Calcification patterns in femoral and carotid atheromatous plaques: A comparative morphometric study.

This comparative study was designed to focus on the mineral patterns in human atherosclerotic plaques based on quantitative measurements of calcium deposits through the morphometric method. A total of 101 atherosclerotic plaques were harvested by conventional transluminal angioplasty from the carotid artery (CA) and different segments of the femoral-popliteal axis (FPA), fixed in formalin and sent for histological processing. The histological grade of the atherosclerotic plaque and the calcification pattern were evaluated, followed by a morphometric analysis of the mineral deposits. Regarding the localization, the advanced plaques (VII and VIII types) developed predominantly at the level of the superficial femoral artery (SFA) compared to the CA (P<0.001). This significant difference was maintained even if they were divided into low grade (IV and V) and high grade categories (VI, VII and VIII) (P<0.05). Compared with that in the carotid plaques, in the FPA plaques the mineralized surface increased in parallel with the narrowing of the vascular lumen diameter. The image analysis of the total pathological calcification score (pCS) showed a significant difference between the CA plaques and distal SFA (dSFA) plaques (P=0.038) and between the proximal SFA (pSFA) and dSFA plaques (P=0.013). In the case of the simple nodular pattern, calcification occupied significantly larger areas in the plaques developed in the dSFA and popliteal artery (PA) in comparison with the CA plaques (P=0.0007 and P=0.0009). pCSs calculated in plaques with extensive calcification pattern showed a lower value in the CA vs. the pSFA plaques (P=0.004). A less pronounced, but significant difference was observed between the pCS of pSFA and dSFA plaques (P=0.017). Femoral and carotid plaques exhibited different morphology and tendency for calcification. In parallel with the narrowing of the vascular lumen diameter, the mineralized surface increased at the level of different FPA segments. These results suggest that the mechanism is site-specific, and wall structure-dependent.