These results imply that pulmonary vasculopathy in patients with CPFE could occur in the whole lung tissue. This may explain the tendency for it to lead to the development of pulmonary hypertension in CPFE cases.

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Accumulating evidence has shown that oxidized low-density lipoprotein (LDL) is a useful marker for cardiovascular disease. Oxidized LDL contributes to atherogenesis in a wide range of stages, such as impairing vascular endothelial cells, promoting expression of adhesion factors of vascular endothelial cells, and facilitating monocyte migration and accumulation of lipids under the vascular endothelium by being captured by macrophages [1]. Previous studies have shown that oxidized LDL levels are elevated in patients with coronary artery disease [2,3]. Oxidized LDL levels are especially increased in acute coronary syndrome (ACS) compared with stable angina pectoris [4]. Furthermore, elevated oxidized LDL levels are predictive of future cardiovascular events in healthy men and predict an increased risk of future myocardial infarction in apparently healthy people [5]. These

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