Spectral Differences Between Normal and Atherosclerotic Aorta

Ischemic heart disease associated with coronary artery atherosclerosis is a leading cause ofdeath in the world today. In addition to standard treatments such as balloon angioplasty, laser mediated angioplasty is being considered as a potential adjuvant or replacement. Nevertheless, experiments and clinical experience have demonstrated that laser angioplasty is associated with damage to normal vessel tissue, which can cause serious complications. To study the possibility of minimizing these effects by directing laser energy more specifically to atherosclerotic lesions, data concerning the spectral characteristics of normal and diseased artery are necessary. In the current study, the absorbance, reflection and fluorescence spectra of normal and atherosclerotic aortic wall tissue are defined, revealing that (i) spectral characteristics of atherosclerotic aorta wall samples are significantly differed from that of healthy vascular wall samples and (ii) based on a spectral analysis of vascular wall, it is possible to distinguish morphological types of atherosclerotic plaques (i.e., lipidic, calcified). The current study contributes to a more complete understanding of laser-tissue interactions that may, following more experimentation and technique development, result in an improvement of clinical laser angioplasty technique.

Role of autophagy in aneurysm and dissection of the ascending aorta

Maintenance of physiologically balanced levels of autophagy is crucial for cellular homeostasis and in the normal vessel wall, balanced autophagy can be considered a cytoprotective mechanism that preserves endothelial function and prevents cardiovascular disease. Recent studies pointed out the importance of the modulation of the autophagic flux in the pathogenesis of aortic dissection and aneurysms of the ascending aorta. Notably, shear stress (and its receptor p62), IL-6, Rab7 and Atg5/IRE1α pathways of autophagy may be considered the novel super-selective therapeutic target for the preventive and postoperative treatment of aortic aneurysm and aortic dissection. This review intends to summarize current evidences in this field trying to enlighten new avenues for future researches.

The research of Secretogranin III in periperal blood and vitreous of diabetic retinopathy

Background: Secretory granulin III (SCG3) is a member of the secretory granule protein family that regulates the production of secretory granules. SCG3 has a role in reducing retinal vascular leakage and neovascularization in an animal model of diabetic retinopathy. This study aimed to study SCG3 in periperal blood and vitreous of human. Methods ： (1) Collecting diabetic retinopathy(DR) patients required vitrectomy, and patients requiring vitrectomy for other non-diabetic factors, retaining some of the vitreous, ELISA was used to detect SCG3 in vitreous. The grouping was divided according to the patients’ blood lipids, BMI (Body Mass Index, BMI) and analyzed. (2) Collecting peripheral blood of DR and non-diabetic patients, ELISAwas performed. Results: (1) A total of 43 cases with DR were collected, and 34 cases non-diabetic patients were collected. SCG3 in DR patients was higher than that of non-diabetic. After refinement grouping, it was found that SCG3 with DR and hyperlipidemia was higher than that of non-diabetic patients without hyperlipidemia. SCG3 with DR and hyperlipidemia was higher than that of DR patients without hyperlipidemia. SCG3 of patients with DR and high BMI was higher than that of non-diabetic with normal BMI. SCG3 with DR and high BMI was higher than that of non-diabetic patients with normal BMI. (2) SCG3 in plasma was minimal or could not be detected. Conclusion： In DR patients, up-regulation of vitreous SCG3 may be closely related to the pathogenesis of DR. However, SCG3 is almost difficult to detect in normal vessel vasculature, which may highlight its advantages in using anti-SCG3 drugs in babies and children in future.

Numerical and experimental analysis of balloon angioplasty impact on flow hemodynamics improvement

Purpose: The paper focuses on the numerical and experimental evaluation of the fluid flow inside chosen fragments of blood vessels. In the first stage of the study, the experimental tests were conducted using a research test stand, designed to be used in this evaluation. The study evaluated the blood flow through a silicone vessel with an implanted coronary stent. Methods: The PIV method was used in order to visualize the flow vectors inside a silicone vessel. Deformed vessel geometry implemented for computational fluid dynamics purposes was obtained owing to a non-linear simulation of the stent expansion (angioplasty process) in a silicone vessel. Additionally, a vessel model with a statistical 55% area stenosis and an irregular real vessel with an atherosclerotic plaque were also subjected to analysis from the hemodynamic flow point of view. A vessel with a statistical stenosis was also used to simulate the angioplasty process, which resulted in obtaining a flow domain for the vessel with an atherosclerotic plaque after the stent implantation. Results: For each case, distributions of parameters such as OSI or TAWSS were also analyzed and discussed. The areas of low TAWSS values appear close to the stent struts. Conclusions: Stents with increased diameters, compared to the normal vessel diameter, create a higher risk of occurrence of the areas with low WSS values. Excessive stent deformation can cause inflammation by injuring the vessel and can initiate the restenosis and thrombotic phenomena through the increased vessel diameter.

