Effect of TEVAR Combined with Drugs and Drug Therapy Alone on the Efficacy and Safety of Stable Standford B Aortic Dissection.

Objective: Stanford type B aortic dissection is a condition in which the intima of the aorta tears, and TEVAR is an interventional treatment to manage this dissection through intimal repair. To evaluate the medium-term clinical efficacy of endovascular repair (TEVAR) for Aortic dissection and drug Conservative management for Stanford B Aortic dissection aneurysms and further explore whether the former is superior to drug Conservative management in the medium-term efficacy. Methods: The clinical data of 70 patients with stable Standford type B Aortic dissection admitted to our hospital from March 2016 to March 2020 were retrospectively analyzed. They were divided into the treatment group (n = 47) and the control group (n = 23). The control group patients were treated solely with medication, while the treatment group patients were treated with TEVAR on the basis of the control group patients. The treatment efficacy and safety of the two groups of patients were compared and analyzed. All patients will be followed up once a month for 12 months after discharge and every 2 months thereafter (for a total of 3 years). Results: The findings highlight the need to carefully weigh the benefits and harms in the treatment of Stanford type B aortic dissection, especially when considering TEVAR surgery. Future research should focus on reducing postoperative complications to optimize treatment strategies and improve overall patient outcomes.TEVAR surgery significantly reduces hospital mortality, but is also associated with significantly increased postoperative complications, emphasizing the complexity of treatment decisions. This finding provides critical information about weighing the risks and survival benefits of surgery, helping medical teams and patients make informed treatment choices. The hospital mortality rate of patients in the treatment group was 12.77%, while the hospital mortality rate of patients in the control group was 21.74%. The difference between the two groups was statistically significant (P < .05). The incidence of postoperative complications in the treatment group was 23.40%, while the control group did not experience any major complications. The difference between the two groups was statistically significant (P < .05). The mortality rate of patients in the treatment group within 30 days of discharge was 0%, while the mortality rate of patients in the control group within 30 days of discharge was 11.11%. The difference between the two groups was statistically significant (P < .05). The Kaplan Meier curve showed that the survival rates at 3 years of the control and treatment groups were 56.52% and 95.12%, respectively. The log-rank test showed a statistical difference between the two groups. Univariate and multivariate regression analysis showed that postoperative neurological complications (HR = 32.41; P = .00) and preoperative Aortic valve regurgitation (HR = 3.91; P = .00) were risk factors for medium-term death. Conclusion: The TEVAR combination drug is a safe and effective treatment for stable Stanford B Aortic dissection. It can reduce mortality. Compared with drug treatment, it has obvious advantages in medium-term treatment effects. Early rising for high-risk patients can make them have better long-term outcomes. Limitations of the study include its retrospective nature and the use of data from only a single medical center, which may limit the external generalizability of the results.

Construction of a high-throughput aorta smooth muscle-on-a-chip for thoracic aortic aneurysm drug screening.

Thoracic aortic aneurysm (TAA), in which arteries enlarge asymptomatically over time until dissection or rupture occurs, is a serious health risk. The mainstay of TAA treatment remains surgical repair due to the lack of effective drugs. The complex etiology and pathogenesis of TAA, including hemodynamic alterations and genetic factors, lead to inaccuracies in preclinical models for drug screening. Previously, our group designed an aorta smooth muscle-on-a-chip to emulate human aorta physiology and pathophysiology and screened three promising therapeutic drugs targeting mitochondrial dynamics in TAA. On this foundation, we updated the one-channel chip to an eighteen-well chip platform with four polydimethylsiloxane layers. Benefiting from this high-throughput chip, we rapidly screened multiple drugs simultaneously using distinct cell lines in vitro. In addition, we observed the abnormal activation of hypoxia-inducible factor 1-alpha (HIF-1alpha) in aortas from TAA patients by Western blot and bioinformatics analyses. Intriguingly, this phenomenon was replicated only when smooth muscle cells (SMCs) were strained on the chip. We then screened seven specific HIF-1alpha inhibitors and selected the two most effective drugs (2-methoxyestradiol and digoxin) by quantitative PCR and colorimetric methods. The results demonstrated that these two drugs can improve respiratory chain function and rescue the SMC contractile phenotype, showing applicability for the clinical treatment of TAA. This high-throughput aorta smooth muscle-on-a-chip will become a potential preclinical model for TAA drug screening.

