Sequelae of limited amputation.

Ninety patients underwent toe amputations because of vascular disease; 21% required higher amputation and 21% healed without further surgery (i.e., revascularization). Of 60 patients who required bypass surgery, 52 underwent successful first amputations and eight required higher amputations. No difference was seen between diabetic and nondiabetic patients in eventual limb salvage; however, men fared better than women. Without bypass surgery, 11 of 30 patients required a higher level of amputation. No patient's toe amputation site healed with an ankle-to-brachial index of less than 0.35. The judicious use of toe amputation remains an important tool in the surgeon's quest for limb salvage.

The effect of withdrawal of drugs treating intermittent claudication.

BACKGROUND: Pharmacologic treatment for intermittent claudication is a management option. This study evaluated the effect of withdrawal of drug therapies, cilostazol and pentoxifylline, on the walking ability of peripheral artery disease patients. METHODS: Single-blind placebo crossover from a randomized, double-blind trial; 45 claudication patients received either cilostazol 100 mg orally twice daily (n = 16), pentoxifylline 400 mg orally three times daily (n = 13), or placebo (n = 16) for 24 weeks. After 24 weeks of double-blind therapy, treatment for all groups was placebo only, and follow-up continued through week 30. Treatment efficacy was established with treadmill testing. RESULTS: Profile analysis demonstrated a highly significant loss of treatment benefit after crossover (P = 0.001) for cilostazol-treated patients, but no significant change after crossover was observed with pentoxifylline. CONCLUSIONS: Drug withdrawal worsened the walking of claudicants who had benefited from cilostazol therapy. This decline with crossover to placebo suggests that the initial improvement with cilostazol treatment was due to the drug's action. Withdrawal of pentoxifylline did not adversely affect walking.

Internal iliac artery aneurysm following aortic reconstruction.

Fewer than 100 internal iliac artery aneurysms have been reported in the English literature. Of these the incidence of true aneurysms occurring after aortic reconstruction is exceedingly low. A 73-year old man presented with 7 cm asymptomatic left internal iliac artery aneurysm 12 years after repair of an abdominal aortic aneurysm with a bifurcation graft. We report our experience with this patient along with a review of the literature and recommendations for aneurysm surveillance.

Acute aortic occlusion secondary to Aspergillus endocarditis in an intravenous drug abuser.

A 55-year-old black man, an intravenous substance abuser who had an acute arterial embolus to the distal aorta originating from his mitral valve, was noted on pathologic examination of the clot to have aspergillosis emboli. The infective endocarditis also resulted in emboli to the brain with subsequent death.

Heparin treatment enhances the recovery of neoendothelial acetylcholine-induced vascular relaxation after balloon catheter injury in the rabbit aorta.

BACKGROUND: After catheter injury, the neoendothelium that grows is abnormal in morphology and in acetylcholine-induced generation of endothelium-derived relaxing factor (EDRF). Heparin has been shown to have stimulatory effects on vascular endothelial growth in vitro. Its effect in vivo on neoendothelial cell morphology and metabolism after injury has not been described. We investigated the effect of heparin treatment on the neoendothelium formed after injury. METHODS AND RESULTS: Four groups of New Zealand White rabbits were studied. Group 1 rabbits underwent catheter denudation and were killed 4 weeks after injury without receiving treatment (NO Tx, n = 8). Groups 2 and 3 underwent similar aortic injury, received 2 weeks of treatment with either heparin (n = 7) or low molecular weight heparin (LMWH, n = 5), and were killed at 4 weeks. Group 4 underwent sham operation (SHAM, n = 8). EDRF generation was determined by the relaxation of precontracted aortic rings in an organ bath in response to acetylcholine. The heparin-treated group exhibited a significant improvement in acetylcholine-induced relaxation (27%) versus both LMWH-treated (14%, P = .035) and untreated groups (11%, P = .004), although relaxation was only 50% of that observed in the uninjured control vessels (52%, P = .001). The neoendothelium formed in the heparin-treated group exhibited a more normal histological appearance and was aligned with the direction of blood flow as compared with that observed in the untreated or LMWH-treated groups. CONCLUSIONS: These results demonstrate that in vivo heparin administration enhanced the recovery of EDRF generation and augmented normalization of the morphologic appearance of the neoendothelium.

Angiopeptin enhances acetylcholine-induced relaxation and inhibits intimal hyperplasia after vascular injury.

The effects of the somatostatin analogue, angiopeptin (BIM-23014), on neoendothelial function, as evidenced by formation of prostaglandin (PG) I2 and by acetylcholine-induced relaxation (formation of endothelial-derived relaxing factor), were investigated in the rabbit aorta. A balloon catheter injury of the thoracic and abdominal aorta was induced in New Zealand White rabbits. Animals treated with angiopeptin for 2 or 4 wk were compared with untreated rabbits at 2 or 4 wk after the induction of injury, as well as to sham-operated controls. When the rabbits were killed, vascular rings were assessed for arachidonic acid-stimulated PGI2 formation, acetylcholine-induced relaxation, and the degree of intimal hyperplasia. Vascular rings from animals treated with angiopeptin exhibited enhanced acetylcholine-induced relaxation; however, angiopeptin treatment had no effect on arachidonic acid-stimulated PGI2 formation. Intimal hyperplasia in treated animals was reduced by 36%. Treatment with another somatostatin analogue, BIM-23030, did not enhance relaxation or inhibit intimal hyperplasia. These data suggest that treatment with angiopeptin may inhibit intimal hyperplasia in part by its beneficial effect on neoendothelial function.

