Description

Peripheral arterial occlusive disease (PAOD) is defined as the partial or total obstruction of one or more lower extremity arteries, most often of atherosclerotic origin. It is a common disease whose 5-years mortality is near 30%.The positive diagnosis is based on clinical examination and measurement of the ankle-brachial index (ABI), which is the ratio of systolic pressure of ankle and brachial systolic pressure. The threshold value for the diagnosis is <0.90. Physiopathologically, mitochondria have the predominant role of providing the ATP necessary for the energetic needs of myocytes, which increase drastically during muscle contraction during exercise. This energy production is of course conditioned by the availability of oxygen. In patients with PAOD, the decrease in blood flow secondary to significant stenosis has the direct consequence of disrupting oxygen delivery to distal muscles and thus limiting muscular performance. Because mitochondrial respiration is the only metabolic pathway capable of providing the energy needed to sustain an effort of several minutes, intermittent claudication in PAOD has logically been related to a hemodynamic mechanism of intermittent muscle hypoperfusion. Recently, an increasing number of histological or functional studies have suggested that episodes of ischemia-reperfusion could induce mitochondrial dysfunction. Medical treatment of patients frequently includes statins while a direct deleterious effect on mitochondrial function has been suspected, inducing a deterioration of the muscular oxidative capacity which would increase the factors hemodynamics and may accumulate in mitochondrial myopathy. In the light of these elements, it is clear that there would be a benefit in being able to distinguish and quantify 1) the part of the reduction of mitochondrial activity secondary to the hemodynamic factor alone due to a decreased muscle perfusion 2) the mitochondrial involvement (mitochondriopathy) potentially induced by oxidative stress in PAOD. 2 sub-groups are distinguished to identify the statin-induced mitochondrial dysfunction.