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Following surgical repair of acute type A aortic dissection(ATAAD), distal aortic degeneration and growth may occur. Previous evidence has suggested that false lumen(FL) communications and flow may influence postoperative aortic remodeling, although the contribution of branch vessel dissection and FL communications is unclear. Patients who underwent ATAAD repair from 2017 to 2023 at a single center with at least 1 year of follow-up imaging were included in this study. Patients were grouped based on aortic pathology and surgical repair. Preoperative and postoperative measurements were taken at the level of zone 1 and between zones 4/5. 63 patients were included in this study. 87.3% received a hemiarch repair, 34.9% received hemiarch + AMDS Hybrid prosthesis, and 12.7% received a total arch replacement. Proximal aortic remodeling was not reliably predicted by the presence of FL communications or surgical approach. Distal aortic growth was independently associated with ≥ 3 or 4 visceral vessel dissections( p  = 0.04 − 0.005). In conclusion, distal aortic remodeling following ATAAD repair was predicted by visceral vessel involvement. While the aortic arch is often emphasized at the time of ATAAD repair, features of the distal aorta may help to risk stratify patients for long-term adverse events, helping to guide initial management and post-ATAAD repair follow-up.

The present study aimed to identify aortic morphological features associated with the occurrence of acute type B aortic dissection (aTBAD) and establish a risk prediction model. Patients in the control group were age- and sex-matched in a 1:1 ratio with the aTBAD group. Morphological parameters of the ascending aorta and aortic arch were measured on the GE Healthcare Advantage Workstation. The length and diameter of the ascending aorta and aortic arch in the aTBAD group increased significantly (all P  < 0.001). The tortuosity and angulation of ascending aorta were significantly larger in the aTBAD group ( P  < 0.001 and P  = 0.021, respectively), with no significant difference in the aortic arch ( P  = 0.757 and P  = 0.212, respectively). The height and angle of the ascending aorta increased significantly in the aTBAD group ( P  < 0.001 and P  = 0.039, respectively). The height, width, and angle of the aortic arch were significantly larger in the aTBAD group (all P  < 0.05). Multivariable logistic regression showed that distal left common carotid artery diameter, aortic arch height, and ascending aorta tortuosity were associated with the occurrence of aTBAD. The area under the curve of the risk prediction model and the validation dataset were 0.8415 and 0.8319, respectively. The width, height, and angle of the ascending aorta and aortic arch were associated with the occurrence of aTBAD.

Background Aortic structural damage (ASD) may complicate the course of patients with giant cell arteritis (GCA). However the frequency and outcome of ASD has not been assessed in long term prospective studies. Methods In a previous screening of 54 biopsy proven GCA patients, significant ASD was detected in 12 (22.2%) after a median follow-up of 5.4 years. These patients were periodically evaluated (every 4 years) over a median of 10.3 years (range 4–16.6 years) in order to investigate the development of new ASD and the outcome of previously detected abnormalities. Results 18 of the 54 patients abandoned the study due to death or other reasons. The remaining 36 patients were subjected to a second screening and 14 to a third screening. 12 (33.3%) of the 36 patients re-screened and 16 (29.6%) of the initial cohort developed ASD, all but one in the thoracic aorta. Aortic diameters at the ascending and descending aorta significantly increased over time. One patient (1.9% of the initial cohort) died from aortic dissection. Surgery was advised in eight (50%) patients with ASD but could only be performed in three patients (37.7%). The development of ASD was not associated with persistence of detectable disease activity. Conclusions The incidence of ASD is maximal within the first 5 years after diagnosis but continues developing over time, affecting up to 33.3% of individuals after long term follow-up. Once ASD occurs, dilatation increases over time, underlining the need for periodic evaluation. Surgical repair is feasible in about one-third of candidates.

