10 CTA identifies calcium very well when used as an adjunctive noninvasive diagnostic test however, extensive VC decreases the diagnostic accuracy of CTA because it creates a “blooming artifact,” which can make the lesion appear more severe. Extravascular ultrasound (EVUS) can noninvasively identify the extent and location of calcific lesions, but the shadowing of the lumen by calcium may limit the ability to determine systolic flow velocities in the underlying vessel. 9 The exact anatomic location and severity of a lesion can then be visualized with noninvasive imaging modalities. Although an ABI 1.3 due to noncompressible lower extremity arteries. The ABI is a simple test to begin the diagnostic workup of PAD and VC. 6 Alternatively, a meta-analysis by Renneberg et al demonstrated that arterial or valvular calcification carries a separate additional risk of broad cardiovascular events and mortality, and Yang et al showed that just the presence of VC was linked to not only mortality but also limb-specific outcomes, with increased risk of limb amputation in patients with PAD. It is well known that the presence of PAD correlates with cardiovascular mortality, and this holds true even when correcting for coexisting cardiovascular risk factors and can help prognosticate potential outcomes. Its prevalence increases with age and in patients with diabetes mellitus, chronic kidney disease, obesity, and dyslipidemia. Medial VC is more commonly seen in the femoral artery than the popliteal artery and poses special challenges when it is present below the knee (which is common) since it affects both diagnostic accuracy (eg, noncompressible vessels lead to falsely elevated ankle-brachial index ) and interventional considerations.
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The distribution of medial calcification extends contiguously throughout the vascular bed, resulting in arterial stiffening and decreased compliance. 5 Increased bone turnover leads to the release of circulating nucleational complexes that act with apoptotic cells as substrate for VC. Secondly, activation of vascular osteoblast-like cells induces mineralization of vascular smooth muscle cells. 2,4 More specifically, associated mechanisms of medial VC include an accompanying decrease in inhibition of antimineralization factors, such as pyrophosphate, which is expressed by blood vessels. Medial calcification (Mönckeberg sclerosis) is more prevalent in intra-abdominal and lower extremity arteries, and the complex pathophysiology of medial arteriosclerosis is thought to be associated with an upregulation of bone-associated proteins and osteoblast differentiation factors.
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Intimal calcification occurs in association with a classically obstructive atherosclerotic plaque. When it occurs, calcium deposition is typically seen in two of the three anatomic layers of arteries, specifically the intima and media. Calcification of the vasculature is triggered by inflammation as an active pathologic response to systemic disease.
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1-3 The pathophysiology of VC was previously attributed to elevated serum calcium levels however, this theory has recently fallen out of favor. This is especially true because VC is ubiquitous, found in up to 47% to 72% of PAD patients. Vascular calcification (VC) in peripheral artery disease (PAD) presents a treatment challenge.