Ortner syndrome secondary to saccular thoracic aneurysm.

Mechanical stretching of the left laryngeal nerve secondary to an enlarged left atrium was first described by Dr Norbert Ortner in 1987. An extensive literature search revealed only 76 reported cases of Ortner syndrome, with the more recent reports describing other causes of the syndrome such as pulmonary hypertension, aortic dissection, and a thoracic aneurysm. We recently encountered this rare pathologic entity in an elderly man who had presented with severe hoarseness, presumed to be due to one of the aforementioned vascular anomalies. In the present report, we have highlighted the pathology and hybrid repair of this challenging entity.

Brescia-Cimino AV Fistula Complicated by Steal Syndrome.

The Brescia-Cimino AV fistula is most commonly performed and rarely associated with steal syndrome. A case is presented with details regarding its correction.

Rapid Degradation and Subsequent Endovascular Salvage of Upper Extremity Cryogenic Allograft Bypass.

It has long been reported that cryogenic allografts have suboptimal mid- and long-term patencies and consequently are only used in the absence of autologous vein, predominantly in lower extremity limb salvage situations. As such, we felt that our recent experience with an upper extremity bypass for limb salvage using a cryogenic saphenous vein allograft, which aneurysmally degenerated after one month and required multiple endovascular rescues, serves to re-emphasize such concerns and the importance of continuous postoperative surveillance.

Genesis of Crural Revascularization.

BACKGROUND: The purpose of this study is to recognize those investigators responsible for initiating progress in limb salvage where runoff beyond the arterial blockage was limited to the crural vasculature and to also describe how crural bypass has evolved into the contemporary setting where endovascular options have become increasingly prominent. METHODS: An extensive literature review of articles published from 1960 to 1979 was the basis for selecting and recognizing surgeons who pioneered infrageniculate revascularization. Documentation of patency and amputation rates were tabulated for these early series of distal limb bypass. Cases performed in the decade of interest, but not published until the 1980s, are also recognized and recorded separately. RESULTS: Subsequent to the first tibial bypass performed in 1961 by McCaughan, a total of 746 crural bypasses were defined in the decades of interest, where possible, with overall 6-, 12-, and 36-month patencies of 76%, 59%, and 48%, respectively. There was an overall amputation rate of 17%. Life table analysis and other statistical methods were also adopted during this time. CONCLUSIONS: Performance of crural bypass from 1960 to 1979 was analyzed in groups according to the distal anastomosis site. These results confirm the satisfactory early progress leading to further refinement in subsequent decades. It is essential that the current generation of vascular surgeons recognize the value of these early open procedures as a stable force for securing limb salvage in conjunction with evolving endovascular techniques.

Aberrant splenic artery complicated by aneurysm during pregnancy.

The aberrant splenic artery is an uncommon anomaly. It may become a challenging problem when it is associated with an aneurysm diagnosed during pregnancy. Our experience with a patient who underwent two interventions, each performed in the postpartum period without incident, highlights the need to employ techniques that ensure aneurysm closure and thus avoid recurrence and need for repetitive procedures.

Endovascular rescue of long-term vascular graft implants and need for continuous surveillance.

We present two cases of vascular graft degradation after long-term implantation. In both patients, endovascular techniques were employed to effect continued graft patency and function. Furthermore, these cases lend further credence to the doctrine of lifelong surveillance of all vascular interventions regardless of graft material. Postoperative surveillance of vascular interventions is generally recommended to avoid failures by identifying "the failing graft"1 at the earliest possible time to facilitate corrective procedures. There is a tendency that with continued function, over time, surveillance methods are spread farther apart and in fact often discontinued. Recent experiences with two cases illustrate the vital importance of lifelong continuous surveillance regardless of the site, graft material, or absence of symptoms. Clearly, the patient's compliance is essential. Both patients consented to the publication of their cases.

True Aneurysm of the Anterior Tibial Artery.

Most anterior tibial aneurysm cases described in the literature are pseudoaneurysms resulting from trauma. Since 1967, only 8 cases published on true anterior tibial artery aneurysms were atraumatic. Recent experience with an atraumatic aneurysm of the anterior tibial artery prompted a literature review regarding their incidence, and accordingly, we feel the need exists for greater recognition and understanding of this entity.

Pseudoaneurysm of the subclavian-vertebral artery junction--case report and review of the literature.

Pseudoaneurysm of the subclavian-vertebral artery junction (SVJ) is a rare complication of internal jugular vein catheter placement. Because of its retroclavicular location, arterial injury at the SVJ poses a significant therapeutic challenge. A case report and review of the literature are presented.

Cholinergic antiinflammatory pathway inhibition of tumor necrosis factor during ischemia reperfusion.

