Atherosclerotic lesions produce luminal narrowing, thrombosis, embolization, and occulation.
Characterized by local accumulation of lipid in the vessel wall located either in the extracellular matrix or inside foam cells.
Thories of atherogenesis
Lipid insudation hypothesis
Intima cell mass hypothesis
Major components of plaque : smooth muscle cells, connective tissue (matrix), lipid, and inflammatory cells (predominantly macrophages)
The presence of lipid within these lesions is a prominent distinguishing feature in comparison to other arteriopathies.
Position of lesion
commonly involved the infrarenal abdominal aorta, iliofemoral arteries (especially the superficial femoral artery), popliteal arteries, carotid bifurcation, and proximal coronary arteries
Upper extremity vessels, as well as the common carotid, renal, and mesenteric arteries (beyond their origins), are also usually spared.
Positive family history
Studies have demonstrated a strong positive correlation between atherosclerotic cardiovascular disease and elevated total and LDL cholesterol and an equally strong negative correlation with HDL levels.
The mechanism for the effects of smoking is likely to involve direct toxicity of tobacco metabolites on the vascular endothelium, probably by creating oxidant stress .
another important independent risk factor for coronary atherosclerosis, with a continuous increase in relative risk associated with each increment of pressure .
Diabetic patients are also at markedly increased risk for atherosclerosis, often manifesting a particularly virulent form of the disease, leading to higher rates of myocardial events, stroke, and amputation.
Excessive alcohol use
Peripheral arterial insufficiency
Atherosclerotic plagues become large enough to narrow the arterial lumen and cause atherosclerosis occlusion
a complex, chronic inflammatory process that affects the elastic and muscular arteries.
Atherosclerotic plaques continuous progression and secondary thrombosis cause stricture or obstruction of arteries and often results in chronic or acute ischemic symptoms of lower limbs
Atherosclerotic plaques are dynamic lesions that may undergo progression or regression over time. Similarly, the underlying arterial wall also undergoes adaptive remodeling.
Arterial enlargement is a well-established feature of atherosclerosis and often results in relative preservation of luminal area until plaque volume reaches a threshold size (approximately 40% stenosis) beyond which compensation fails and lumen narrowing becomes progressive.
Decreased amplitude of the pulses
Pallor of foot on elevation
Ischemic rest pain
Ulceration/ nonhealing of wounds
Atrophy and gangrene
Low ankel-brachial index (ABI)
Pain or fatigue in muscles of the lower extremity caused by walking and relieved by rest
Typically,symptoms are completely relieved after 2-5 minutes of inactivity
Does not occur at rest
Commonly occurs in the calf muscles
Ischemic rest pain
Caused by ischemic neuritis and tissue necrosis
Indicate an advanced stage of ischemia
Localized to the vicinity of an ischemic ulcer or pregangrenous toe
Aggravated by elevation of the extremity
Relieved sometimes when patients stand erect, as gravity aids the delivery of arterial blood
Ankel-brachial index (ABI)
Determined by dividing the pressure obtained at the ankle by the brachial arterial pressure
Normally, the ABI is 1.0 or greater
A value below 1.0 indicates occlusive disease proximal to the point of measurement
Rest pain usually appears when the ratio is 0.3 or lower
Noninvasive Hemodynamic Assessment
segmental pressure technique
Exercise (treadmill) testing
Doppler and Duplex Ultrasonography
Computed tomography angiography (CTA)
Magnetic resonance angiography (MRA)
Digital subtraction angiography (DSA)
Low MW dextrans:500ml iv qd
Antispasmodic,nacotic and artery dilated drugs
Morphine and dolantin
Sympathetic nerve blocker such as phentolamine
Percutaneous transluminal angiography(PTA)
The classic approach is to advance a guide (or a long sheath) across the stenosis over the previously placed guide wire; the vascular stent is then passed through the guide and positioned at the lesion, the guide is withdrawn, and the stent is deployed