Mechanisms of Medial Wall Thinning in Chronic Total Occlusion.

Abstract

The success rate of percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) is lower and the risk for complications higher compared with other non-CTO PCI. Although interventionalists focus on intimal plaque characteristics, the coronary media is an important (especially for techniques involving antegrade dissection and re-entry) but poorly understood structure in CTO PCI. The aim of the present study was to investigate coronary medial wall thinning in CTO lesions and determine how this thinning might affect CTO PCI. A total of 2,586 sections were investigated, from arteries with evidence of CTO from 54 subjects (n=1,383 sections) and arteries without evidence of CTO from 54 subjects with non-coronary-related deaths (n=1,203 sections) after matching for age, gender, body weight, and body height. The medial thickness in subjects with CTO was lower than that in those with non-coronary-related death (P<0.001). In subjects with CTO, CTO lesions had thinner medial walls compared with those with lower luminal narrowing (P< 0.001). At the CTO distal segments, the 6- to 12-mm distal segment from the distal end of the CTO had significantly less luminal narrowing (P< 0.001), and similar medial thickness, compared with the distal end of the CTO. Immunohistochemical analysis revealed that short-duration CTO had more cleaved caspase-3-positive cells in media and had significantly more CD3+, CD4+, CD8+, and CD4+CD28null T cells compared with long-duration CTO. CTO lesions demonstrated coronary medial thinning compared with non-CTO lesions. Further investigation of the cause-and-effect relationship among inflammation, apoptosis, and coronary medial wall thinning is warranted in future mechanistic studies.