Extensive research has been conducted to elucidate and substantiate the crucial role of the Renin-Angiotensin System (RAS) in the pathogenesis of hypertension, cardiovascular disorders, and renal diseases. Furthermore, the role of oxidative stress in maintaining vascular balance has been well established. It has been observed that many of the cellular effects induced by Angiotensin II (Ang II) are facilitated by reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In this paper, we present a comprehensive overview of the role of ROS in the physiology of human blood vessels, specifically focusing on its interaction with RAS. Moreover, we delve into the mechanisms by which clinical interventions targeting RAS influence redox signaling in the vascular wall.

Background: Despite the increasing use of transcatheter aortic valve procedures, many patients still require surgical aortic valve replacement (SAVR). Assessing arterial properties in patients undergoing SAVR for aortic valve stenosis can be challenging, and the existing evidence is inconclusive. Our study aimed to investigate the impact of SAVR on vascular stiffness and the quality of life, as well as the different effects of valve type on arterial properties. Methods: We included 60 patients (mean age 70.25 ± 8.76 years, 65% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness (cfPWV, baPWV) and vascular parameters (AIx@75, central pressures, SEVR) were measured at baseline, pre-discharge, and 1-year post-operation. The QOL was assessed using the generic questionnaire—short-form health survey 36 (SF-36) pre-operatively and at 1 year. Results: Post-SAVR, cfPWV increased immediately (7.67 ± 1.70 m/s vs. 8.27 ± 1.92 m/s, p = 0.009) and persisted at 1 year (8.27 ± 1.92 m/s vs. 9.29 ± 2.59 m/s, p ≤ 0.001). Similarly, baPWV (n = 55) increased acutely (1633 ± 429 cm/s vs. 2014 ± 606 cm/s, p < 0.001) and remained elevated at 1 year (1633 ± 429 cm/s vs. 1867 ± 408 cm/s, p < 0.001). Acute decrease in Alx@75 (31.16 ± 10% vs. 22.48 ± 13%, p < 0.001) reversed at 1 year (31.16 ± 10% vs. 30.98 ± 9%, p = 0.71). SEVR improved (136.1 ± 30.4% vs. 149.2 ± 32.7%, p = 0.01) and persisted at 1 year (136.1 ± 30.4% vs. 147.5 ± 30.4%, p = 0.01). SV had a greater cfPWV increase at 1 year (p = 0.049). The QOL improved irrespective of arterial stiffness changes. Conclusions: After SAVR, arterial stiffness demonstrates a persistent increase at 1-year, with valve type having a slight influence on the outcomes. These findings remain consistent despite the perceived QOL.

BACKGROUND: Left atrial (LA) myxoma’s clinical manifestation depends on the size, location, mobility, and architecture of the tumor. The clinical presentation consists of cardiac (67%), embolic (29%), and systemic (34%) symptoms, even sudden cardiac death. CASE PRESENTATION: We present an interesting case and images of a patient with severe mitral valve dysfunction and syncope, who was diagnosed with a giant mass in the left atrium and left ventricle as myxomas. Open heart surgery was performed and the mass was detected and successfully removed. The histopathology confirmed the diagnosis of myxoma of the left atrium. CONCLUSION: Myxoma may be challenging to diagnose, but with imaging techniques, such as transthoracic (TTE), transesophageal (TEE) echocardiograms, when a high index of clinical suspicion exists, early diagnosis and therefore curative intervention in the majority of the cases is more likely.

Background: Assessing arterial properties in patients with aortic valve stenosis undergoing surgical aortic valve replacement (SAVR) is difficult, and the results to date have been inconclusive. Purpose: We sought to investigate how SAVR affects vascular stiffness in the short and long term. Methods: We included 69 patients (mean age 70.8±8.4 years, 62% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness was assessed using the carotid femoral pulse wave velocity (cfPWV) and brachial-ankle pulse wave velocity (baPWV). Measurements in patients with an ankle-brachial index (ABI) <0.9 were excluded from the analysis for baPWV measurments because a low ABI can affect the accuracy of baPWV. Augmentation index corrected for heart rate (Alx@75), central pressures and subendocardial viability ratio (SEVR) were assessed with arterial tonometry. Measurements were conducted at baseline, in the acute phase and 1 year after the operation. Results: Immediately after SAVR there was an increase in cfPWV (8.04±1.3 m/s vs 8.54±1.6 m/s, p=0.02) that was sustained at 1 year (8.04±1.3 m/s vs 9.42±2.4 m/s, p≤0.001). Similarly, baPWV (n=55) increased in the acute phase (1633±429 cm/s vs 2014±606 cm/s, p<0.001) and persisted 1 year postoperatively (1633±429 cm/s vs 1867±408 cm/s, p<0.001). Post-SAVR we also observed a decrease in Alx@75 (31.02±10% vs 22.73±12%, p≤0.001) that was attenuated 1 year later (31.02±10% vs 26.65±8%, p≤0.001), and an increase in SEVR (136.1±30.4% vs 149.2±37.7%, p=0.01) which remained improved at 1 year (136.1±30.4% vs 147.5±30.4%, p=0.01). Conclusions: After SAVR the arterial system shows an increase of stiffness in response to the acute relief of the obstruction, which is retained in the long term. Funding Acknowledgement: Type of funding sources: None.