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The last few years have seen a surge of interest in the measurement of coronary artery calcification to predict and monitor the presence of coronary atherosclerosis. In addition, the rising clinical burden of valvar calcification in the aging population has highlighted the importance of understanding the processes of calcification within vascular tissues.
Vascular calcification occurs in both the intima and the media of arteries, and there is evidence that these two sites of calcification are distinct entities (table 1). Intimal calcification only occurs within atherosclerotic plaques and is seen as early as the second decade of life, just after the fatty streak stage.1 In contrast, medial calcification occurs independently of intimal calcification and atherosclerosis. It commonly occurs in the peripheral arteries of the lower limbs in otherwise healthy elderly patients (Monckeberg's sclerosis), where it is seen as “rail tracking” on plain radiographs. However, it also occurs in younger patients with diabetes and chronic renal failure. In diabetic patients, medial calcification appears to be a strong independent predictor of cardiovascular mortality and occurs particularly in those with neuropathy.2 Its presence can make palpating pulses and hearing Korotkoff sounds difficult and can lead to false elevation of cuff systolic blood pressure measurements. It also causes problems with the surgical management of vascular shunts.
More importantly, arterial wall stiffness has been shown to be correlated independently with aortic calcification.3 In theory this increased arterial stiffness from calcification may lead to an increase in cardiac work. In addition the reduction in aortic compliance may result in a decrease in diastolic coronary perfusion, as this is dependent on the recoil of the aorta which has been stretched during systole.4 Furthermore, increased arterial stiffness leads to an increase in pulse pressure, which is a highly significant …