Management of aneurysms involving branches of the celiac and superior mesenteric arteries: A comparison of surgical and endovascular therapy

ObjectiveAneurysms involving branches of the superior mesenteric and celiac arteries are uncommon and require proper management to prevent rupture and death. This study compares surgical and endovascular treatment of these aneurysms and analyzes outcome.MethodsPatients at the Mount Sinai Medical Center in New York who were treated for aneurysms in the branches of the celiac artery and superior mesenteric artery were identified through a search of the institution’s medical records and endovascular database. Patient demographics, history, clinical presentation, aneurysm characteristics, treatments, and follow-up outcome were retrospectively recorded. Significant differences between patients treated by surgical or endovascular therapy were determined by using Student’s t test and χ 2 analysis.ResultsBetween January 1, 1991, and July 1, 2005, 59 patients with 61 aneurysms were treated at a single institution. Twenty-four patients had surgical repair, and 35 underwent endovascular treatment, which included coil embolization and stent-graft therapy. Splenic (28) and hepatic (22) artery aneurysms predominated. Eighty-nine percent of splenic artery aneurysms were true aneurysms and were treated by endovascular and surgical procedures in near equal numbers (14 and 11, respectively). Pseudoaneurysms were significantly more likely to be treated by endovascular means (P < .01). The technical success rate of endovascular treatment for aneurysms was 89%, and failures were successfully treated by repeat coil embolization in all patients who presented for retreatment. Patients treated by endovascular techniques had a significantly higher incidence of malignancy than patients treated with open surgical techniques (P = .03). Furthermore, patients treated by endovascular means had a shorter in-hospital length of stay (2.4 vs 6.6 days, P < .001).ConclusionEndovascular management of visceral aneurysms is an effective means of treating aneurysms involving branches of the celiac and superior mesenteric arteries and is particularly useful in patients with comorbidities, including cancer. It is associated with a decreased length of stay in the elective setting, and failure of primary treatment can often be successfully managed percutaneously

The Toll of Vascular Insufficiency: Implications for the Management of Peripheral Arterial Disease

Peripheral artery disease (PAD) can result in limb loss within six months of diagnosis in a subset of patients who cannot undergo endovascular or surgical revascularization yet continues to maintain a marginal position in cardiovascular research. While a body of literature continues to grow describing the role of danger signaling and innate immunity in cardiac biology, the role of these pathways in the ischemic myopathy associated with PAD has not been extensively studied. The following report will review the current literature on the role of Toll-like receptor (TLR) signaling in cardiovascular biology as well as in nonischemic myopathy. While attenuation of TLR signaling has not been shown to be clinically useful in the treatment of infectious inflammation, it may show promise in the management of severe arterial insufficiency

TLR2 and TLR4 mediate differential responses to limb ischemia through MyD88-dependent and independent pathways.

The danger signal HMGB1 is released from ischemic myocytes, and mediates angiogenesis in the setting of hindlimb ischemia. HMGB1 is a ligand for innate immune receptors TLR2 and TLR4. While both TLR2 and TLR4 signal through myeloid differentiation factor 88 (MyD88), TLR4 also uniquely signals through TIR-domain-containing adapter-inducing interferon-β (TRIF). We hypothesize that TLR2 and TLR4 mediate ischemic myocyte regeneration and angiogenesis in a manner that is dependent on MyD88 signaling.Mice deficient in TLR2, TLR4, MyD88 and TRIF underwent femoral artery ligation in the right hindlimb. Laser Doppler perfusion imaging was used to assess the initial degree of ischemia and the extent of perfusion recovery. Muscle regeneration, necrosis and fat replacement at 2 weeks post-ligation were assessed histologically and vascular density was quantified by immunostaining. In vitro, endothelial tube formation was evaluated in matrigel in the setting of TLR2 and TLR4 antagonism.While control and TLR4 KO mice demonstrated prominent muscle regeneration, both TLR2 KO and TRIF KO mice exhibited marked necrosis with significant inflammatory cell infiltrate. However, MyD88 KO mice had a minimal response to the ischemic insult with little evidence of injury. This observation could not be explained by differences in perfusion recovery which was similar at two weeks in all the strains of mice. TLR2 KO mice demonstrated abnormal vessel morphology compared to other strains and impaired tube formation in vitro.TLR2 and TRIF signaling are necessary for muscle regeneration after ischemia while MyD88 may instead mediate muscle injury. The absence of TLR4 did not affect muscle responses to ischemia. TLR4 may mediate inflammatory responses through MyD88 that are exaggerated in the absence of TLR2. Additionally, the actions of TLR4 through TRIF may promote regenerative responses that are required for recovery from muscle ischemia

Elastic Laminar Reorganization Occurs with Outward Diameter Expansion during Collateral Artery Growth and Requires Lysyl Oxidase for Stabilization

When a large artery becomes occluded, hemodynamic changes stimulate remodeling of arterial networks to form collateral arteries in a process termed arteriogenesis. However, the structural changes necessary for collateral remodeling have not been defined. We hypothesize that deconstruction of the extracellular matrix is essential to remodel smaller arteries into effective collaterals. Using multiphoton microscopy, we analyzed collagen and elastin structure in maturing collateral arteries isolated from ischemic rat hindlimbs. Collateral arteries harvested at different timepoints showed progressive diameter expansion associated with striking rearrangement of internal elastic lamina (IEL) into a loose fibrous mesh, a pattern persisting at 8 weeks. Despite a 2.5-fold increase in luminal diameter, total elastin content remained unchanged in collaterals compared with control arteries. Among the collateral midzones, baseline elastic fiber content was low. Outward remodeling of these vessels with a 10–20 fold diameter increase was associated with fractures of the elastic fibers and evidence of increased wall tension, as demonstrated by the straightening of the adventitial collagen. Inhibition of lysyl oxidase (LOX) function with β-aminopropionitrile resulted in severe fragmentation or complete loss of continuity of the IEL in developing collaterals. Collateral artery development is associated with permanent redistribution of existing elastic fibers to accommodate diameter growth. We found no evidence of new elastic fiber formation. Stabilization of the arterial wall during outward remodeling is necessary and dependent on LOX activity

Interplay between TLR4, TLR2, MyD88 and TRIF in mediating inflammation, muscle regeneration and angiogenesis after muscle ischemia.

<p>Interplay between TLR4, TLR2, MyD88 and TRIF in mediating inflammation, muscle regeneration and angiogenesis after muscle ischemia.</p

Hind limb perfusion was determined by LDPI measurements and presented as ratios that compared the perfusion of the ischemic to nonischemic limb.

<p>(A) The perfusion for control, TLR2 KO, TLR4 KO, MyD88KO and TRIFKO mice at 1 and 13 days after femoral artery ligation. (N = 4–8 per group) is shown (N = 5–7 per group). (B) Representative 13 day LDPI in experimental groups demonstrating extent of perfusion recovery after ischemia.</p