目的： 探讨茜素红S（alizarin red S）染色在血管钙化疾病中的应用价值。 方法： 选择钙盐含量高、中、低的组织共31例分别进行茜素红S染色和von Kossa硝酸银染色，对比2种不同染色法的一致性。对58例慢性肾病，17例动脉粥样硬化以及13例主动脉夹层血管组织进行茜素红S染色观察钙化情况。 结果： 茜素红S染色和硝酸银染色对高、中、低钙含量组织31例均能明确着色，结果差异无统计学意义（P>0.05），但在钙盐颗粒信号显示方面，茜素红S染色明显强于硝酸银染色，且前者比后者更易识别杂质。在染色时间方面，茜素红S染色明显短于硝酸银染色法（40 s比30 min）。使用茜素红S法染色：53%（31/58）慢性肾病、13例（13/17）动脉粥样硬化和13例（13/13）主动脉夹层组织可见钙盐沉积，获得双盲一致的结果。 结论： 茜素红S染色和硝酸银染色的检测结果一致，但前者相比后者具有操作快捷简便的特点，且阳性信号更容易识别，可作为血管钙化疾病中显示钙盐沉积的首选方法推荐。.

BACKGROUND: Bicuspid aortic valves (BAV) are frequently associated with ascending aortic aneurysms. The etiology is incompletely understood, but genetic factors, in addition to flow perturbations, are likely involved. Since loss of contractility and elaboration of extracellular matrix in the vessel wall are features of BAV-associated aortopathy, phenotypic modulation of smooth muscle cells (SMCs) may play a role.
METHODS: Ascending aortic tissue was collected intra-operatively from 25 individuals with normal (i.e., tricuspid) aortic valves (TAV) and from 25 individuals with BAVs. For both TAV and BAV, 10 patients had non-dilated (ND) and 15 patients had dilated (D) aortas. SMCs were isolated and cultured from a subset of patients from each group. Aortic tissue and SMCs were fluorescently immunolabeled for SMC phenotypic markers (i.e., alpha-smooth muscle actin (ASMA, contractile), vimentin (synthetic) and p16INK4a and p21Cip1 (senescence). SMCs were also analyzed for replicative senescence in culture.
RESULTS: In normal-sized and dilated BAV aortas, SMCs switched from the contractile state to either synthetic or senescent phenotypes, as observed by loss of ASMA (ND: P = 0.001, D: P = 0.002) and associated increases in vimentin (ND: P = 0.03, D: P = 0.004) or p16/p21 (ND: P = 0.03, D: P<0.0001) compared to TAV. Dilatation of the aorta exacerbated SMC phenotypic switching in both BAV and TAV aortas (all P<0.05). In SMCs cultured from normal and dilated aortas, those isolated from BAV reached replicative senescence faster than those from TAV aortas (all P = 0.02). Furthermore, there was a stark inverse correlation between ASMA and cell passage number in BAV SMCs (ND: P = 0.0006, D: P = 0.01), but not in TAV SMCs (ND: P = 0.93, D: P = 0.20).
CONCLUSIONS: The findings of this study provide direct evidence from cell culture studies implying that SMCs switch from the contractile state to either synthetic or senescent phenotypes in the non-dilated BAV aorta. In cultured SMCs from both non-dilated and dilated aortas, we found that this process may precede dilatation and accompany aneurysm development in BAV. Our findings suggest that therapeutically targeting SMC phenotypic modulation in BAV patients may be a viable option to prevent or delay ascending aortic aneurysm formation.

