Aortic aneurysm and aortic dissection (AA/AD) are critical aortic diseases with a hidden onset and sudden rupture, usually resulting in an inevitable death. Several pro- and anti-angiogenic factors that induce new capillary formation in the existing blood vessels regulate angiogenesis. In addition, aortic disease mainly manifests as the proliferation and migration of endothelial cells of the adventitia vasa vasorum. An increasing number of studies have shown that angiogenesis is a characteristic change that may promote AA/AD occurrence, progression, and rupture. Furthermore, neocapillaries are leaky and highly susceptible to injury by cytotoxic agents, which promote extracellular matrix remodeling, facilitate inflammatory cell infiltration, and release coagulation factors and proteases within the wall. Mechanistically, inflammation, hypoxia, and angiogenic factor signaling play important roles in angiogenesis in AA/AD under the complex interaction of multiple cell types, such as smooth muscle cells, fibroblasts, macrophages, mast cells, and neutrophils. Therefore, based on current evidence, this review aims to discuss the manifestation, pathological role, and underlying mechanisms of angiogenesis involved in AA/AD, providing insights into the prevention and treatment of AA/AD.

UNASSIGNED: Vasa vasorum (VVs) is a Latin word representing vessels of vessels. VVs are usually found on the adventitia of the parent vessel and infrequently reach the media and intima, depending on the size and type of the parent vessels and physiological and pathological conditions. The VVs include arteries, capillaries, veins, and lymphatic vessels, involving the oxygenation and nourishment of the vessel\'s wall to sustain its healthy state. Accumulated studies have revealed that VVs are involved in various intracranial lesions, including atherosclerotic diseases, aneurysms, and shunt diseases. The current review aims to review and integrate past and recent findings and knowledge on VVs and to facilitate our understanding of VVs and intracranial pathology involving VVs.
UNASSIGNED: A literature review was carried out with a focus on the role of VVs by searching the Pubmed database.
UNASSIGNED: We identified 71 articles that discuss the role of VVs. We discussed the anatomical structure, physiological significance, and pathological significance of the VV.
UNASSIGNED: VV is not only involved in the nutrition and metabolism of the vascular wall but is also deeply involved in the pathogenesis of inflammation, ischemia, and thrombosis of the vascular wall. In addition, in the central nervous system, intracranial vascular wall nutrient particularities and VVs are closely related to the pathogenesis of cerebral aneurysms, subarachnoid hemorrhage, arteriovenous shunt disease, atherosclerotic lesions, and other conditions.

Intracranial atherosclerotic stenosis (ICAS) is a pathological condition characterized by progressive narrowing or complete blockage of intracranial blood vessels caused by plaque formation. This condition leads to reduced blood flow to the brain, resulting in cerebral ischemia and hypoxia. Ischemic stroke (IS) resulting from ICAS poses a significant global public health challenge, especially among East Asian populations. However, the underlying causes of the notable variations in prevalence among diverse populations, as well as the most effective strategies for preventing and treating the rupture and blockage of intracranial plaques, remain incompletely comprehended. Rupture of plaques, bleeding, and thrombosis serve as precipitating factors in the pathogenesis of luminal obstruction in intracranial arteries. Pericytes play a crucial role in the structure and function of blood vessels and face significant challenges in regulating the Vasa Vasorum (VV)and preventing intraplaque hemorrhage (IPH). This review aims to explore innovative therapeutic strategies that target the pathophysiological mechanisms of vulnerable plaques by modulating pericyte biological function. It also discusses the potential applications of pericytes in central nervous system (CNS) diseases and their prospects as a therapeutic intervention in the field of biological tissue engineering regeneration.

The vasa vasorum of the large pulmonary vessels is involved in the pathology of COVID-19. This specialized microvasculature plays a major role in the biology and pathology of the pulmonary vessel walls. We have evidence that thrombosis of the vasa vasorum of the large and medium-sized pulmonary vessels during severe COVID-19 causes ischemia and subsequent death of the pulmonary vasculature endothelium. Subsequent release of thrombi from the vasa interna into the pulmonary circulation and pulmonary embolism generated at the ischemic pulmonary vascular endothelium site, are the central pathophysiological mechanisms in COVID-19 responsible for pulmonary thromboembolism. The thrombosis of the vasa vasorum of the large and medium-sized pulmonary vessels is an internal event leading to pulmonary thromboembolism in COVID-19.