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH) and sleep fragmentation (SF). Currently, the potential role of SF has not been extensively explored with animal models and it remains unclear to what extent recurring arousals and sleep disruption that characterize sleep fragmentation in OSA contribute to an early cardiovascular dysfunction. To determine early changes in cardiovascular anatomy, we set up studies with a middle-aged rat model of SF exposed for 1 month. We evaluated biomechanical responses parameters such as elasticity, histomorphological changes, inflammation, oxidative stress, and blood serum molecule extracellular vesicles in a population exposed to such SF compared to a control group. Our experiments enabled us to show that 30 days of SF normoxia in adult rats induced aortic remodeling, with an increase in diameter of thoracic aortas and fiber disorganization associated with an increase in biomechanical elasticity as well as slight alterations in blood serum biomarkers. An increase in extracellular vesicles content of CD31 was observed in SF rats. Matrix metalloproteinases-9 (MMP9) has also been identified as a potential remodeling biomarker linked to aortic elasticity. We observed an increase in release of MMP9 in our model, the same way as we obtained an increase in ox-LDL that is another oxidative stress marker associated with atherosclerosis. Our preliminary findings support that SF alters aortic function, structure and biomechanical properties and release extracellular vesicles; and therefore these should be considered in preventive cardiovascular health programs.

Hypertension causes aortic wall thickening until the original wall stress is restored. We hypothesized that this regulation involves stress fiber (SF) tension transmission to the nucleus in smooth muscle cells (SMCs) and investigated the strain in the SF direction as a condition required for this transmission. Thoracic aortas from Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHRs) were examined. SFs in aortic SMCs were fluorescently labeled and observed under a confocal microscope while stretched along the circumferential ( θ ) axis. Three conditions were studied: WKY physiological (WKY phys ; blood pressure changes from diastolic to systolic for WKY), high-strain state (WKY high ; diastolic to hypertensive level for WKY simulating initial hypertension), and SHR physiological (SHR phys ; diastolic to systolic for SHR simulating after wall-thickening). SF strain and direction were measured. The SF inclination angle from the θ axis was 18° ± 3° in WKY phys, 13° ± 2° in WKY high , and 20° ± 1° in SHR phys . SF strain was 0.01 ± 0.02 in WKY phys , 0.20 ± 0.04 in WKY high , and 0.02 ± 0.02 SHR phys . SF strain was minimal in WKY phys , significantly increased in WKY high , and reduced to approximately zero in SHR phys . These findings support SFs function as mechanosensors in response to hypertension.

To identify magnetic resonance (MR) angiography derived predictors of progressive dilatation and surgery of the aortic root in Marfan syndrome. We retrospectively included 111 patients (32.7±16.5 years, range: 7-75 years) with a total of 446 MR angiographies. Aortic diameter growth rates of the entire thoracic aorta and Z-scores were estimated from annual diameter measurements. Aortic root shape was subdivided into three different types: (T0) normal; (T1) localized dilatation; (T2) generalized aortic root dilatation. Aortic diameter, Z-score, age, and aortic root shape at baseline were tested as predictors of aortic root dilatation using a multivariate logistic regression model. The highest aortic growth rate was observed at the level of the sinuses of Valsalva. Higher aortic root diameters and Z-scores at baseline predicted an increased growth of the aortic root (p = 0.003 and p<0.001). Young age (<30 years) was a predictor for the increase of Z-scores when compared to patients ≥30 years (p = 0.019). 25/111 patients (22.5%) had a T0 aortic root shape, 59/111 patients (53.2%) had a T1 aortic root shape, and 27/111 patients (24.3%) had a T2 aortic root shape. Aortic root shape did not predict further aortic growth (p>0.05). However, significantly more patients undergoing surgery had a generalized aortic dilatation (19/28, 76.9%) than a localized aortic root dilatation (9/28, 32.1%) (p = 0.001). Larger baseline aortic root diameter and Z-score as well as young age predict solely progressive aortic root dilatation in Marfan patients. MR angiography derived type of aortic root shape does not predict aortic growth, but patients with generalized aortic root dilatation are referred more frequently for aortic surgery.

Patients with aortic enlargement are recommended to undergo serial imaging and clinical follow-up until they reach surgical thresholds. This study aimed to identify aortic diameter and care of patients with aortic imaging before aortic dissection (AD). In a retrospective cohort of AD patients, we evaluated previous imaging results in addition to ordering providers and indications. Imaging was stratified as >1 or <1 year: 62 patients (53% men) had aortic imaging before AD (most recent test: 82% echo, 11% computed tomography, 6% magnetic resonance imaging). Imaging was ordered most frequently by primary care physicians (35%) and cardiologists (39%). The most frequent imaging indications were arrhythmia (11%), dyspnea (10%), before or after aortic valve surgery (8%), chest pain (6%), and aneurysm surveillance in 13%. Of all patients, 94% had aortic diameters below the surgical threshold before the AD. Imaging was performed <1 year before AD in 47% and aortic size was 4.4 ± 0.8 cm in ascending aorta and 4.0 ± 0.8 cm in sinus. In patients whose most recent imaging was >1 year before AD (1,317 ± 1,017 days), the mean ascending aortic diameter was 4.2 ± 0.4 cm. In conclusion, in a series of patients with aortic imaging before AD, the aortic size was far short of surgical thresholds in 94% of the group. In >50%, imaging was last performed >1 year before dissection.

