Journal of vascular surgery
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The clinical significance of isolated calf vein thrombosis (ICVT) remains controversial. Several studies have shown that the majority of ICVT do not propagate above the knee while other studies have suggested ICVT propagation and recommend full anticoagulation. The purpose of this study was to determine the progression of ICVT, identify risk factors for clot propagation, and to evaluate further thrombotic events associated with it. ⋯ ICVT can be safely observed in asymptomatic patients without therapeutic anticoagulation. In our study, patients who have had orthopedic procedures, those with malignancy, and those that were immobile seemed to have a higher incidence of clot propagation. In this group, we recommend full anticoagulation until the patient is ambulatory or the follow-up duplex scan is negative. Our data also suggest that a follow-up duplex scan is not beneficial when performed within 72 hours or after 3 months.
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Aneurysm growth after endovascular aneurysm repair (EVAR) in patients with type II endoleak is associated with adverse outcomes. This study evaluated the long-term success of embolization of type II endoleaks in preventing aneurysm sac growth. ⋯ Embolization of type II endoleaks is successful early in preventing aneurysm sac growth and rupture after EVAR. However, a significant number of patients require more than one procedure, and at 5 years, many patients who underwent embolization of a type II endoleak continued to experience sac growth. Patients with hyperlipidemia who undergo coil embolization are more likely to require a second embolization procedure, and patients who smoke have a higher likelihood of AAA sac expansion after embolization. Continued long-term surveillance is necessary in this cohort of patients.
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Meta Analysis
Polymorphisms of genes involved in extracellular matrix remodeling and abdominal aortic aneurysm.
Abdominal aortic aneurysm (AAA) has a multifactorial etiology and the relevance of genetic factors is getting increasing interest, in particular those related to the destructive remodeling of extracellular matrix. ⋯ These findings suggest that polymorphisms in MMP2, MMP3, MMP-13, and ELN genes may independently contribute to the pathogenesis of AAA.