UNASSIGNED: Acute Type A Aortic Dissection (AAAD) is one of the most life-threatening diseases, often associated with transient hyperglycemia induced by acute physiological stress. The impact of stress-induced hyperglycemia on the prognosis of ST-segment elevation myocardial infarction has been reported. However, the relationship between stress-induced hyperglycemia and the prognosis of AAAD patients remains uncertain.
UNASSIGNED: The clinical data of 456 patients with acute type A aortic dissection were retrospectively reviewed. Patients were divided into two groups based on their admission blood glucose. Cox model regression analysis was performed to assess the relationship between stress-induced hyperglycemia and the 30-day and 1-year mortality rates of these patients.
UNASSIGNED: Among the 456 patients, 149 cases (32.7%) had AAAD combined with stress-induced hyperglycemia (SIH). The results of the multifactor regression analysis of the Cox model indicated that hyperglycemia (RR = 1.505, 95% CI: 1.046-2.165, p = 0.028), aortic coarctation involving renal arteries (RR = 3.330, 95% CI: 2.237-4.957, p < 0.001), aortic coarctation involving superior mesenteric arteries (RR = 1.611, 95% CI: 1.056-2.455, p = 0.027), and aortic coarctation involving iliac arteries (RR = 2.034, 95% CI: 1.364-3.035, p = 0.001) were independent influences on 1-year postoperative mortality in AAAD patients.
UNASSIGNED: The current findings indicate that stress-induced hyperglycemia measured on admission is strongly associated with 1-year mortality in patients with AAAD. Furthermore, stress-induced hyperglycemia may be related to the severity of the condition in patients with AAAD.

Aortic aneurysm (AA) refers to the persistent dilatation of the aorta, exceeding three centimeters. Investigating the pathophysiology of this condition is important for its prevention and management, given its responsibility for more than 25000 deaths in the United States. AAs are classified based on their location or morphology. various pathophysiologic pathways including inflammation, the immune system and atherosclerosis have been implicated in its development. Inflammatory markers such as transforming growth factor β, interleukin-1β, tumor necrosis factor-α, matrix metalloproteinase-2 and many more may contribute to this phenomenon. Several genetic disorders such as Marfan syndrome, Ehler-Danlos syndrome and Loeys-Dietz syndrome have also been associated with this disease. Recent years has seen the investigation of novel management of AA, exploring the implication of different immune suppressors, the role of radiation in shrinkage and prevention, as well as minimally invasive and newly hypothesized surgical methods. In this narrative review, we aim to present the new contributing factors involved in pathophysiology of AA. We also highlighted the novel management methods that have demonstrated promising benefits in clinical outcomes of the AA.

A rare transthoracic echocardiographic image of left sinus of Valsalva aneurysm complicated by thrombus formation.

OBJECTIVE: In the endovascular aneurysm repair (EVAR) era, open surgical repair (OSR) is performed for ruptured abdominal aorta aneurysm (RAAA) in patients with complex aneurysm neck and technical difficulties. Understanding the risk factors of OSR is essential for the clinical selection of the ideal surgical procedure. We aimed to re-evaluate the outcomes of OSR and treatment options for RAAA.
METHODS: Patients who underwent OSR for RAAA between January 2010 and December 2022 were enrolled in this single-center, retrospective observational study. Preoperative status, operative findings, and postoperative course were retrospectively reviewed. The Cox proportional hazards model was used to evaluate the association between age and early postoperative mortality.
RESULTS: Among 142 patients, 43 (30.3%) and 99 (69.7%) were aged ≥80 and <80 years, respectively. Postoperative mortality within 30 days occurred in 24 (16.9%) patients (11/43 [25.6%] and 13/99 [13.1%] patients aged ≥80 and <80 years, respectively; hazard ratio [HR]=1.95; P=0.069). In a multivariable analysis, increased postoperative mortality within 30 days was associated with age ≥80 years (adjusted HR, aHR=2.36; P=0.049), the presence of pre- or intraoperative cardiopulmonary arrest (aHR=12.0; P<0.001), and postoperative gastrointestinal disorder (aHR=4.42; P=0.003).
CONCLUSIONS: EVAR may be preferable in older people; however, its use in cases of pre- or intraoperative cardiopulmonary arrest or perioperative gastrointestinal disorders remains controversial, and a careful discussion on the surgical indications is needed in such cases.

