Project description:IntroductionExtrinsic left atrial compression caused by a displaced, crooked descending thoracic aorta is rare. This anomaly may mimic primary cardiac tumors or metastatic neoplasms from the first look.Case presentationWe reported a 78-year-old woman presented to our emergency room with back pain, increased exercise intolerance and intermittent angina. She also had one syncopal event 1 month ago and gastric cancer post gastrectomy history. Subsequent chest plain film showed no mediastinum widening.Two-dimensional echocardiography was performed and revealed a heterogeneous mass as large as 2.3 x 2.4 cm occupying the left atrium (LA). Three-dimensional echocardiography vividly demonstrated that LA was constrained between the aortic valve (AV) and a luminal structure with pulsatile character suggestive of the aorta.ConclusionsWe successfully demonstrated the detailed structure and location of an anomalous descending aorta on the oblique imaging plane of RT-3DE, which may not be readily available by traditional 2D method.
Project description:Abdominal Aortic Aneurysm (AAA) affects 4-5% of men over 65, and Aortic Dissection (AD) is a life-threatening aortic pathology associated with high morbidity and mortality. Initiators of AAA and AD include smoking and arterial hypertension, whilst key pathophysiological features of AAA and AD include chronic inflammation, hypoxia, and large modifications to the extra cellular matrix (ECM). As it stands, only surgical methods are available for preventing aortic rupture in patients, which often presents difficulties for recovery. No pharmacological treatment is available, as such researchers are attempting to understand the cellular and molecular pathophysiology of AAA and AD. Upregulation of matrix metalloproteinase (MMPs), particularly MMP-2 and MMP-9, has been identified as a key event occurring during aneurysmal growth. As such, several animal models of AAA and AD have been used to investigate the therapeutic potential of suppressing MMP-2 and MMP-9 activity as well as modulating the activity of other MMPs, and TIMPs involved in the pathology. Whilst several studies have offered promising results, targeted delivery of MMP inhibition still needs to be developed in order to avoid surgery in high risk patients.
Project description:The self-healing phenomenon can be found in the elastase-induced abdominal aortic aneurysm (AAA) model, and an enlarging AAA model was successfully induced by coarctation. Unfortunately, aortic coarctation in these enlarging models is generally not found in human AAA disease. This study aimed to create an experiment model of enlarging AAA in rabbits to better mimic human aortic aneurysm disease. Eighty-four male New Zealand white rabbits were randomly divided into three equal groups: two aneurysm groups (A and B) and a SHAM group. Aneurysm group rabbits underwent extrinsic aortic stenosis below the right renal artery and received a 10-minute incubation of 60 μl elastase (1 unit/μl). Absorbable suture was used in Group A and nonabsorbable cotton thread was used in Group B. A sham operation was performed in the SHAM group. Aortic diameter was measured after 1, 3, 7, and 15 weeks; thereafter animals were sacrificed for histopathological, immunohistochemical and quantitative studies. Two rabbits died at 29 and 48 days, respectively, after operation in Group B. All aneurysms formed and enlarged progressively by 3 weeks in the Aneurysm groups. However, diameter enlargement in Group A was significantly lower than that in Group B at 7 weeks. Aneurysm groups developed intimal hyperplasia; intima-media thickness (IMT) increased significantly by week 7, and aortic media thickness and intima-media ratio (IMR) increased significantly by week 15. Marked destruction of elastin fibers and smooth muscle cells (SMCs) occurred 1 week later and increased progressively thereafter. Intimal hyperplasia and SMCs content in Group A increased significantly by week 15 compared with Group B. Aneurysm groups exhibited strong expression of matrix metalloproteinases 2 and 9 and RAM11 by week 1, and decreased progressively thereafter. In conclusion, this novel rabbit AAA model enlarges progressively without coarctation and is capable of better mimicking human aortic aneurysm disease.
