Survival is not improved by elective repair of abdominal aortic aneurysms smaller than 5.5 cm, even when operative mortality is low.

Background:We previously reported the prevalence and associations of abdominal aortic aneurysm (AAA) in 73451 veterans aged 50 to 79 years who underwent ultrasound screening.

No abstract

Anatomic observations were made during 200 consecutive transaxillary surgical procedures performed in 175 patients because of unremitting signs and symptoms of nerve or vascular compression at the thoracic outlet. There were 160 cases of brachial plexus compression and 40 cases of arterial or venous occlusion. In 132 (66%) of these cases, single or multiple abnormalities were recognized that represented developmental variations previously described in anatomic dissections or in embryologic studies. There were 17 cases of cervical rib or first thoracic rib abnormalities and 20 supernumerary scalene muscles. Developmental variations were identified in 86 scalene and 39 subclavius muscles or their insertions. Comparisons revealed a higher percentage of developmental anomalies in this group of patients than in consecutive anatomic investigations reported in unselected populations. This information was interpreted in light of recent embryologic studies and histochemical and morphometric ultrastructural studies of scalene muscle. The preponderance of evidence suggests that neurovascular compression in the region of the thoracic outlet derives from a combination of these factors: predisposing morphologic variations, structural modifications conditioned by functional requirements, and changes in fiber type or myosin isoform consequent to trauma. The correlation of clinical syndrome with morphologic characteristics alone was significant only for the Paget-Schroetter syndrome.

Reductions in nitric oxide (NO) activity persist after arterial intimal injury and may be a factor in the development of intimal hyperplasia. NO inhibits in vitro platelet aggregation, leukocyte adhesion, and smooth muscle cell growth, all of which are key components in the process of intimal hyperplasia. We hypothesized that long-term supplementation with L-arginine, the precursor of NO, would increase NO production and thereby improve endotheliumdependent vasorelaxation and simultaneously reduce intimal hyperplasia. Twenty-six New Zealand White male rabbits were fed standard rabbit chow either with or without 2.25% L-arginine in their drinking water for 3 weeks. Then the animals underwent unilateral iliac artery angioplasty and were continued on their respective diets. Four weeks after angioplasty, the iliac arteries were harvested for functional and M echanically induced vascular intimal injury is characterized by prolonged reduction of endothelial cell nitric oxide (NO) release and concurrent development of intimal hyperplasia. Current evidence suggests that these phenomena may be causally related. Alterations in NO-mediated vasodilation persist in injured arterial segments even after regrowth of an endothelial cell monolayer.1 Recent in vitro experiments have shown that NO inhibits platelet aggregation, leukocyte adhesion, and smooth muscle cell growth, all of which are key components in the development of intimal hyperplasia. 25 Furthermore, administration of L-arginine, the NO precursor, to hypercholesterolemic rabbits has been shown to reverse defects in NO activity and reduce the development of proliferative atherosclerotic lesions. 6 We hypothesized that long-term administration of L-arginine would increase endothelial cell NO release at the site of balloon angioplasty injury, therefore increasing endotheliumdependent vasorelaxation while simultaneously reducing the intimal hyperplastic response to this injury. Methods AnimalsTwenty-six New Zealand White male rabbits (3.5 to 5.0 kg body weight) were studied. All animals were housed individually in a controlled-temperature, standard light/dark environment and allowed to acclimate before any intervention or morphometric studies. The iliac arteries from several animals from each group were processed for study by electron microscopy. Maximal endothelium-dependent vasorelaxation in injured arteries was significantly greater in L-arginine-supplemented animals (mean±SEM, 71.8±4.1%; n=6) than controls (51.4±4.0%, n=7; P<.05). Furthermore, the intimal area in injured arteries was significantly reduced in L-arginine-supplemented animals (0.22±0.03 mm 2 , n=5) compared with controls (0.34±0.03 mm 2 , n=6; P<.05). These data suggest that L-arginine supplementation enhances NO production at sites of vascular healing and may reduce intimal hyperplasia. Animals were continued on their respective diets after angioplasty until they were killed, at which time the iliac arteries were excised and studied for vasomotor function and histomorphometry. The L-arginin...

Heparin-associated thrombocytopenia and thrombosis (HATT) is an unusual but serious complication of heparin therapy. Twenty-five patients (13 men and 12 women) had thrombocytopenia and arterial or venous thrombosis 1 to 10 days (mean, 6.3 days) after the start of heparin administration. The vessels in the affected extremity had been entered for catheterization, arteriography, or passage of a balloon counterpulsation device in 19 of the 25 patients. In vitro platelet aggregation with heparin was seen in all patients. Additional studies were performed to see whether other lots or sources of heparin also produced in vitro aggregation. Four separate lots of beef lung heparin, commercial heparin from porcine intestinal mucosa, and two types of low molecular weight heparin were all highly stimulatory in this system. However, Org 10172, a heparinoid, did not induce aggregation in any of 13 patient plasmas tested. Inhibition of platelet aggregation by aspirin was also examined. Aspirin abolished in vitro aggregation in 9 of 16 cases and decreased the degree of aggregation from 85% to 55% (p = 0.02) in the remaining seven cases. We conclude that in patients with HATT platelet aggregation is equally induced by beef lung, porcine intestinal, and some forms of low molecular weight heparin. Org 10172 does not stimulate platelet aggregation in plasma from these patients in vitro. Finally, there may be a role for aspirin in treating patients with HATT.

A case of widely disseminated mucormycosis involving Cunninghamella bertholletiae is reported. This represents the first report of Cunninghamella infection in a transplant patient and, to our knowledge, only the eighth reported case of human infection by this saprophytic fungus. The clinical course was similar to most of the previously reported cases in that the patient was immunocompromised prior to the infection and the diagnosis was made too late for appropriate therapeutic intervention. The current case is unique in that it involved a renal allograft recipient; that the major clinical signs and symptoms mimicked myocardial infarction; and that there was more widespread dissemination than in earlier cases. The histologic and laboratory identification of the fungus are presented and correlated with the clinical parameters (signs, symptoms, and therapy) of this case as well as the cases previously reported in the literature.

Postischemic extremities exhibited a transient, early burst of TNF release on reperfusion, which likely represented washout of TNF produced during ischemia. Suppression of TNF activity with an antibody to TNF-alpha resulted in a salutary increase in postischemic flow rates, suggesting that TNF may play a role in the no-reflow phenomenon.