We analyzed the associations of the mechanical strength of dilated ascending aorta wall (intraoperative samples from 30 patients with non-syndromic aneurysms) with tissue MMPs and the cytokine system. Some samples were stretched to break on an Instron 3343 testing machine and the tensile strength was calculated; others were homogenized and the concentrations of MMP-1, MMP-2, MMP-7, their inhibitors (TIMP-1 and TIMP-2), and pro- and anti-inflammatory cytokines were determined by ELISA. Direct correlations between aortic tensile strength and concentrations of IL-10 ( r =0.46), TNFα ( r =0.60), and vessel diameter ( r =0.67) and an inverse correlation with patient’s age ( r =-0.59) were revealed. Compensatory mechanisms supporting the strength of the ascending aortic aneurysm are possible. No associations of MMP-1, MMP-7, TIMP-1, and TIMP-2 with tensile strength and aortic diameter were found.

Vascular calcification (VC) is a major risk factor for cardiovascular mortality in chronic renal failure (CRF) patients, but the pathogenesis remains partially unknown and effective therapeutic targets should be urgently explored. Here we pursued the therapeutic role of rapamycin in CRF-related VC. Mammalian target of rapamycin (mTOR) signal was activated in the aortic wall of CRF rats. As expected, oral rapamycin administration significantly reduced VC by inhibiting mTOR in rats with CRF. Further in vitro results showed that activation of mTOR by both pharmacological agent and genetic method promoted, while inhibition of mTOR reduced, inorganic phosphate-induced vascular smooth muscle cell (VSMC) calcification and chondrogenic/osteogenic gene expression, which were independent of autophagy and apoptosis. Interestingly, the expression of Klotho, an antiaging gene that suppresses VC, was reduced in calcified vasculature, whereas rapamycin reversed membrane and secreted Klotho decline through mTOR inhibition. When mTOR signaling was enhanced by either mTOR overexpression or deletion of tuberous sclerosis 1, Klotho mRNA was further decreased in phosphate-treated VSMCs, suggesting a vital association between mTOR signaling and Klotho expression. More importantly, rapamycin failed to reduce VC in the absence of Klotho by using either siRNA knockdown of Klotho or Klotho knockout mice. Thus, Klotho has a critical role in mediating the observed decrease in calcification by rapamycin in vitro and in vivo.

Genetic studies in patients reveal that mutations to genes that encode contractile proteins in medial smooth muscle cells can cause thoracic aortic aneurysms and dissections. Mouse models of such mutations, including Acta2(-/-) and Myh11(R247C/R247C), surprisingly do not present with any severe vascular phenotype under normal conditions. This observation raises the question whether these mutations nevertheless render the thoracic aorta increasingly vulnerable to aneurysms or dissections in the presence of additional, epigenetic, factors such as hypertension, a known risk factor for thoracic aortic disease. Accordingly, we compared the structure and biaxial mechanical properties of the ascending and descending thoracic aorta from male wild-type and Myh11(R247C/R247C) mice under normotension and induced hypertension. On average, the mutant aortas exhibited near normal biomechanics under normotensive hemodynamics and near normal adaptations to hypertensive hemodynamics, yet the latter led to intramural delaminations or premature deaths in over 20% of these mice. Moreover, the delaminated vessels exhibited localized pools of mucoid material, similar to the common histopathologic characteristic observed in aortas from humans affected by thoracic aortic aneurysms and dissections. The present findings suggest, therefore, that mutations to smooth muscle cell contractile proteins may place the thoracic aorta at increased risk to epigenetic factors and that there is a need to focus on focal, not global, changes in aortic structure and properties, including the pooling of glycosaminoglycans/proteoglycans that may lead to thoracic aortic dissection.