Transforming Growth Factor-ß and the Renin-Angiotensin System in Syndromic Thoracic Aortic Aneurysms: Implications for Treatment.

Thoracic aortic aneurysms (TAAs) are permanent pathological dilatations of the thoracic aorta, which can lead to life-threatening complications, such as aortic dissection and rupture. TAAs frequently occur in a syndromic form in individuals with an underlying genetic predisposition, such as Marfan syndrome (MFS) and Loeys-Dietz syndrome (LDS). Increasing evidence supports an important role for transforming growth factor-ß (TGF-ß) and the renin-angiotensin system (RAS) in TAA pathology. Eventually, most patients with syndromic TAAs require surgical intervention, as the ability of present medical treatment to attenuate aneurysm growth is limited. Therefore, more effective medical treatment options are urgently needed. Numerous clinical trials investigated the therapeutic potential of angiotensin receptor blockers (ARBs) and ß-blockers in patients suffering from syndromic TAAs. This review highlights the contribution of TGF-ß signaling, RAS, and impaired mechanosensing abilities of aortic VSMCs in TAA formation. Furthermore, it critically discusses the most recent clinical evidence regarding the possible therapeutic benefit of ARBs and ß-blockers in syndromic TAA patients and provides future research perspectives and therapeutic implications.

Inhibition of interleukin-1ß decreases aneurysm formation and progression in a novel model of thoracic aortic aneurysms.

BACKGROUND: Thoracic aortic aneurysms (TAAs) are common, but experimental TAA models are limited and the role of interleukin-1ß (IL-1ß) is undetermined. METHODS AND RESULTS: IL-1ß protein was measured in human TAAs and control aortas, and IL-1ß protein was increased ≈20-fold in human TAAs. To develop an experimental model of TAAs, 8- to 10-week-old male C57Bl/6 mice (wild type [WT]) underwent thoracotomy with application of periadventitial elastase (WT TAA) or saline (WT control; n=30 per group). Elastase treatment to thoracic aortas resulted in progressive dilation until day 14 with maximal dilation of 99.6±24.7% compared with 14.4±8.2% for WT saline control (P<0.0001). WT TAAs demonstrated elastin fragmentation, smooth muscle cell loss, macrophage infiltration, and increased IL-1ß expression. Next, TAAs were induced in mice deficient of IL-1ß (IL-1ß knockout) or IL-1 receptor (IL-1R knockout; n=10 each). Genetic deletion of IL-1ß and IL-1R significantly decreased thoracic aortic dilation (IL-1ß knockout=54.2±16.8% and IL-1R knockout=62.6±17.2% versus WT TAA=104.7±23.8%; P<0.001for both). IL-1ß knockout and IL-1R knockout aortas demonstrated preserved elastin and smooth muscle cells with fewer inflammatory cells. Correspondingly, IL-1ß and IL-1R knockout aortas had decreased inflammatory cytokine and matrix metalloproteinase 9 expression. Separately, WT mice pretreated with either IL-1R antagonist anakinra (100 mg/kg per day) or vehicle alone (control) underwent elastase treatment. Pretreatment of WT mice with anakinra attenuated TAA formation (control: 99.2±15.5% versus anakinra: 68.3±19.2%; P<0.005). Finally, to investigate treatment of small TAAs, WT mice were treated with anakinra 3 days after TAA induction. Anakinra treatment in WT mice with small TAAs reduced aortic dilation on day 14 (control treatment: 89.1±18.6% versus anakinra treatment: 59.7±25.7%; P=0.01). CONCLUSIONS: Periadventitial application of elastase to murine thoracic aortas reproducibly produced aneurysms with molecular and histological features consistent with TAA disease. Genetic and pharmacological inhibition of IL-1ß decreased TAA formation and progression, indicating that IL-1ß may be a potential target for TAA treatment.

Rare cause of dyspnea: yin-yang thoracic aortic aneurysm.

Aortic aneurysmal diseases, mostly found incidentally, have high mortality and morbidity. Complications mostly are associated with and accelerated in the presence of systemic hypertension, aortic valve disease, or aortic atherosclerosis. Presenting signs and symptoms can be nonspecific and need immediate and accurate recognition. We present a case of incidental finding of a large descending aortic aneurysm with "yin-yang" sign and discuss the importance of differentiating pseudoaneurysm versus intramural thrombus.