Search

BackgroundThe proximal anastomosis is an important procedure during the acute type A aortic dissection (AAAD) surgery. The conventional method is a double patch sandwich technique with Teflon felt. Adventitial eversion and prosthesis eversion technique as a novel approach has been applied to many patients in our center. Herein, This technique would be introduced, and the perioperative and 1-year follow-up results of the two different anastomosis methods were also evaluated.MethodsBetween December 2017 and May 2021, 143 AAAD patients who underwent total arch replacement (TAR) and frozen elephant trunk (FET) implantation were included in this retrospective study. Patients were divided into the eversion technique group (adventitial eversion and prosthesis eversion technique for proximal anastomosis, n = 64) and the sandwich technique group (n = 79).ResultsThe medical records were analyzed and compared between the groups. The mean operation time was 466 ± 73 min in the eversion technique group and 513 ± 81 min in the sandwich technique group (P < 0.001). Compared with the sandwich technique group, the eversion technique group also showed a shorter time on proximal anastomosis (38 ± 12 min vs. 58 ± 20 min, P < 0.001), cardiopulmonary bypass (195 ± 26 vs. 211 ± 40 min, P = 0.003), and aortic cross-clamp (120 ± 23 min vs. 134 ± 27 min, P = 0.002). Furthermore, a decreased proportion of >600 ml fresh frozen plasmas transfusion was observed in eversion technique group (10.9% vs. 34.2%, P = 0.002). No statistical differences were found in the postoperative morbidities and 1-year follow-up outcomes.ConclusionProximal anastomosis with adventitial eversion and prosthesis eversion technique is a promising surgical option for AAAD patients, with favorable perioperative and 1-year follow-up results.

anomalous pulmonary veins drain into the right side of the left atrium is an uncommon variety of anomalous pulmonary venous return. Rarely, anomalous pulmonary venous drainage combined with cor triatriatum and atrial septal defect. We presented the imaging findings of a male patient who had anomalous pulmonary venous drainage which has not previously been described.

Background: More evidence was required to guide the management of left subclavian artery (LSA) during thoracic endovascular aortic repair (TEVAR). The present study aimed to compare the outcomes of LSA coverage with LSA revascularization. Another purpose of this study was to share our experience of LSA revascularization with castor single-branched stent-graft. Methods: From January 2016 to December 2019, 134 patients with type B aortic dissection (TBAD) or intramural hematoma (IMH) were enrolled and divided into two groups, the LSA-covered group (n = 61) and the LSA-revascularized group (with castor single-branched stent-graft, n = 73). The results, such as in-hospital and 30-day mortality, stroke, paraplegia, left arm ischemia, operation time, endoleak, were compared between the two groups. Results: The incidence of 30-day stroke in the LSA-covered group (8.2%) was significantly higher compared with the LSA-revascularized group (0%, P = 0.018). 30-day ischemia of left arm occurred in more patients in the LSA-covered group (11.5%, P = 0.003). No statistical difference was found in the incidences of paraplegia, endoleak, in-hospital mortality, and 30-day mortality. Conclusions: LSA should be revascularized during TEVAR to reduce the incidences of stroke and left arm ischemia. Castor single-branched stent-graft was feasible and safe for treating TBAD or IMH.

Objective To study the risk factors of oxygenation impairment in patients with type-A acute aortic dissection who underwent total arch replacement with a stented elephant trunk. Methods In this study, 169 consecutive patients were enrolled who were diagnosed with type-A acute aortic dissection and underwent a total arch replacement procedure at the Qilu Hospital of Shandong University between January 2015 and February 2017. Postoperative oxygenation impairment was defined as arterial oxygen partial pressure/inspired oxygen fraction ≤ 200 with positive end expiratory pressure ≥ 5 cm H2O that occurred within 72 hours of surgery. Perioperative clinical characteristics of all patients were collected and univariable analyses were performed. Risk factors associated with oxygenation impairment identified by univariable analyses were included in the multivariable regression analysis. Results The incidence of postoperative oxygenation impairment was 48.5%. Postoperative oxygenation impairment was associated with prolonged mechanical ventilation time, intensive care unit stay, and hospital stay. Multivariable regression analysis demonstrated that body mass index (odds ratio [OR], 1.204; 95% confidence interval [CI], 1.065-1.361; P = .003), preoperative oxygenation impairment (OR, 9.768; 95% CI, 4.159-22.941; P Conclusions Postoperative oxygenation impairment is a common complication of surgery for type-A acute aortic dissection. Body mass index, preoperative oxygenation impairment, preoperative homocysteine, circulatory arrest time, and plasma transfusion were independent risk factors for oxygenation impairment after a total arch replacement procedure.

