The Society for Vascular Surgery (SVS) and the American Venous Forum (AVF) have developed clinical practice guidelines for the care of patients with varicose veins of the lower limbs and pelvis. The document also includes recommendations on the management of superficial and perforating vein incompetence in patients with associated, more advanced chronic venous diseases (CVDs), including edema, skin changes, or venous ulcers. Recommendations of the Venous Guideline Committee are based on the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system as strong (GRADE 1) if the benefits clearly outweigh the risks, burden, and costs. The suggestions are weak (GRADE 2) if the benefits are closely balanced with risks and burden. The level of available evidence to support the evaluation or treatment can be of high (A), medium (B), or low or very low (C) quality. The key recommendations of these guidelines are: We recommend that in patients with varicose veins or more severe CVD, a complete history and detailed physical examination are complemented by duplex ultrasound scanning of the deep and superficial veins (GRADE 1A). We recommend that the CEAP classification is used for patients with CVD (GRADE 1A) and that the revised Venous Clinical Severity Score is used to assess treatment outcome (GRADE 1B). We suggest compression therapy for patients with symptomatic varicose veins (GRADE 2C) but recommend against compression therapy as the primary treatment if the patient is a candidate for saphenous vein ablation (GRADE 1B). We recommend compression therapy as the primary treatment to aid healing of venous ulceration (GRADE 1B). To decrease the recurrence of venous ulcers, we recommend ablation of the incompetent superficial veins in addition to compression therapy (GRADE 1A). For treatment of the incompetent great saphenous vein (GSV), we recommend endovenous thermal ablation (radiofrequency or laser) rather than high ligation and inversion stripping of the saphenous vein to the level of the knee (GRADE 1B). We recommend phlebectomy or sclerotherapy to treat varicose tributaries (GRADE 1B) and suggest foam sclerotherapy as an option for the treatment of the incompetent saphenous vein (GRADE 2C). We recommend against selective treatment of perforating vein incompetence in patients with simple varicose veins (CEAP class C(2); GRADE 1B), but we suggest treatment of pathologic perforating veins (outward flow duration ≥500 ms, vein diameter ≥3.5 mm) located underneath healed or active ulcers (CEAP class C(5)-C(6); GRADE 2B). We suggest treatment of pelvic congestion syndrome and pelvic varices with coil embolization, plugs, or transcatheter sclerotherapy, used alone or together (GRADE 2B).

Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade various components of the extracellular matrix (ECM). Members of the MMP family include collagenases, gelatinases, stromelysins, matrilysins and membrane-type MMPs. ProMMPs are cleaved into active forms that promote degradation of ECM proteins. Also, recent evidence suggests direct or indirect effects of MMPs on ion channels in the endothelium and vascular smooth muscle, and on other mechanisms of vascular relaxation/contraction. Endogenous tissue inhibitors of metalloproteinases (TIMPs) reduce excessive proteolytic ECM degradation by MMPs. The balance between MMPs and TIMPs plays a major role in vascular remodeling, angiogenesis, and the uterine and systemic vasodilation during normal pregnancy. An imbalance in the MMPs/TIMPs activity ratio may underlie the pathogenesis of vascular diseases such as abdominal aortic aneurysm, varicose veins, hypertension and preeclampsia. Downregulation of MMPs using genetic manipulations of endogenous TIMPs, or synthetic pharmacological inhibitors such as BB-94 (Batimastat) and doxycycline, and Ro-28-2653, a more specific inhibitor of gelatinases and membrane type 1-MMP, could be beneficial in reducing the MMP-mediated vascular dysfunction and the progressive vessel wall damage associated with vascular disease.

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C hronic venous disease is often overlooked by primary and cardiovascular care providers because of an underappreciation of the magnitude and impact of the problem. The importance of chronic venous disease is related to the number of people with the disease and the socioeconomic impact of its more severe manifestations. Unfortunately, the literature concerning the prevalence and incidence of chronic venous disease has varied greatly because of differences in the methods of evaluation, criteria for definition, and the geographic regions analyzed. The most common manifestations of chronic venous disease are dilated cutaneous veins, such as telangiectases and reticular veins, and varicose veins. The term chronic venous insufficiency (CVI) describes a condition that affects the venous system of the lower extremities with venous hypertension causing various pathologies including pain, swelling, edema, skin changes, and ulcerations. Although the term CVI is often used to exclude uncomplicated varicose veins, varicose veins have incompetent valves with increased venous pressure leading to progressive dilation and tortuosity. We will use the term CVI to represent the full spectrum of manifestations of chronic venous disease.Varicose veins have an estimated prevalence between 5% to 30% in the adult population, with a female to male predominance of 3 to 1, although a more recent study supports a higher male prevalence. 1 The Edinburgh Vein Study screened 1566 subjects with duplex ultrasound for reflux finding CVI in 9.4% of men and 6.6% of women, after age adjustment, which rose significantly with age (21.2% in men Ͼ50 years old, and 12.0% in women Ͼ50 years old). 2 The San Valentino Vascular Screening Project found among the 30 000 subjects evaluated by clinical assessment and duplex ultrasound a prevalence of 7% for varicose veins and 0.86% for "symptomatic" CVI. 3 As in previous studies, CVI was more common with increasing age, but there was no significant sex difference. The rate of varicose vein development may be estimated from the Framingham Heart Study, which found an annual incidence of 2.6% in women and 1.9% in men. 4 Risk factors found to be associated with CVI include age, sex, a family history of varicose veins, obesity, pregnancy, phlebitis, and previous leg injury. 5,6 There also may be environmental or behavioral factors associated with CVI such as prolonged standing and perhaps a sitting posture at work. 6,7 Varicose veins have a significant impact on healthcare resources, with millions of people seeking medical attention for their cosmetic appearance annually. Although often minimized, the cosmetic consequences may adversely affect an individual's quality of life and are associated with other manifestations.The more serious consequences of CVI such as venous ulcers have an estimated prevalence of Ϸ0.3%, although active or healed ulcers are seen in Ϸ1% of the adult population. 8 It has been estimated that Ϸ2.5 million people have CVI in the United States, and of those, Ϸ20% develop venous ulcers. 9 The ov...

Most data regarding early thrombus removal strategies are of low quality but do suggest patient-important benefits with respect to reducing postthrombotic morbidity. We anticipate revision of these guidelines as additional evidence becomes available.

Objective-Reactive hyperemia is the compensatory increase in blood flow that occurs after a period of tissue ischemia, and this response is blunted in patients with cardiovascular risk factors. Key Words: endothelium Ⅲ cardiovascular risk Ⅲ surrogate markers Ⅲ reactive hyperemia Ⅲ flow-mediated dilation R eactive hyperemia is a complex response that occurs after a period of tissue ischemia and primarily depends on local production of adenosine and other non-endothelium-dependent vasodilators that dilate tissue microvessels. 1 Studies in humans have shown that endothelium-derived nitric oxide also contributes to reactive hyperemia. 2,3 Peak brachial artery hyperemic flow velocity after 5-minute cuff occlusion of the arm relates inversely to traditional cardiovascular disease risk factors 4 and to markers of inflammation 5 in the Framingham Heart Study. Smaller scale mechanistic studies suggest that the nitric oxide-dependent component of reactive hyperemia may be particularly affected by risk factors. 3 The relation of reactive hyperemia to the incidence of cardiovascular disease events in atherosclerosis has not been previously studied.

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