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Background: Severely calcified coronary artery stenting remains a challenge due to stent thrombosis, target vessel failure, and higher mortality. Moreover, optimal vessel preparation for calcified plaque with a crack formation pattern has not been established yet. We aimed to identify the effect of crack formation in calcified plaque in the coronary artery on the lumen area after stenting.Materials and Methods: We evaluated 50 consecutive patients undergoing drug-eluting stent implantation for severely calcified lesions by using optical frequency domain imaging (OFDI) (54 lesions); we analyzed OFDI image slices every 3 mm and evaluated the segments of 242 images in those who had the arc of calcium more than 180°. Crack formation in calcified plaque was classified into three types: type 0, no cracks; type 1, no dissection between calcified plaque and vessel wall; and type 2, any dissection between calcified plaque and vessel wall.Results: Type 2 had a significantly higher area expansion ratio between preballooning and poststenting (type 0, 196% (interquartile range (IQR), 163-244); type 1, 210% (IQR, 174-244); type 2, 237% (IQR, 203-294)).Conclusions: The dissection between calcified plaque and vessel wall was a significant factor affecting lumen area expansion after stenting. [ABSTRACT FROM AUTHOR]

Atherosclerosis is the main pathological basis for the occurrence of most cardiovascular diseases, the leading global health threat, and a great burden for society. It has been well established that atherosclerosis is not only a metabolic disorder but also a chronic, sterile, and maladaptive inflammatory process encompassing both innate and adaptive immunity. Macrophages, the major immune cell population in atherosclerotic lesions, have been shown to play critical roles in all stages of atherosclerosis, including the initiation and progression of advanced atherosclerosis. Macrophages have emerged as a novel potential target for antiatherosclerosis therapy. In addition, the macrophage phenotype is greatly influenced by microenvironmental stimuli in the plaques and presents complex heterogeneity. This article reviews the functions of macrophages in different stages of atherosclerosis, as well as the phenotypes and functions of macrophage subsets. New treatment strategies based on macrophage-related inflammation are also discussed. [ABSTRACT FROM AUTHOR]