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The objective of this study is to demonstrate the safety and reproducibility of our surgical technique for implanting decellularized vascular xenografts in the carotid artery of sheep.

Autologous vascular arterial or venous graft are not available in 10-40% of patients, due to vascular pathologies, and the utility of decellularized biological scaffolds would be a solution for those cases. The purpose of this research was to obtain a functional acellular xenograft, prior to in-vivo testing as a vascular graft in an experimental animal.

In vascular reconstruction in arterial trauma, ruptured abdominal aortic aneurysm or ruptured aneurysmal arteriovenous fistula, the challenge no longer lies in the surgical procedure itself, but rather the prevention of intimal hyperplasia, thrombosis and aneurysm formation, in parallel with extending as long as possible the patency of the grafts.

An intrapericardial organized haematoma secondary to chronic type A aortic dissection is an extremely rare cause of right heart failure. Imaging studies are essential in recognising and diagnosis of this distinctive medical condition and guiding the anticipated treatment.

Genetic factors play a significant role in the pathogenesis of mitral valve diseases, including mitral valve prolapse (MVP) and mitral valve regurgitation. Genes like Fibrillin-1 (FBN1), Filamin A (FLNA), matrix metalloproteinase 2 (MMP2), and SRY-box transcription factor 9 (SOX9) are known to influence mitral valve pathology but knowledge of the exact mechanism is far from clear. Data regarding serum parameters, transesophageal echocardiography, and genetic and histopathologic parameters were investigated in 54 patients who underwent cardiovascular surgery for mitral valve regurgitation. The possible association between Fibrillin-1, Filamin A, MMP2, and SOX9 gene expressions was checked in relationship with the parameters of systemic inflammatory response. The mRNA expression levels (RQ—relative quantification) were categorized into three distinct groups: low (RQ < 1), medium/normal (RQ = 1–2), and high (RQ > 2). Severe fibrosis of the mitral valve was reflected by high expression of FBN1 and low expression of MMP2 (p < 0.05). The myxoid degeneration level was associated with the mRNA expression level for FBN1 and a low lymphocyte-monocyte ratio was associated with an increased mRNA expression of FBN1 (p < 0.05). A high number of monocytes was associated with high values of FBN1 whereas the increase in the number of lymphocytes was associated with high levels of MMP2. In addition, we observed that the risk of severe hyalinization was enhanced by a low mRNA expression of FLNA and/or SOX9. In conclusion, a lower FLNA mRNA expression can reflect the aging process that is highlighted in mitral valve pathology as a higher risk for hyalinization, especially in males, that might be prevented by upregulation of the SOX9 gene. FBN1 and MMP2 influence the inflammation-related fibrotic degeneration of the mitral valve. Understanding the genetic base of mitral valve pathology can provide insights into disease mechanisms, risk stratification, and potential therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: We hypothesized that an ideal heart valve replacement would be acellular valve root scaffolds seeded with autologous stem cells. To test this hypothesis, we prepared porcine acellular pulmonary valves, seeded them with autologous adipose derived stem cells (ADSCs) and implanted them in sheep and compared them to acellular valves.

Background: Aortic stenosis is the valvulopathy with the highest incidence, having congenital (frequently bicuspid valve) or degenerative etiology. Objective: The purpose of this paper is to present a case of severe cardiac dysfunction due to the aortic stenosis, in which the surgical benefit is impressive, even if the optimal moment has been exceeded. Material and methods: We present a case of a 39 years old male, with bicuspid aortic valve and moderate aortic stenosis, periodically investigated by cardiologists, without indication of surgery at that time who had a sudden decompensation of the clinical status. He had severe fatigue, dyspnea and a thrombophlebitic episode in the lower left limb. The patient was hospitalized in the Cardiovascular Surgery Clinic of the Institute, where we highlighted severe aortic stenosis, severe tricuspid insufficiency, a tumor in the left atrium and severe dysfunction of the left ventricle (EF 30%). Chest CT scan revealed multiple peripheral pulmonary infarctions, probably in the context of the thrombophlebitis. Blood tests revealed liver dysfunction due to the severe tricuspid insufficiency and also the presence of hepatic B virus, undiscovered until then. We practiced aortic valve replacement, tricuspid annuloplasty and myxoma excision from the left atrium. Results: Postoperative, the evolution was favorable, with increasing in the performance of the heart contractility (up to NYHA I, EF 45%), the decrease of the hepatic dysfunction, the improvement of the clinical status and the quality of the patient's life. Conclusions: The replacement of the aortic valve should be performed before the onset of cardiac dysfunction. It may also be beneficial in selected cases, for patients with decompensated stages of the disease, but with good myocardial function in the first decades of life. [ABSTRACT FROM AUTHOR]