CVD: A condition of underestimated severity
Chronic venous disease affects approximately a quarter of the adult population and causes a considerable burden on the health of these patients. The true extent of the severity of the disease is hampered because of reduced public awareness, operational difficulties in diagnosis, and the perception that varicose veins are mainly a cosmetic inconvenience. Consequently the disease receives little attention in public health care systems which focus on life threatening conditions and those which cause obvious morbidity like cancer, cardiac disease and stroke. This review aims to correct these misconceptions by addressing the full scope of CVD, including the postthrombotic syndrome and venous ulceration. The severity of conditions like telangectasiae and edema and the symptoms they cause are frequently underestimated, especially if varicose veins are not present to alert the patient or doctor. The definition, diagnosis, scope, epidemiology, progression and cost of CVD are discussed with evidence to explain how these underestimate the severity of the disease. It is anticipated that once CVD achieves greater recognition this will open up greater opportunities for treatment. These include surgery, endovenous ablation, stenting, compression, venoactive drugs like micronized purified flavonoid fraction and other drugs such as sulodexide and pentoxifylline.
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ABSTRACT: Chronic venous disease encompasses a spectrum of disorders caused by an abnormal venous system. They include chronic venous insufficiency, varicose veins, lipodermatosclerosis, post-thrombotic syndrome, and venous ulceration. Some evidence suggests a genetic predisposition to chronic venous disease due to gene polymorphisms associated mainly with vein wall remodelling. The literature exploring these polymorphisms has not been reviewed and compiled thus far. In this narrative and systematic review, we present the current evidence available on the role of polymorphisms in genes involved in vein wall remodelling and other pathways as contributors to chronic venous disease. We searched the EMBASE, Medline, and PubMed databases from inception to 2013 for basic science or clinical studies relating to genetic associations in chronic venous disease, and obtained 38 relevant studies for this review. Important candidate genes/proteins include the matrix metalloproteinases (extracellular matrix degradation), vascular endothelial growth factors (angiogenesis and vessel wall integrity), FOXC2 (vascular development), HFE (venous ulceration and iron absorption) and various types of collagen (contributors to vein wall strength). The data on associations between these genes/proteins and the post-thrombotic syndrome is limited and additional studies are required. These associations might have future prognostic and therapeutic implications.
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ABSTRACT: Venous and arterial disease probably share a number of common risk factors. From the pathophysiological point of view a similar triggering mechanism was proposed for atherosclerosis and venous disease: subclinical inflammation. Life-threatening thrombotic events may also go through similar pathways in both entities and the culprit is probably dysfunctional endothelial cell in the vessel wall. In available clinical and population based studies, however, unequivocal data are presented regarding association between arterial and venous diseases and their risk factors. In our studies, we found a higher prevalence of lower ankle brachial index in women with chronic venous disease of the lower extremities At the same time, nevertheless we found no strong evidence of a direct link between preclinical atherosclerosis and the occurrence of venous thrombosis in patients with thrombophilias; in the latter group, however, we found a link between hypertension and thromboembolic events. Arterial and venous disease may thus be favorably managed by already well-established and available tools used in prevention of atherosclerotic cardiovascular disease. Evidence of a possible impact of pharmacotherapy on both arterial and venous disease stems from a large clinical study in which treatment with hypolipemic drug, rosuvastatin, significantly decreased not only incidence of cardiovascular events but also of venous thromboembolic events. Another promising drug for the treatment of both arterial and venous disease could be glycosaminoglycan sulodexide.
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To evaluate the impact of delaying interventional treatment on varicose vein disease progression, complications, and health care costs in a real-world setting.
Materials and methods:
This was a retrospective analysis of adults diagnosed with varicose veins between January 2008 and June 2010. Patients were followed for 2 years after diagnosis and categorized into three cohorts based on the timing of interventional therapy: early (≤ 2mo), intermediate (> 2mo but ≤ 6mo), and late (> 6 mo). Disease progression and all-cause health care costs were evaluated.
A total of 44,206 patients were included, with 43% classified as receiving early interventional therapy, 33% as intermediate, and 24% as late. Early interventional treatment was associated with lower disease progression rates (29.2%) compared with intermediate (42.5%; P < .0001) and late treatment (52.2%; P < .0001). Also, early interventional treatment was associated with lower costs ($17,564) than intermediate ($17,923; P > .05) and late treatment ($18,399; P < .05). Each 30-day delay in treatment initiation was associated with a 7% higher risk of disease progression (P < .0001) and a 1% increase in costs (P < .0001).
Findings suggest that early initiation of interventional varicose vein treatment was significantly associated with a decreased risk of disease progression and costs.
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