What’s new in vascular surgery

This article covers the period from October 2000 through September 2001 and focuses primarily on clinical advances in vascular and endovascular surgery. Surgical, medical, and radiologic journals were surveyed during this period and peer-reviewed publications form the bulk of this article. Although aortic stent graft treatment of aortic aneurysm (AAA) continues to dominate the vascular surgical literature, initial enthusiasm for this technique is now being moderated with caution and concerns centering on durability and longterm complications. Carotid angioplasty and stenting continue to enjoy enthusiastic reports as this technology advances with the introduction of cerebral protection devices, but durability again is emerging as an important issue that may limit the application of this approach. In addition to higher rates of significant restenosis on longterm followup, carotid angioplasty and stenting, to date, have failed to produce better or equivalent outcomes in comparison to wellperformed carotid endarterectomy (CEA). There have been many advances in the field of venous disease, particularly with the introduction of new antithrombotic agents and refinements in conventional antithrombotic therapy to tailor length of therapy according to risk factors and effectively prevent recurrent venous thromboembolism. Although there have been few seminal reports in the area of lower extremity arterial disease, there have been many publications that have more sharply delineated the relative benefits of surgical, interventional radiologic, and medical treatments. Outcomes analyses and epidemiologic studies are becoming increasingly important in the field of vascular disease, with many recent reports documenting that trained vascular surgeons “do it better.” CEREBROVASCULAR DISEASE Plaque morphology and noninvasive testing Tegos and colleagues characterized the echomorphology of 50% to 99% stenotic plaques in symptomatic patients and correlated computer-generated gray scale images with emboli detected by transcranial Doppler and brain CT infarction patterns. Emboli and CT scan evidence of discrete cortical infarcts were statistically more frequent in the presence of low plaque echodensity. Low plaque echodensity was more predictive of emboli and infarction than severity of carotid stenosis. In a followup study, these investigators documented that symptomatic plaques were associated with hypoechoic and predominately homogeneous echo patterns; asymptomatic ones were associated with hyperechoic and less predominant homogeneous patterns. In a corroborative study, Mathiesen and colleagues noted that echolucent carotid plaques have increased risk of ischemic cerebrovascular events independent of degree of stenosis and cardiovascular risk factors. Patients at high risk for cerebrovascular ischemic events may be identified by ultrasonographic assessment of plaque morphology. Events and factors leading to plaque instability that causes an asymptomatic plaque to become symptomatic are of considerable interest. Loftus and colleagues measured blood levels of matrix metalloproteinases (MMPs) and their inhibitors, and correlated these with the embolic potential of plaques in patients undergoing CEA. They noted that MMP-9 levels were elevated in patients with spontaneous plaque embolization. Numerous studies have reported the detection of Chlamydia pneumoniae in atherosclerotic plaques. In an interesting study, Nadareishvili and colleagues showed a preferential increase of CD8 T cells in symptomatic carotid artery plaques positive for C pneumoniae. They postulated that the presence of C pneumoniae in plaques may recruit these T cells, and that immune inflammatory responses may predispose to plaque rupture and ischemic complications. How C pneumoniae becomes incorporated in carotid plaques is anybody’s guess. But the implications of Received October 30, 2001; Accepted October 30, 2001. From the Division of Vascular Surgery, University of Texas Southwestern Medical Center, Dallas, TX. Correspondence address: G Patrick Clagett, MD, Division of Vascular Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9157.