The Hypothesis Regarding the Benefit of Carotid Endarterectomy Under Locoregional Anesthesia in Prevention of Stroke May be Unanswered

A recent trial attempted to investigate the role of locoregional anesthesia (LA) in carotid endarterectomy (CEA) compared with general anesthesia. The hypothesis regarding the advantage of LA is based on the intraprocedural neurologic evaluation and the early identification of neurologic deficit. The trial has not demonstrated the superiority of the rocoregional anesthesia versus general anesthesia and revealed equal results concerning the prevention of stroke. We analyze the reasons which explain why the hypothesis regarding the advantage of LA in CEA, in comparison to general anesthesia cannot be answered

An update on markers of carotid atherosclerosis in patients with Type 2 diabetes

Carotid atherosclerosis constitutes an important cause of ischemic brain attack and stroke, accounting for up to 40% of cases of ischemic cerebrovascular disease. Type 2 diabetes mellitus is an independent risk factor for stroke and its recurrence. Thus, identifying diabetic patients who are at high risk of developing stroke is of great clinical importance. Noninvasive measurements of surrogate markers of atherosclerosis, such as novel serum biomarkers, can be helpful in detecting subclinical carotid disease, especially among individuals at the highest cardio-/cerebro-vascular risk. Previous studies have proposed an expanding body of serum biomarkers, such as C-reactive protein, fibrinogen, adipokines, cytokines and growth factors, as novel indicators of carotid atherosclerosis development that predict carotid-related clinical outcomes. Furthermore, those biomarkers are expected to assess the efficacy of both pharmaceutical and interventional strategies. Accordingly, it is increasingly clear that measuring biomarkers may improve the definition of cerebrovascular risk profile in patients with Type 2 diabetes mellitus

What a vascular surgeon should know and do about atherosclerotic risk factors

Atherosclerosis is a systematic disease presenting with a significant overlapping of cardiovascular disorders implicating coronary heart disease and its equivalents, peripheral arterial disease, carotid arterial disease, and aneurysm disease. Evaluating patient’s atherosclerotic risk profile is essential to guide primary and secondary prevention. Atherosclerotic risk factor modifications reduce, significantly, cardiovascular disease mortality and morbidity, particularly in high-risk patients. This article provides a reference guide for all conventional (eg, smoking, dyslipidemia, hypertension) and evolving (eg, homocysteine, C-reactive protein, fibrinogen, inflammatory markers) risk factors of atherosclerosis and recommends the currently effective strategies for an overall cardiovascular risk reduction. As vascular surgeons, by definition, conduct the overall management of patients with vascular disease understanding of the development, assessment, and management of atherosclerotic risk factors should remain among their highest priorities. (J Vasc Surg 2009;49:1348-54.

Decreased Expression of the CD3ζ Chain in T Cells Infiltrating the Synovial Membrane of Patients with Osteoarthritis

Osteoarthritis (OA) is a heterogeneous disease which rheumatologists consider to be noninflammatory. However, recent studies suggest that, at least in certain patients, OA is an inflammatory disease and that patients often exhibit inflammatory infiltrates in the synovial membranes (SMs) of macrophages and activated T cells expressing proinflammatory cytokines. We report here that the expression of CD3ζ is significantly decreased in T cells infiltrating the SMs of patients with OA. The CD3ζ chain is involved in the T-cell signal transduction cascade, which is initiated by the engagement of the T-cell antigen receptor and which culminates in T-cell activation. Double immunofluorescence of single-cell suspensions derived from the SMs from nine patients with OA revealed significantly increased proportions of CD3ɛ-positive (CD3ɛ(+)) cells compared with the proportions of CD3ζ-positive (CD3ζ(+)) T cells (means ± standard errors of the means, 80.48% ± 3.92% and 69.02% ± 6.51%, respectively; P = 0.0096), whereas there were no differences in the proportions of these cells in peripheral blood mononuclear cells (PBMCs) from healthy donors (94.73% ± 1.39% and 93.79% ± 1.08%, respectively; not significant). The CD3ζ(+) cell/CD3ɛ(+) cell ratio was also significantly decreased for T cells from the SMs of patients with OA compared with that for T cells from the PBMCs of healthy donors (0.84 ± 0.17 and 0.99 ± 0.01, respectively; P = 0.0302). The proportions of CD3ɛ(+) CD3ζ(+) cells were lower in the SMs of patients with OA than in the PBMCs of healthy donors (65.04% ± 6.7% and 90.81% ± 1.99%, respectively; P = 0.0047). Substantial proportions (about 15%) of CD3ɛ(+) CD3ζ-negative (CD3ζ(−)) and CD3ɛ-negative (CD3ɛ(−)) CD3ζ(−) cells were found in the SMs of patients with OA. Amplification of the CD3ζ and CD3δ transcripts from the SMs of patients with OA by reverse transcriptase PCR consistently exhibited stronger bands for CD3δ cDNA than for CD3ζ cDNA The CD3ζ/CD3δ transcript ratio in the SMs of patients with OA was significantly lower than that in PBMCs from healthy controls (P < 0.0001). These results were confirmed by competitive MIMIC PCR. Immunoreactivities for the CD3ζ protein were detected in the SMs of 10 of 19 patients with OA, and they were of various intensities, whereas SMs from all patients were CD3ɛ(+) (P = 0.0023). The decreased expression of the CD3ζ transcript and protein in T cells from the SMs of patients with OA relative to that of the CD3ɛ transcript is suggestive of chronic T-cell stimulation and supports the concept of T-cell involvement in OA

Abdominal aortic endograft proximal collapse resulting in aortic aneurysm rupture

An 82-year-old man was transferred to our emergency department due to acute abdominal pain. He had undergone an endovascular abdominal aortic aneurysm repair (EVAR) six years ago. An intravenous contrast-enhanced abdominal computed tomography revealed the rupture of the abdominal aortic aneurysm (AAA) with a large retroperitoneal hematoma. A Talent (Medtronic, Santa Rosa, CA, USA) modular bifurcated endoprosthesis had vertically collapsed approximately 7 cm after losing its infrarenal fixation. As a result, it led to the repressurization of the aneurysm sac and rupture. The patient was successfully treated by placing three Talent (Medtronic) aortic cuffs. To our knowledge, this is the first reported case of endograft collapse that has manifested with aortic aneurysm rupture. Although they are gradually declining, considerable rates of complications create the ‘Achilles’ heel of endovascular repair of AAAs. A lifelong follow-up strategy for patients treated for AAA with EVAR is essential for the early detection and treatment of complications of the procedure

Endograft Accommodation on the Aortic Bifurcation: An Overview of Anatomical Fixation and Implications for Long-term Stent-Graft Stability

In light of the results of randomized trials, it seems that despite the favorable short and midterm outcomes of standard endografts, concern over endograft migration has escalated, as this event will be responsible for almost all late complications in endovascular aneurysm repair (EVAR). Migration forces, both caudal and sideways, depend heavily on blood pressure, inlet diameter, and angulation of the stent-graft, while the bifurcation generates more force than any other segment of the stent-graft. It thus seems that the position of the endograft’s flow divider influences force distribution and migration risk. Additionally, due to concomitant ongoing aortic degeneration, postoperative dilatation of the infrarenal aortic neck poses a threat to EVAR patients as soon as the diameter of the infrarenal neck reaches the dimensions of the proximal graft. This review evaluates the significance of endograft accommodation on the aortic bifurcation and cumulative experience of the only endografts utilizing this feature: the Zenith Composite and the Powerlink. J Endovasc Ther. 2011; 18: 462-47