Long-term consequences of trans-radial catheterization on the radial artery

Background: The radial artery (RA) is often utilized for diagnostic coronary angiography and percutaneous intervention. Recent high-level evidence supports RA use in preference to saphenous vein as a conduit for coronary revascularization. Aim: To demonstrate gross and histologic changes of the RA following transradial access. Methods: We present two patients who had open RA harvest for coronary bypass surgery after transradial catheterization. Results: Examination 8 years after transradial catheterization demonstrated thickened intima and dissection, and examination 12 years following transradial catheterization with percutaneous coronary intervention demonstrated chronic dissection with thickened intima and near occlusion of the lumen. Conclusion: Transradial access via the RA, even after several years, is associated significant injury, making it unusable as a conduit for surgical coronary revascularization. A RA that has been utilized for catheterization should not be considered for coronary revascularization.

Vulnerability to shear stress caused by altered peri-endothelial matrix is a key feature of Moyamoya disease

Moyamoya disease (MMD) is characterized by progressive bilateral stenotic changes in the terminal portion of the internal carotid arteries. Although RNF213 was identified as a susceptibility gene for MMD, the exact pathogenesis remains unknown. Immunohistochemical analysis of autopsy specimens from a patient with MMD revealed marked accumulation of hyaluronan and chondroitin sulfate (CS) in the thickened intima of occlusive lesions of MMD. Hyaluronan synthase 2 was strongly expressed in endothelial progenitor cells in the thickened intima. Furthermore, MMD lesions showed minimal staining for CS and hyaluronan in the endothelium, in contrast to control endothelium showing positive staining for both. Glycosaminoglycans of endothelial cells derived from MMD and control induced pluripotent stem cells demonstrated a decreased amount of CS, especially sulfated CS, in MMD. A computational fluid dynamics model showed highest wall shear stress values in the terminal portion of the internal carotid artery, which is the predisposing region in MMD. Because the peri-endothelial extracellular matrix plays an important role in protection, cell adhesion and migration, an altered peri-endothelial matrix in MMD may contribute to endothelial vulnerability to wall shear stress. Invading endothelial progenitor cells repairing endothelial injury would produce excessive hyaluronan and CS in the intima, and cause vascular stenosis.

Superficial Temporal Artery-Middle Cerebral Artery Bypass Using a Thick STA after Endarterectomy: A Rescue Technique

Background and Objective Superficial temporal artery (STA)-middle cerebral artery (MCA) bypass is a procedure to reconstruct cerebral blood flow in the MCA territory. In some cases, the STA wall is thickened and the size discrepancy between STA and MCA is apparent. In such a situation, STA-MCA bypass is challenging. We present two patients who underwent STA-MCA bypass using STA in which a thickened intima was removed. We discuss the usefulness of this rescue technique. Patients and Results A patient with an atherosclerotic MCA occlusion and another with an occluded internal carotid artery are included. Endarterectomy of STA was performed before or during anastomosis, and the intima-resected STA was anastomosed to MCA. In both cases, the STA was thick and hard, and it was difficult to anastomose the STA as it was to the MCA. Patency of the bypass was confirmed by postoperative angiography. Conclusion Endarterectomy of a thickened STA might be an effective rescue technique in cases with severely atherosclerotic STA in STA-MCA bypass.

Atomic Force Microscopy Study of Atherosclerosis Progression in Arterial Walls

Cardiovascular disease remains the leading cause of mortality worldwide. Here we suggest a novel approach for tracking atherosclerosis progression based on the use of atomic force microscopy (AFM). Using AFM, we studied cross-sections of coronary arteries with the following types of lesions: Type II—thickened intima; Type III—thickened intima with a lipid streak; Type IV—fibrotic layer over a lipid core; Type Va—unstable fibrotic layer over a lipid core; Type Vc—very thick fibrotic layer. AFM imaging revealed that the fibrotic layer of an atherosclerotic plaque is represented by a basket-weave network of collagen fibers and a subscale network of fibrils that become looser with atherosclerosis progression. In an unstable plaque (Type Va), packing of the collagen fibers and fibrils becomes even less uniform than that at the previous stages, while a stable fibrotic plaque (Vc) has significantly tighter packing. Such alterations of the collagen network morphology apparently, led to deterioration of the Type Va plaque mechanical properties, that, in turn, resulted in its instability and propensity to rupture. Thus, AFM may serve as a useful tool for tracking atherosclerosis progression in the arterial wall tissue.

Abstract 190: Continuous Vascular Remodeling Related To Development Of Arteriosclerosis Or Atherosclerosis In Kawasaki Disease ~ Immunohistochemical Study using an Animal Model ~

Background: Atherosclerotic coronary heart disease has recently emerged as a clinical issue among young individuals with a history of Kawasaki disease (KD), which is a systemic vasculitis unique to children. However, whether or not and how KD promotes atherosclerosis remains unclear. We hypothesized that, analogous to the pathogenesis of arteriosclerosis or atherosclerosis, endothelial injury and the resultant intimal thickening are induced in coronary arteries after attenuation of vasculitis. Methods: We used a rabbit model of KD developed by Onouchi et al. and performed histopathological analysis of the coronary arteries at acute (1, 3, 5, and 7 days) and chronic (3 months) phases of the disease. Results: In these rabbit models, a pan-arteritis with significant intimal cellular hypertrophy was histologically detected in the acute phase, and arterial intimal thickening was observed during the chronic phase. Immunohistochemical analysis of the coronary arteries revealed that the thickened intimal lesions observed during the chronic phase comprised abundant α-smooth muscle actin (α-SMA)-positive cells, most of which concomitantly expressed vascular cell adhesion molecule-1 and nuclear factor-κB. Although macrophages positive for RAM11 were barely detected, macrophage colony stimulating factor was strongly expressed in migrating smooth muscle cells in the intimal layer. In addition, the accumulation of proteoglycan as extracellular matrix was distinctly visible in the thickened intima, indicating progressive accumulation of lipids and proliferation of smooth muscle cells within the lesion. Conclusions: These findings suggest that, in KD-associated vasculitis, the migration of α-SMA-positive cells into the thickened intima might induce continuous vascular inflammation and remodeling, which might progress to coronary arteriosclerosis or atherosclerosis.