OBJECTIVE: It was previously believed that atherosclerotic (AS) plaque starts to develop from the intima and that intraplaque vasa vasorum (VV) hyperplasia promotes adventitial VV (AVV) hyperplasia. However, recent studies have shown that arterial AVV hyperplasia precedes early intimal thickening, suggesting its possible role as an initiating factor of AS. To provide further insight into this process, in this study, we examine the evolution of AAV and VV development in a preclinical model of early AS with longitudinal ultrasound imaging.
METHODS: Models of early AS were established. Duplex ultrasound scanning and contrast-enhanced ultrasound were performed for diagnosis. Pearson correlation tests were used to analyze the relationships between AVV hyperplasia and VV hyperplasia, or between AVV hyperplasia and intima-media thickness (IMT).
RESULTS: During 0-12 wk of high-fat feeding, AVV gradually increased and intima-media thickened gradually in the observation area; in the 2nd wk of high-fat feeding, the observation area showed obvious AVV proliferation; at the 4th wk, the intima-media membrane became thicker; at the 12th wk, early plaque formation and intraplaque VV proliferation were observed. There was a strong positive correlation between AVV proliferation and IMT thickening and a strong negative correlation between AVV proliferation and the change rate of vessel diameter.
CONCLUSIONS: This study demonstrated that AVV proliferation in the arteries occurred earlier than IMT thickening and was positively correlated with IMT. At present, the indicators of ultrasonic diagnosis of AS, such as IMT, Intraplaque VV, Echo property, all appear in the advanced stage of AS. The AVV may be an innovative diagnostic target for the early stage of AS plaque.

Abdominal aortic aneurysm (AAA) is a vascular disease that involves aortic wall dilation. Cigarette smoking is an established risk factor and rupture, and nicotine may be a major contributor to the onset of AAA. In humans the condition is associated with stenosis of the vasa vasorum (VV), which may be caused by nicotine. In this study, we evaluated the effects of nicotine on VV pathology. After 4 weeks of nicotine administration to rats using an osmotic pump, the VV patency rate in the nicotine administration group was significantly lower than that in the control group. The levels of Ki-67, a cell proliferation marker, were significantly increased in the regions containing VV in the nicotine group, as were hypoxia inducible factor-α levels. Collagen levels around VV were significantly lower in the nicotine group than in the controls. Our data suggest that nicotine can cause VV stenosis by inducing abnormal proliferation of smooth muscle cells in the VV. The increased risk of AAA development due to cigarette smoking may be partially explained by nicotine-induced VV denaturation and collagen fiber degradation.

UNASSIGNED: Nonalcoholic fatty liver disease (NAFLD) affects a quarter of the world\'s population and encompasses a spectrum of liver conditions, from non-alcoholic steatohepatitis (NASH) to inflammation and fibrosis. In addition, NAFLD also links to extrahepatic conditions like diabetes or obesity. However, it remains unclear if NAFLD independently correlates with the onset and progression of atherosclerosis.
UNASSIGNED: This cross-sectional study aimed to explore the relationship between NAFLD severity, assessed via liver biopsy, and early atherosclerosis using adventitial vasa vasorum (VV) density. It included 44 patients with obesity (33 with steatosis, 11 with NASH) undergoing bariatric surgery.
UNASSIGNED: Results revealed no significant differences in adventitial VV density between steatosis and NASH groups, neither in the mean values [0.759 ± 0.104 vs. 0.780 ± 0.043, P=0.702] nor left-right sides. Similarly, carotid intima-media thickness (cIMT) did not vary between these groups. Additionally, no linear correlation existed between VV density and cIMT. Only gender showed an association with VV density.
UNASSIGNED: These findings suggest that NASH severity doesn\'t independently drive early atherosclerosis or affects cIMT. Gender might play a role in early atherosclerotic disease in NAFLD, impacting VV density and cIMT. This highlights the need to consider other risk factors when evaluating cardiovascular risk in NAFLD patients.

