intraluminal graft that allows dilatation of the lesion and simultaneous placement of a supportive endoprosthesis to prevent recoil of the arterial wall. The graft is made of continuous, woven, stainless steel wire. The resulting tubular mesh has a wall thickness of 200-450 micron and 80% open surface. The grafts, mounted on angioplasty catheters, are introduced through 8-12-F Teflon sheaths. Eleven grafts of 6, 8, and 10 mm in diameter by 20 mm long were placed in the aorta, common carotid, superior mesenteric, iliac, and renal arteries of dogs. Six grafts showed no stenosis in follow-up studies of up to 8 weeks. Two grafts had moderate stenosis as a result of neointimal hyperplasia. Two partial and one complete graft thrombosis occurred in nonheparinized animals in which the graft outflow was restricted. Anticoagulant was not used on a long-term basis. Light and electron microscopy studies showed complete covering of the graft's inner surface by endothelium at 3 weeks.
Arterial collaterals in the hilus of the liver may develop in a variety of clinical situations including neoplasm, atherosclerosis, operative ligation and other vascular stenoses, and cirrhosis. They are normally present but are not demonstrated angiographically unless they are functioning as collaterals. Hilar collaterals are an important factor in maintaining liver viability following accidental or purposeful hepatic arterial ligation. The authors base their discussion on personal experience with 16 cases. INDEX TERMS: Liver, blood supply. Arteries, hepatic Radiology 94: 575-579, March 1970 T H E POSSIBILITIES for the development of collateral blood flow to an occluded hepatic artery depend primarily on the site of the occlusion (3). If the celiac or common hepatic artery is occluded, several potential routes exist for collateral circulation (1,4). The main pathway is through the pancreaticoduodenal arcades and the gastroduodenal artery. With proper hepatic artery occlusion, these major collateral channels cannot be utilized, and the liver becomes dependent upon small collaterals in the hepatic ligaments and around the common bile duct. If the occlusion is located in the right or left hepatic arteries or their branches, collateral vessels may develop between these arteries in the hilus of the liver. These hilar communications between hepatic arteries are an important but poorly recognized entity. We are, therefore, presenting 16 patients in whom such collaterals were demonstrated at angiography. METHODS AND MATERIALSThe 16 patients underwent celiac and superior mesenteric angiography for a variety of reasons. The angiograms were obtained by the percutaneous femoral technique, using thin-walled, red Kifa catheters (LD./O.D. = 1.4/2.2). Renografin 76 per cent (Squibb) was injected into the celiac and superior mesenteric arteries at a rate of 12 ml/sec. for three seconds, and serial films were obtained at 2 per second for five seconds, 1 per second for five seconds, and 1 every other second for ten seconds. The angiograms were evaluated to determine (a) the direction of the blood flow through the collateral vessels and (b) the cause for the development of the collateral flow. In addition, the relevant visceral vascular anatomy and its contribution to the pattern of development of collateral flow were assessed. RESULTSHilar collaterals developed subsequent to vascular stenosis in 7 patients, to operative ligation in 5, to tumor in 2, and to cirrhosis in 2. The vascular stenoses were secondary to atherosclerosis in 4 patients, but in 3 younger patients they were probably caused by diaphragmatic crus or were congenital. The operative stenoses were seen in 3 patients following liver resection
In an attempt to demonstrate the cause of change in bruit with respiration, the author observed changes in the configuration of the celiac axis during deep inspiration and deep expiration lateral aortography of 12 patients. Three of the 12 had no bruits during quiet respiration, but in deep expiration a bruit occurred; compression by the median arcuate ligament of the diaphragm caused a notch on the cephalad surface of the celiac artery. A fourth patient had an epigastric bruit during quiet respiration; aortography showedapproximately 80% stenosis of the celiac artery during inspiration and occlusion during expiration.
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