Condition "Vasa Vasorum" in Patients with Thoracic Aortic Aneurysm.

It is known that vasa vasorum contributes substantially to the blood supply and nutrition of one-third of the wall of the ascending thoracic aorta. Therefore, we focused on studying the relationship between inflammatory cells and vasa vasorum vessels in patients with aortic aneurysm. The material for the study was biopsies of thoracic aortic aneurysms taken from patients during an aneurysmectomy (34 men, 14 women, aged 33 to 79 years). The biopsies belonged to patients with non-hereditary thoracic aortic aneurysm. An immunohistochemical study was carried out using antibodies to antigens of T cells (CD3, CD4, CD8); macrophages (CD68); B cells (CD20); endothelium (CD31, CD34, von Willebrand factor (vWF)); and smooth muscle cells (alpha actin). Samples without inflammatory infiltrates contained less vasa vasorum in the tunica adventitia than samples with inflammatory infiltrates, and this difference was statistically significant p < 0.05. T cell infiltrates in the adventitia of aortic aneurysms were found in 28 of 48 patients. In the vessels of the vasa vasorum, surrounded by inflammatory infiltrates, T cells that adhered to the endothelium were found. The same cells were also localized in the subendothelial area. The number of adherent T cells in patients with inflammatory infiltrates in the aortic wall dominated the number of these cells in patients without inflammation of the aortic wall. This difference was statistically significant, p < 0.0006. Hypertrophy and sclerosis of the arteries of the vasa vasorum system, the narrowing of their lumen, and, as a result, impaired blood supply to the aortic wall, were found in 34 patients with hypertension. In 18 patients (both in patients with hypertension and in patients without hypertension), T cells that adhered to the vasa vasorum endothelium were found. In nine cases, massive infiltrates of T cells and macrophages were found, which surrounded and squeezed the vasa vasorum, preventing blood circulation. In six patients, parietal and obturating blood clots were found in the vasa vasorum vessels, which disrupted the normal blood supply to the aortic wall. We believe that this indicates the importance of the state of the vessels of the vasa vasorum in the development of an aortic aneurysm. In addition, pathological changes in these vessels may not always play a primary role, but always a very important role, in the pathogenesis of this disease.

Implication of inflammation on Coxsackie virus and Adenovirus receptor expression on cardiomyocytes and the role of platelets in patients with dilated cardiomyopathy.

BACKGROUND: Coxsackie Virus and Adenovirus Receptor (CXADR or CAR) is involved in the pathogenesis of inflammatory dilated cardiomyopathy (DCM). We aimed to examine the relationship of CAR expression on platelets and cardiomyocytes with virus persistence, local and systemic inflammation and platelet activity in patients with DCM. METHODS: Endomyocardial biopsy (EMB) samples of 38 patients (mean age 39.5±11.3 years, 20 male) with DCM were analyzed for CAR expression, local inflammation grade by immunohistochemistry and virus persistence by real-time PCR. Platelet morphology was analyzed in all patients and 30 healthy subjects (HS) using scanning electron microscopy, platelet activity by light transmission aggregation, and CAR persistence by immunofluorescence. Platelets of 20 patients were analyzed for cytomegalovirus and herpes simplex virus 1-2 by immunofluorescence. Serum levels of tumor necrosis factor alpha (TNF α) and Interleukin-6 were assessed using ELISA in all studied subjects. RESULTS: CAR expression in EMB samples was related to the heart failure functional class and the level of IL-6. Platelets from DCM patients showed enhanced spontaneous and ADP induced aggregation. Platelets' CAR expression was >4 fold higher in DCM than HS and was observed predominantly at sites of intercellular communications in microaggregates and leukocyte-platelet aggregates. CAR-positive patients showed significantly higher TNF-α and IL-6 serum levels in CAR-negative patients. Platelets of 6 (30%) DCM patients revealed the mature cytomegalovirus and herpes simplex viruses particles. CONCLUSION: Tight junction protein CAR may serve as a docking pin creating a new type of contact structure that could be responsible for signaling between neighboring cells in pathological conditions.

Thoracic Aortic Aneurysm and Factors Affecting Aortic Dissection.

This study is aimed at investigating the relationship between inflammation, the number of vasa vasorum, and the presence of lipoprotein (a) [Lp(a)] in the aortic aneurysm wall, as well as the relationships of these pathological processes with the development of aneurysm wall dissection. To that end, we examined segments of aortic aneurysm wall, consisting of intima, media, and adventitia, collected from patients during aneurysm prosthetics intervention. The material was collected from 23 men and eight women aged from 33 to 69 years. Monoclonal antibodies to Lp(a), markers of monocytes and macrophages (CD68), T cells (CD3, CD4, and CD8), von Willebrand factor, endothelium NO synthase, and smooth muscle α-actin were used for morphological and morphometric investigation. The present study demonstrated that Lp(a) is not often found in biopsies of patients with thoracic aortic aneurysm. Morphological and morphometric investigation shows the connection of aortic dissection with the process of damage to its wall caused by inflammatory infiltrates, medianecroses, and the appearance of newly formed vasa vasorum in media.