OBJECTIVE: Ischemia-reperfusion injury is a pathologic event characterized by tissue damage. It is mediated by tumor necrosis factor (TNF) and other cytokines that activate complement and proteases and stimulate fibrinolysis, degranulation of white blood cells, and free radical production. We recently reported that vagus nerve stimulation (VNS) suppresses endotoxin-induced cytokine synthesis through alpha bungarotoxin-sensitive cholinergic receptors. VNS protects against endotoxin-induced shock by inhibiting hepatic and cardiac synthesis of TNF. Here, the effects of VNS on suppression of ischemia-reperfusion injury and cytokine release were studied in a rat model of aortic occlusion. METHODS: Adult male Lewis rats were subjected to laparotomy and suprarenal aortic clamping for 15 minutes followed by reperfusion. Blood pressure, heart rate, and respiratory rate were recorded every 3 minutes for 90 minutes. Exposed cervical vagus nerves in the experimental group were stimulated for 5 minutes before and after aortic occlusion, with constant voltage (1 V, 2 ms, 5 Hz); sham-operated animals received no stimulation. TNF levels in serum and organs were measured with enzyme-linked immunosorbent assay ELISA (BioSource International, Camarillo, Calif). Data analysis was performed with the Student t test. RESULTS: Control animals had shock develop (mean, 59% decrease in blood pressure) whereas blood pressure in the stimulated animals did not decrease (control versus stimulated animals, P <.05). VNS significantly inhibited TNF levels in serum (7 +/- 1 ng/mL versus 45 +/- 6 ng/mL; P =.0008), heart (21 +/- 11 ng/g protein versus 85 +/- 15 ng/g protein; P =.01), and liver (16 +/- 2 ng/g protein versus 42 +/- 12 ng/g protein; P =.02). CONCLUSION: VNS significantly attenuates TNF synthesis and shock during reperfusion injury in a standard model of aortic occlusion. Clinical evaluation of VNS for this condition may be warranted.

Globin attenuates the innate immune response to endotoxin.

Hemoglobin is an endotoxin (lipopolysaccharide; LPS)-binding protein that synergistically increases the release of proinflammatory cytokines from the innate immune system in response to LPS. It has been suggested that this activity of hemoglobin facilitates the recognition of Gram-negative bacteria in a wound, thereby maximizing immune efficiency. This synergy may be important to the pathogenesis of a broad spectrum of clinical conditions because elevated hemoglobin levels frequently are observed in patients after the transfusion of red cells, trauma, cardiopulmonary bypass surgery, hemolysis, in addition to other disorders. To determine the molecular basis of the specific hemoglobin-LPS synergy, in this article we tested the effects of globin itself on macrophage responses to LPS. Paradoxically, these studies revealed that globin suppressed tumor necrosis factor (TNF) synthesis in LPS-stimulated murine and human macrophage cultures. LPS comigrated with globin on non-denaturing electrophoretic gels, giving direct evidence for binding. Globin specifically inhibited LPS activity in the standard Limulus assay but did not inhibit interleukin-1beta-mediated TNF synthesis. Iron supplementation of macrophage cultures significantly increased interleukin-1beta-induced TNF release. Intraperitoneal administration of globin protected mice against both LPS-induced lethality and experimentally induced bacterial infection. Thus, the heme-iron moiety of hemoglobin, and not the binding of LPS to globin, enhanced macrophage responses to LPS.

Pharmacological stimulation of the cholinergic antiinflammatory pathway.

Efferent activity in the vagus nerve can prevent endotoxin-induced shock by attenuating tumor necrosis factor (TNF) synthesis. Termed the "cholinergic antiinflammatory pathway," inhibition of TNF synthesis is dependent on nicotinic alpha-bungarotoxin-sensitive acetylcholine receptors on macrophages. Vagus nerve firing is also stimulated by CNI-1493, a tetravalent guanylhydrazone molecule that inhibits systemic inflammation. Here, we studied the effects of pharmacological and electrical stimulation of the intact vagus nerve in adult male Lewis rats subjected to endotoxin-induced shock to determine whether intact vagus nerve signaling is required for the antiinflammatory action of CNI-1493. CNI-1493 administered via the intracerebroventricular route was 100,000-fold more effective in suppressing endotoxin-induced TNF release and shock as compared with intravenous dosing. Surgical or chemical vagotomy rendered animals sensitive to TNF release and shock, despite treatment with CNI-1493, indicating that an intact cholinergic antiinflammatory pathway is required for antiinflammatory efficacy in vivo. Electrical stimulation of either the right or left intact vagus nerve conferred significant protection against endotoxin-induced shock, and specifically attenuated serum and myocardial TNF, but not pulmonary TNF synthesis, as compared with sham-operated animals. Together, these results indicate that stimulation of the cholinergic antiinflammatory pathway by either pharmacological or electrical methods can attenuate the systemic inflammatory response to endotoxin-induced shock.