Abstract

Peripheral arterial disease (PAD) is a clinical condition caused by an atherosclerotic process affecting the arteries of the limbs. PAD has many similarities with the atherosclerotic process in coronary artery disease and shares similar risk factors, including male sex, age, diabetes mellitus, smoking, hypertension, high cholesterol, and renal insufficiency. Furthermore, PAD is known to be associated with a reduction in functional capacity and quality of life, as well as an increased risk for myocardial infarction, stroke, death, and a major cause of limb amputation. However, because PAD is often observed with comorbid conditions, such as hypertension, dyslipidemia, diabetes mellitus, cigarette smoking, and physical inactivity, the pathophysiology of PAD is certainly complex and multifactorial. For this reason, a better physiological understanding of the pathogenesis and treatment options for patients with PAD is necessary. In general, the goal of medical therapy in patients with PAD is to reduce the risk of future cardiovascular morbidity and mortality in patients with high ischemic risk and to improve walking distance and functional status in patients with intermittent claudication. Despite major improvements in surgical endovascular techniques, PAD is still associated with high mortality and morbidity. Unfortunately, most patients are diagnosed late and are not treated optimally. A blood test for PAD, if sufficiently sensitive and specific, would be expected to improve recognition and treatment of PAD-affected patients, but biomarkers to predict the development of PAD are lacking although recently OxPL/apoB levels are shown to be positively associated with risk of PAD.1 Article see p 490 Traditionally, cellular processes and linked gene control were considered to occur via a relatively simple mechanism. Genomic DNA is transcribed into coding mRNA strands that are subsequently translated into proteins, finally carrying out cellular tasks. However, recent discoveries of a new class …

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