Evidence-based management of peripheral vascular disease

Abstract

Peripheral vascular disease (PVD) is very prevalent in the United States and is part of a global vascular problem. PVD patients have a heightened inflammatory state and are at high risk of death from acute cardiovascular problems rather than from progression of PVD. Modifiable risk factors for PVD include smoking, hypertension, diabetes, hyperlipidemia, elevated high sensitivity C-reactive protein, obesity, and the metabolic syndrome. Symptomatic treatment of claudication includes smoking cessation, exercise, cilostazol, statins, and revascularization with percutaneous or surgical therapy. Antithrombotic therapy with aspirin or clopidogrel is important to reduce cardiovascular events but does not affect symptoms of claudication. Patients with rest limb ischemia or ulceration should be revascularized to minimize the chance of limb loss. Percutaneous revascularization is not without significant complications, however, and future research needs to focus on inflammation, thrombosis, and restenosis in the PVD patient. Finally, new devices that tackle difficult lesions, drug-eluting stents, and pharmacologic agents that reduce global atherosclerosis are on the horizon and are likely to become critical components in the management of the PVD patient.

Increased vascular thromboxane generation impairs dilation of skeletal muscle arterioles of obese Zucker rats with reduced oxygen tension

“…These results also suggest that the elevated vascular oxidant stress inherent in metabolic syndrome may contribute to the increased vascular TxA 2 production and may blunt vascular sensitivity to PGI 2. skeletal muscle microcirculation; endothelium-dependent dilation; vascular reactivity; rodent models of obesity METABOLIC SYNDROME represents a series of systemic pathologies that develop sequentially in afflicted individuals and can include obesity, insulin resistance/type II diabetes mellitus, dyslipidemia, and hypertension (25). While each of these pathologies in isolation can increase the future risk for the development of peripheral vascular disease, when present in combination, this risk increases dramatically (24) and can lead to numerous profound alterations to vascular structure/function relationships (26,27). These vascular alterations can impair tissue perfusion-demand matching and can lead to a compromised function (27).…”

“…While each of these pathologies in isolation can increase the future risk for the development of peripheral vascular disease, when present in combination, this risk increases dramatically (24) and can lead to numerous profound alterations to vascular structure/function relationships (26,27). These vascular alterations can impair tissue perfusion-demand matching and can lead to a compromised function (27). An effective animal model for metabolic syndrome in humans is the obese Zucker rat (OZR), a rodent model characterized by its dysfunctional leptin receptor gene, resulting in abrogated leptin signaling and an impaired satiety reflex (10).…”

An autopsy case of internal jugular vein thrombophlebitis involving sepsis following blunt neck injury

“…[19][20][21][22] Partial contribution of the preexisting diabetes may also be considered for the predisposition. [23][24][25] Due to the complicated structure of the neck, composed of three layers involving an outer superficial (investing) layer, a middle (visceral) layer and an internal (prevertebral) layer, surgical treatment is difficult; once infection of the neck organs occurs, and the condition may become critical. 5 The prognosis for this infectious complication is poor, with a mortality rate approaching 40% despite aggressive open drainage and antibiotic therapy.…”

The role of genetic polymorphism in the formation of atherosclerosis in the vessels of lower extremities

“…В связи с местными осложнениями 4% больных проводят ампутацию, 7% -реваскуляризирующие операции [22]. Кроме того, риск смерти от сердечнососудистой патологии у больных атеросклерозом сосудов нижних конечностей почти в 6 раз выше, чем в целом в популяции, а у больных с манифестным течением -выше в 15 раз [2], в первую очередь за счёт гиперкоагуляции [17] и воспаления [14].…”