OBJECTIVE: Assess subsequent cardiovascular events and all-cause mortality in patients with intact AAA treated by EVAR according to the existence of isolated EL2 at 1 year after EVAR implantation.
METHODS: This retrospective, single-centre study included patients treated with EVAR between 2010 and 2017 in the vascular surgery department of the University Hospital of Lyon with a infrarenal AAA > 50 mm. The baseline clinical characteristics collected just before EVAR were retrieved from electronic patient records of our institution. AAA characteristics, procedure and the one-year post-operative CTA were reported. Study endpoints, major adverse cardiovascular events (MACE), major adverse lower extremity events (MALE) and all-cause mortality, were recorded during follow-up. Patients were divided into 2 groups according to the presence of isolated EL2 (EL2 +) or absence (EL2 -) of any endoleak on CTA at 1 year. MACE, MALE and all-cause mortality were compared between both groups.
RESULTS: During the study period, 589 patients were treated by endovascular surgery and 207 were included. According to the CTA results at 1 year, 60 patients (29%) were included in the EL2 + group, and 147 patients (71%) in the EL2 - group. A total of 109 patients (53%) experienced a MACE or MALE; significantly fewer patients in the EL2 + than in the EL2 - group did so (p = .009). There were 47 patients (23%) who experienced at least one MALE, and the frequency was significantly lower in the EL2 + group (p = .017).
CONCLUSIONS: Patients with AAA treated by EVAR who did not develop EL2 at one year, were at higher risk of MALE during follow-up. This might be explained by more frequent symptomatic LEPAD at baseline in this group. These patients therefore require a closer follow-up and strict control of cardiovascular risk factors to prevent cardiovascular morbi-mortality.

暂无摘要。

UNASSIGNED: Vascular smooth muscle cells (VSMCs) are highly plastic. Vessel injury induces a phenotypic transformation from differentiated to dedifferentiated VSMCs, which involves reduced expression of contractile proteins and increased production of extracellular matrix and inflammatory cytokines. This transition plays an important role in several cardiovascular diseases such as atherosclerosis, hypertension, and aortic aneurysm. TGF-β (transforming growth factor-β) is critical for VSMC differentiation and to counterbalance the effect of dedifferentiating factors. However, the mechanisms controlling TGF-β activity and VSMC phenotypic regulation under in vivo conditions are poorly understood. The extracellular matrix protein TN-X (tenascin-X) has recently been shown to bind TGF-β and to prevent it from activating its receptor.
UNASSIGNED: We studied the role of TN-X in VSMCs in various murine disease models using tamoxifen-inducible SMC-specific knockout and adeno-associated virus-mediated knockdown.
UNASSIGNED: In hypertensive and high-fat diet-fed mice, after carotid artery ligation as well as in human aneurysmal aortae, expression of Tnxb, the gene encoding TN-X, was increased in VSMCs. Mice with smooth muscle cell-specific loss of TN-X (SMC-Tnxb-KO) showed increased TGF-β signaling in VSMCs, as well as upregulated expression of VSMC differentiation marker genes during vascular remodeling compared with controls. SMC-specific TN-X deficiency decreased neointima formation after carotid artery ligation and reduced vessel wall thickening during Ang II (angiotensin II)-induced hypertension. SMC-Tnxb-KO mice lacking ApoE showed reduced atherosclerosis and Ang II-induced aneurysm formation under high-fat diet. Adeno-associated virus-mediated SMC-specific expression of short hairpin RNA against Tnxb showed similar beneficial effects. Treatment with an anti-TGF-β antibody or additional SMC-specific loss of the TGF-β receptor reverted the effects of SMC-specific TN-X deficiency.
UNASSIGNED: In summary, TN-X critically regulates VSMC plasticity during vascular injury by inhibiting TGF-β signaling. Our data indicate that inhibition of vascular smooth muscle TN-X may represent a strategy to prevent and treat pathological vascular remodeling.

暂无摘要。