Temporary arterial shunts to maintain limb perfusion after arterial injury: an animal study.

BACKGROUND: Temporary shunt placement can quickly restore perfusion after extremity arterial injury. This study examined the adequacy of limb blood flow with shunt use, non-heparin-bonded shunt patency over prolonged periods, and the safety of this technique. METHODS: Common iliac arteries were divided and 4.0-mm Silastic Sundt shunts placed in 16 anesthetized pigs. Eight (group I) had shunts placed immediately; eight others (group II) were shunted after an hour of limb ischemia and hemorrhagic shock. Physiologic parameters and femoral artery blood flow in both hindlimbs were continuously monitored. Limb lactic acid generation, oxygen utilization, and hematologic and metabolic effects were serially evaluated for 24 hours. RESULTS: Shunts remained patent in 13 of 16 pigs. Shunts thrombosed in two group I animals because of technical errors, but functioned well after thrombectomy and repositioning. Patency could not be maintained in one animal that died from shock. Flow in group I shunted limbs was 57 (+/-11 SD) % of control. For group II animals in shock, shunted limb flow initially averaged 46 +/- 15% of control, but 4 hours after shunt placement, the mean limb blood flow was the same as in group I. Increased oxygen extraction compensated for the lower flow. Lactic acid production was not increased in comparison to control limbs. CONCLUSION: Shunts provided adequate flow in this model of extremity trauma. Correctly placed shunts stayed patent for 24 hours, without anticoagulation, if shunt placement followed resuscitation.

The role of infrapopliteal MR angiography in patients undergoing optimal contrast angiography for chronic limb-threatening ischemia.

PURPOSE: To determine the benefit of infrapopliteal magnetic resonance angiography (MRA) in patients with chronic limb-threatening ischemia who have undergone optimal contrast angiography (CA). PATIENTS AND METHODS: Thirty-four patients (37 limbs) with limb-threatening chronic lower extremity ischemia underwent MRA and CA of the symptomatic extremity. Selective, vasodilator-enhanced digital subtraction angiography of the infrapopliteal vessels was possible for 34 limbs. Two vascular surgeons retrospectively formulated treatment plans based on CA. They then formulated treatment plans based on CA and MRA together. RESULTS: CA clearly visualized 495 of 888 vascular segments as patent, while MRA clearly visualized 412 of 888 segments. Treatment plans differed for at least one of two surgeons in eight limbs, but MRA would possibly have improved clinical outcome in only one. The amount of inflow disease did not appear to influence segment visualization or treatment planning. In eight of 11 limbs that eventually required below- or above-knee amputation, CA clearly visualized more vascular segments than MRA. One patient developed renal insufficiency after CA. CONCLUSION: Most patients undergoing optimal CA for chronic limb-threatening ischemia will not benefit from the addition of MRA. However, MRA should be considered when CA is suboptimal and when it is necessary to conserve contrast material.

Comparative effects of endothelin (ET-1) and U46619 on human saphenous vein and gastroepiploic artery, sources of human autologous grafts.

The effects of endothelin (ET-1) on smooth muscle contractile activity were investigated and compared in human saphenous vein and gastroepiploic artery, vessels frequently used in revascularization procedures. ET-1 contracted saphenous vein and gastroepiploic artery in a concentration-dependent manner. The peptide produced a greater maximal effect in the vein than in the artery and, in both preparations, ET-1 was less efficacious than U46619, an agent which mimics the actions of thromboxane A2 at the thromboxane A2/prostaglandin H2 receptor. The contractile response to ET-1 declined spontaneously at a more rapid rate in the artery than in the vein. The present data indicate that ET-1 has significant contractile activity in both vessels which are used for coronary arterial bypass surgery and suggest that although, a weaker vasoconstrictor than U46619, the peptide could induce vasospasm in both graft vessels.

Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury.

Differential recovery of prostacyclin and endothelium-derived relaxing factor after vascular injury. Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1449-H1457, 1992. The recovery of prostacyclin (prostaglandin I2, PGI2) synthesis and endothelium-derived relaxing factor (EDRF) activity, as demonstrated by acetylcholine (ACh)-induced relaxation, by rabbit aorta was examined up to 8 wk after balloon catheter-induced injury. Following injury, basal 6-keto-PGF1 alpha formation was decreased acutely; however, after 3 wk it was not different from control. Arachidonic acid-stimulated 6-keto-PGF1 alpha formation was decreased, returning to control levels at 3 and 8 wk for thoracic and abdominal aorta, respectively. ACh-induced relaxation did not return to control levels over the 8-wk study. Initiation of reendothelialization with a layer of hyperplastic endothelial cells overlying subendothelial fibrosis and intimal hyperplasia were present at 2-3 wk. Intimal hyperplasia appeared 2 wk after injury and progressed throughout the period of the study. These data indicate that following balloon catheter-induced injury the formation of both PGI2 and EDRF is reduced and that recovery follows a differential time course. In addition, the recovery of PGI2 formation did not coincide with the attenuation of intimal hyperplasia, whereas the relationship between EDRF formation and intimal hyperplasia is uncertain.