PubMed · 13830982
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J de KLERK. 1960-11-12. [Bladder neck stenosis].. https://pubmed.ncbi.nlm.nih.gov/13830982/
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The accuracy of 16-row multidetector CT in the visualization of different peripheral artery stents and in the appraisal of in-stent stenosis was assessed. Nine different stent types (nitinol and stainless steel) with three diameters (6, 8 and 10 mm) were used; altogether 27 stents were analyzed in a barrel-shaped vascular model. Low-grade (<40%) and high-grade (>60%) in-stent stenoses were simulated by polyurethane sticks (70 HU) of differing diameters (2-6 mm). Imaging was performed with 16x0.75-mm detector collimation, 130 mAs, 120 kV, 12-mm table feed/rotation, 1.0-mm slice thickness and 0.5-mm increment. The stent diameter, strut thickness, in-stent attenuation values, degree and degree of in-stent stenosis were evaluated. Nitinol stents showed significantly (P<10-6) less stent lumen narrowing, artificial strut thickening and overestimation of the degree of in-stent stenoses than stainless steel stents. In-stent attenuation values and artificial strut thickening were significantly (P<10-6) lower in 10- and 8-mm stents than in 6-mm stents. Stent lumen narrowing was significantly less in 10-mm stents than in 8-mm (P<10-4) or 6-mm (P<10-6) stents. In-stent stenoses were significantly overestimated, irrespective of the stent diameter. In 6-mm stents overestimation was significantly higher than in 8-mm (P<0.01) or 10-mm stents (P<10-6). Under in-vitro conditions 16-row MDCT allowed an accurate identification of in-stent stenosis, but significantly overestimated the effective degree of the stenosis.
May-Thurner syndrome is an uncommon process in which the right common iliac artery compresses the left common iliac vein, possibly resulting in pain, severe edema of the left leg or in left iliofemoral deep vein thrombosis [May R, Thurner J. The cause of the predominately sinistral occurrence of thrombosis of the pelvic veins. Angiology 1957; 8: 419-427 .]. Corrective surgical treatment requires extensive dissection. Therefore, endovascular venous stenting is currently used in these patients [Lamont JP, Pearl GJ, Patetsios P, Warner MT, Gable DR, Garrett W, et al. Prospective evaluation of endoluminal venous stents in the treatment of the May-Thurner syndrome. Ann Vasc Surg. 2002 Jan; 16(1): 61-4. Epub 2002 Jan 17 .]. We present a case of migration of two iliacal vein stents into the right ventricle in a patient with May-Thurner syndrome.
During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.