Abstract
Chronic venous disease (CVD) is a multifactorial condition affecting an important percentage of the global population. It ranges from mild clinical signs, such as telangiectasias or reticular veins, to severe manifestations, such as venous ulcerations. However, varicose veins (VVs) are the most common manifestation of CVD. The explicit mechanisms of the disease are not well-understood. It seems that genetics and a plethora of environmental agents play an important role in the development and progression of CVD. The exposure to these factors leads to altered hemodynamics of the venous system, described as ambulatory venous hypertension, therefore promoting microcirculatory changes, inflammatory responses, hypoxia, venous wall remodeling, and epigenetic variations, even with important systemic implications. Thus, a proper clinical management of patients with CVD is essential to prevent potential harms of the disease, which also entails a significant loss of the quality of life in these individuals. Hence, the aim of the present review is to collect the current knowledge of CVD, including its epidemiology, etiology, and risk factors, but emphasizing the pathophysiology and medical care of these patients, including clinical manifestations, diagnosis, and treatments. Furthermore, future directions will also be covered in this work in order to provide potential fields to explore in the context of CVD.
Highlights
Chronic venous disease (CVD) is a persistent, progressive, and frequently underestimated condition widely represented in the general population, having a huge socioeconomic, physical, and psychological impact associated [1,2]
Veins are conformed by three layers: (1) tunica intima or inner layer, mainly conformed by endothelial cells (ECs); (2) the tunica media or media layer, represented by vascular smooth muscle cells (SMCs) and little elastic fibers; and (3) tunica adventitia or outer layer, which is composed by connective tissue, with an important development of elastic fibers, giving the vessel an important support and elasticity [7]
Secondary CVD are those cases in which the manifestation of the disease is caused by a previous event that, as mentioned below, could be subdivided into secondary intravenous— when the vein wall and valves are adversely affected—and secondary extravenous, in which there is no evidence of vein damage, but the local or systemic venous hemodynamic is impaired [77]
Summary
Chronic venous disease (CVD) is a persistent, progressive, and frequently underestimated condition widely represented in the general population, having a huge socioeconomic, physical, and psychological impact associated [1,2]. Clinical signs may affect any vein in the body, the venous system located in the lower limbs is often the most vulnerable structure to suffer CVD [5]. The calf muscle, often named the “peripheral heart”, is especially considered the most prominent enhancer of venous return from lower limbs to heart [10] Failures in both systems are crucial to understand the pathogenesis and progression of CVD leading to a venous reflux and to venous stasis [11,12,13,14]. CEAP (clinical–etiology–anatomy–pathophysiology) classification is a globally accepted method to study venous disorders It is based on different medical features that permits to accurately analyze the clinical, etiological, anatomical, and pathological status of veins [17]. SsaSsytuyussppbtteeeoermmrtfhfii,,ccttisihhaailedel vevmmsee,aiainnjjsoossurrmrmccrooioigngnuhthtnrrttidibtbtreruuadattnnoosbrsrpspysoooorafrftttthtfthhaheeseevcvbibeealnlnolooooocududossmttrhrhepertrtouaourururtngmgn.hh.DeDtntehhetee.eeppsCsvaavapepleihfhnineesmnsnaouaoruresuecssalacejjuucccnopnomcucmttmipioopapnnanssniieaisadenndtdbdhbyettyhhameneanpopaesraettrrreftforieomyrrr,ayapnt,tooeonrrrrevtvravevenesieit,nnsas,ssnoattdnouodrsttckhhseeekeleetddotleaeeelteaapmpslsvmuvueesruncnelsooecauulanesst abpopthrospidreiast,esdurbrloouonddreedtubrynafrfoasmciathl ecolmowpearrtlmimenbst. aCnadlfimt ius sfcrleeqpuuenmtplyisdethsiegmneodstaismtphoer“tapnetrispohuerrcaelthoeaasrstu”r.eVaennoapups rroepturiranteids abllsooopderremtuitrtnedfrobmy tthheeplorweseernlciemobfsvaenndouitsisvafrlevqeus,ewnthlyicdheasrigeneesdseanstitahleto“pperreivpehnetrabllohoeadrtr”e.flVuexn. oTuhserceytutoranricshaitlescotupreermofittthede vbeyinthceopmrpesreisnecsethorfeveemnoauins vlaaylveress,,iwnthimicha,amreedesiase, nantidalatdovpernetviteina,t wbliothodunreiqfluuex.pTrohpeecrytiteosa.rchitecture of the vein comprises three main layers, intima, media, and adventitia, with unique properties
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