Project description:Aims: We describe a new aortic arch dissection (AcD) classification, which we have called the Fuwai classification. We then compare the clinical characteristics and long-term prognoses of different classifications. Methods: All AcD patients who underwent surgical procedures at Fuwai Hospital from 2010 to 2015 were included in the study. AcD procedures are divided into three types: Fuwai type Cp, Ct, and Cd. Type Cp is defined as the innominate artery or combined with the left carotid artery involved. Type Cd is defined as the left subclavian artery or combined with the left carotid artery involved. All other AcD surgeries are defined as type Ct. The Chi-square test was adopted for the pairwise comparison among the three types. Kaplan-Meier was used for the analysis of long-term survival and survival free of reoperation. Results: In total, 1,063 AcD patients were enrolled from 2010 to 2015: 54 patients were type Cp, 832 were type Ct, and 177 were type Cd. The highest operation proportion of Cp, Ct and Cd were partial arch replacement, total arch replacement, and TEVAR. The surgical mortality in type Ct was higher compared to type Cd (Ct vs. Cd = 9.38 vs. 1.69%, p < 0.01) and type Cp (Ct vs. Cp = 9.38 vs. 1.85%, p = 0.06). There was no difference in surgical mortality of type Cp and Cd (p = 0.93). There were no significant differences in the long-term survival rates (p = 0.38) and free of aorta-related re-operations (p = 0.19). Conclusion: The Fuwai classification is used to distinguish different AcDs. Different AcDs have different surgical mortality and use different operation methods, but they have similar long-term results.
Project description:Aneurysmatic and dissection cells show a specific alteration of gene expression, which allow a disease specific distinction. We used microarrays to analyse the cellular gene expression of controls, thoracic aortic aneurysm, and aortic dissection.
Project description:Thoracic aortic aneurysm is a potentially life-threatening condition in that it places patients at risk for aortic dissection or rupture. However, our modern understanding of the pathogenesis of thoracic aortic aneurysm is quite limited. A genetic predisposition to thoracic aortic aneurysm has been established, and gene discovery in affected families has identified several major categories of gene alterations. The first involves mutations in genes encoding various components of the transforming growth factor beta (TGF-?) signaling cascade (FBN1, TGFBR1, TGFBR2, TGFB2, TGFB3, SMAD2, SMAD3 and SKI), and these conditions are known collectively as the TGF-? vasculopathies. The second set of genes encode components of the smooth muscle contractile apparatus (ACTA2, MYH11, MYLK, and PRKG1), a group called the smooth muscle contraction vasculopathies. Mechanistic hypotheses based on these discoveries have shaped rational therapies, some of which are under clinical evaluation. This review discusses published data on genes involved in thoracic aortic aneurysm and attempts to explain divergent hypotheses of aneurysm origin.
Project description:The aortic arch repair is one of the most complex surgeries and carries a high risk of complications as well as mortality. Since 1975, when the arch repair was first done by Randall B. Griepp using hypothermic circulatory arrest, many new technologies were introduced. But even with the use of antegrade and retrograde perfusion techniques and improvement of surgical techniques and grafts, the rate of mortality, cerebral, spinal, and visceral damage was much higher as compared to any other cardiac surgeries. With further developments aimed at less invasive approaches, thoracic endovascular aortic repair (TEVAR) along with de-branching of supra-aortic vessels or the frozen elephant trunk was introduced. Here, in this article, we review the myriad of approaches to the aortic arch and have come to a conclusion that while traditional open surgery is considered as the gold standard for treatment of extensive aortic arch pathologies, one school of thought suggests hybrid techniques such as the frozen elephant trunk and aortic arch vessel de-branching as more appropriate procedures for high-risk patients, where co-morbidities may contraindicate cardiopulmonary bypass and longer operative times required for traditional repair. No randomized trials are present to compare between open and hybrid or endovascular procedure in normal or high-risk patients. The meta-analysis of most of the studies defines open surgery as the gold standard for arch pathology because the hybrid procedures did not provide any proven survival benefits or decrease in stroke rate and spinal ischemia when compared to open surgery in early, mid, or long-term results.