P3644Plaque progression from normal vessel wall to fibroatheroma: lessons from over 5-year follow-up optical coherence tomography study

Background Progression of atherosclerosis is a non-uniform process characterized by coexistence of normal vessel wall (NVW) and advanced fibroatheroma within the same cross-section (Figure). Plaque progression from NVW to fibroatheroma usually takes years, that has never been investigated in human. Purpose To investigate the incidence and related factors associated with atherosclerotic progression from NVW to fibroatheroma using long-term serial optical coherence tomography (OCT) follow-up data over 5 years. Methods We enrolled 47 vessels in 30 patients who had undergone serial OCT imaging over 5 years (average: 6.8 years). Baseline and follow-up OCT images were matched for longitudinal and circumferential location and OCT cross-sections that had NVW >30 degrees were enrolled. NVW was defined as vessel wall having OCT-detectable three-layer structure with intimal thickening ≤300μm. Cross-sections were diagnosed as +Progression when NVW in the cross-section reduced by >30 degrees during >5-year follow-up. Results In the present study, atherogenic progression from NVW to fibroatheroma was observed only in 37.2% of the enrolled cross-sections. On the other hand, despite an average long-term follow-up period of 6.8 years, the extent of NVW was maintained in 62.8% of cross-sections. The incidence of microchannel in adjacent fibroatheroma within the same cross-section (23.6% vs. 13.1%, p=0.023), eccentric plaque distribution (21.7% vs. 11.4%, p=0.019), and concave shape (6.6% vs. 0%, p=0.001) at baseline was significantly higher in cross-sections with +Progression than those without Progression. Average intimal thickness of NVW (187.2±64.9μm vs. 170.7±68.6μm; p=0.048) at baseline was significantly thicker in cross-sections with +Progression than those without. Multivariate analysis demonstrated that the presence of microchannel, eccentric plaque distribution and thicker average intimal thickness of NVW at baseline were independently associated with plaque progression during the follow-up. Atheroma progression Conclusion The presence of microchannel in adjacent fibroatheroma, eccentric plaque distribution, and thicker intimal thickening of NVW were potentially associated with plaque progression from NVW to fibroatheroma.

Drug-Coated Balloons Applications in Interventional Cardiology

Backgrounds: Drug coated balloons (DCBs) are new on stented-based anti-proliferative drug delivery systems, recently introduced in interventional cardiology. Their primary aim is to transfer an anti-proliferative drug to reduce the subsequent neo-intima hyperplasia and to maintain the normal vessel diameter and function. Methods: A review of the most recent influential studies about DCBs in all the fields of interventional cardiology has been performed. Results: As demonstrated by different studies, DCBs have different theoretical advantages over Drug Eluting Stents (DESs), especially for the treatment of some endovascular lesions, as In-Stent Restenosis (ISR), coronary bifurcations, small vessels disease and peripheral artery disease at femoropopliteal and below the knee sites. Conclusion: Despite the need of further studies are needed to elucidate the optimal use of DCBs their current use in interventional cardiology appears promising.

Brief serotonin exposure initiates arteriolar inward remodeling processes in vivo that involve transglutaminase activation and actin cytoskeleton reorganization

Inward remodeling of the resistance vasculature is strongly associated with life-threatening cardiovascular events. Previous studies have demonstrated that both actin polymerization and the activation of transglutaminases mediate early stages of the transition from a structurally normal vessel to an inwardly remodeled one. Ex vivo studies further suggest that a few hours of exposure to vasoconstrictor agonists induces inward remodeling in the absence of changes in intraluminal pressure. Here we report that a short, 10-min, topical exposure to serotonin (5-HT) + Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME) was sufficient to initiate inward remodeling processes in rat cremasteric feed arterioles (100–200 μm lumen diameter), in vivo. Addition of the transglutaminase inhibitor, cystamine, blocked the in vivo remodeling. We further demonstrate that, in isolated arterioles, 5-HT + l-NAME activates transglutaminases and modulates the phosphorylation state of cofilin, a regulator of actin depolymerization. The 5-HT + l-NAME-induced remodeling process in isolated arterioles was also inhibited by an inhibitor of Lim Kinase, the kinase that phosphorylates and inactivates cofilin. Therefore, our results indicate that a brief vasoconstriction induced by 5-HT + l-NAME is able to reduce the passive structural diameter of arterioles through processes that are dependent on the activation of transglutaminases and Lim kinase, and the subsequent phosphorylation of cofilin.

Surgical Management of a Giant Right Coronary Artery Aneurysm

<p>Coronary artery aneurysm (CAA) is a rare entity, defined as localized dilation that exceeds the normal vessel diameter by a factor of 1.5. A giant CAA is described as a very large dilation, when diameter exceeds 20 mm. CAA has a preva-lence of 0.02% [Markis 1976]. Different factors may lead to CAA formation, including Kawasaki disease, atherosclerosis, congenital malformations, autoimmune and infectious disor-ders, and percutaneous interventions [Hartnell 1985]. Man-agement of these patients remains controversial due to a lack of data from large series studies.</p><p>We reported a case of a young female patient, who pre-sented with an acute inferior infarction and was diagnosed with a giant right coronary artery (RCA) aneurysm. She underwent aneurysmectomy and revascularization on a beat-ing heart through a right lateral thoracotomy. Due to the minimally invasive nature of this procedure, the patient was able to recover quickly without substantial cosmetic changes.</p>