The pathophysiology of pulmonary hypertension (PH) is not fully understood. Here, we tested the hypothesis that hypoxic perfusion of the vasa vasorum of the pulmonary arterial (PA) wall causes PH. Young adult pig lungs were explanted and placed into a modified ex vivo lung perfusion unit (organ care system, OCS) allowing the separate adjustment of parameters for mechanical ventilation, as well as PA perfusion and bronchial arterial (BA) perfusion. The PA vasa vasorum are branches of the BA. The lungs were used either as the control group (n = 3) or the intervention group (n = 8). The protocol for the intervention group was as follows: normoxic ventilation and perfusion (steady state), hypoxic BA perfusion, steady state, and hypoxic BA perfusion. During hypoxic BA perfusion, ventilation and PA perfusion maintained normal. Control lungs were kept under steady-state conditions for 105 min. During the experiments, PA pressure (PAP) and blood gas analysis were frequently monitored. Hypoxic perfusion of the BA resulted in an increase in systolic and mean PAP, a reaction that was reversible upon normoxic BA perfusion. The PAP increase was reproducible during the second hypoxic BA perfusion. Under control conditions, the PAP stayed constant until about 80 min of the experiment. In conclusion, the results of the current study prove that hypoxic perfusion of the vasa vasorum of the PA directly increases PAP in an ex situ lung perfusion setup, suggesting that PA vasa vasorum function and wall ischemia may contribute to the development of PH.NEW & NOTEWORTHY Hypoxic perfusion of the vasa vasorum of the pulmonary artery directly increased pulmonary arterial pressure in an ex vivo lung perfusion setup. This suggests that the function of pulmonary arterial vasa vasorum and wall ischemia may contribute to the development of pulmonary hypertension.

OBJECTIVE: Treatment of hypovascular tumors, such as pancreatic adenocarcinoma, is challenging owing to inefficient drug delivery. This report examines the potential mechanism of localized drug delivery via transarterial microperfusion (TAMP) using a proprietary adjustable double-balloon occlusion catheter in a porcine model.
METHODS: Adult Yorkshire swine (N = 21) were used in the Institutional Animal Care & Use Committee-approved protocols. The RC-120 catheter (RenovoRx, Los Altos, California) was positioned into visceral, femoral, and pulmonary arteries with infusion of methylene blue dye, gemcitabine, or gold nanoparticles. Transmural delivery was compared under double-balloon occlusion with and without side-branch exclusion, single-balloon occlusion, and intravenous delivery. Intra-arterial pressure and vascular histologic changes were assessed.
RESULTS: Infusion with double-balloon occlusion and side-branch exclusion provided increased intra-arterial pressure in the isolated segment and enhanced perivascular infusate penetration with minimal vascular injury. Infusates were predominantly found in the vasa vasorum by electron microscopy.
CONCLUSIONS: TAMP enhanced transmural passage mediated by localized increase in arterial pressure via vasa vasorum.

BACKGROUND: Morphologically, the risk of aortic aneurysm rupture is mainly evaluated based on its type (e.g., fusiform or saccular) and diameter. Based on the finite element analysis, peak wall stress has been identified as a more sensitive and specific predictor of rupture in recent years. Moreover, in finite analysis, the neck of aneurysm is the highest peak wall stress and is associated with the rupture point.
METHODS: A saccular aortic aneurysm (84 mm) was incidentally detected during preoperative examination for chronic empyema in a 74-year-old male patient with a history of polycythemia. Aortic arch graft replacement using an open stent was performed.
CONCLUSIONS: Morphologically, this case was associated with a very high risk of rupture; nevertheless, it did not rupture. In this case, a mural thrombus (likely formed due to polycythemia) covered the neck of aneurysm that is experiencing the highest peak wall stress and is associated with the rupture point. The mural thrombus decreased peak wall stress and could reduce the risk of rupture even for huge saccular aneurysms. Furthermore, the mural thrombus was fully occupied in aneurysms, such as during coil embolization. Thus, polycythemia could decrease the risk of rupture of huge saccular aneurysms.