ObjectivesWe sought to explore and create a reliable, convenient, and economic hyperkinetic pulmonary artery hypertension (PAH) model and confirm the exact time of establishing a reversible or irreversible model to serve as a platform for future studies.MethodsWe used a common carotid artery and jugular vein shunt with an anastomosis and cuff to create a hyperkinetic PAH model in rabbits. At 1, 2, 3, 6, and 12 months postoperatively, the systolic pressure, mean pulmonary arterial pressure, and mean arterial pressure were measured by catheterization and the right ventricle hypertrophy index was calculated. Pathologic changes in the small pulmonary arteries were observed with hematoxylin and eosin staining, and the Heath-Edwards classification system was used to evaluate PAH.ResultsThe anastomosis and cuff graft groups both increased in systolic pressure, mean pulmonary arterial pressure (P

Aims Growing evidence suggests a close association of plaque angiogenesis with atherosclerotic plaque formation and progression, and an important role of matrix metalloproteinase (MMP) in angiogenesis and atherosclerosis. We attempted to investigate the functional involvements of MMP8 in angiogenesis. Methods and results Knockdown of MMP8 in human umbilical vein endothelial cells (HuVECs) with MMP-8 shRNA lentivirus resulted in a decrease in in vitro capillary-like network formation, cell proliferation and migration, and impaired its capacity of in vivo angiogenesis. Less nuclear accumulation of β-catenin and lower β-catenin target gene expression levels was observed in the HuVECs expressing lower levels of endogenous MMP8. Knockdown of endogenous MMP8 in HuVECs down-regulated platelet/endothelial cell adhesion molecule-1 (PECAM-1) expression by converting less angiotensin I to II, which is an inducer for PECAM-1 gene expression. Aortic rings isolated from MMP8−/−/apoE−/− mice had less endothelial cell sprouting, and endothelial cells in MMP8−/−/apoE−/− mice had a lower ability to migrate into Matrigel plugs and less capacity of proliferation and angiogenesis. Moreover, immunohistochemical analyses revealed that MMP8 was expressed in microvessels within human atherosclerotic plaques and aneurysm. Finally, analyses of MMP8−/−/apoE−/− and MMP8+/+/apoE−/− mice fed a Western diet for 12 weeks showed that MMP8-deficient mice had small lesion size and less endothelial cells within atherosclerotic lesions. Conclusion We demonstrated for the first time that MMP8 plays an important role in angiogenesis in vitro and in vivo . Our findings provide new insights into the molecular mechanisms of plaque angiogenesis and suggest that MMP8 is a potential therapeutic target of cardiovascular diseases.

Rationale: Accumulating evidence indicates that stem/progenitor cells (SPCs) represent an important source of cells in atheromas and contribute to lesion formation and progression. Objective: We investigated whether matrix metalloproteinase-8 (MMP8) played a role in SPC migration and their recruitment into atheromas. Methods and Results: We found that SPCs in atheromas expressed MMP8 and that MMP8 knockout significantly reduced SPC numbers in atherosclerotic lesions in apolipoprotein E (ApoE)–deficient mice fed a Western diet. Further in vivo experiments showed that ApoE −/− /MMP8 −/− mice injected with stem cells isolated from bone marrows of ApoE −/− /MMP8 −/− mice had fewer SPCs in atheromas and smaller lesions than ApoE −/− /MMP8 −/− mice injected with stem cells isolated from bone marrows of ApoE −/− /MMP8 +/+ mice. Ex vivo experiments showed that MMP8 deficiency inhibited the ability of SPCs to migrate from the arterial lumen and the adventitia into atherosclerotic lesions. In vitro assays indicated that MMP8 facilitated SPC migration across endothelial cells and through Matrigel or collagen I. We also found that MMP8 cleaved a-disintegrin-and-metalloproteinase-domain-10 and that MMP8 deficiency reduced mature a-disintegrin-and-metalloproteinase-domain-10 on SPCs. Knockdown of MMP8 or incubation with the a-disintegrin-and-metalloproteinase-domain-10 inhibitor GI254023X decreased E-cadherin shedding on SPCs. The decrease in migratory ability of SPCs with MMP8 knockdown was reduced by incubation of such cells with culture supernatant from SPCs without MMP8 knockdown, and this compensatory effect was abolished by an antibody against soluble E-cadherin. Conclusions: MMP8 plays an important role in SPC migration and their recruitment into atherosclerotic lesions.

Background Recently, genome-wide association studies have revealed an association between single-nucleotide-polymorphisms (SNPs) in a genomic region containing the ADAMTS7 (a disintegrin-like and metalloprotease with thrombospondin type 1 motif, 7) gene and susceptibility to coronary artery disease (CAD). However, it has remained unclear as to what biological mechanisms underlie this genetic association. We sought to assess possible functional effects of the non-synonymous SNP rs3825807, an adenine (A) to guanosine (G) change that results in a serine (Ser) to proline (Pro) substitution in the propeptide domain of the ADAMTS7 protein, as the G allele of this SNP has been shown to be associated with reduced risk of CAD. Methods and Results In a population-based, prospective study, we observed an inverse relationship between the rs3825807 G allele and prevalence and severity of carotid atherosclerosis determined by carotid ultrasound (Table 1). In immunohistochemical analyses of coronary and carotid atherosclerotic plaques, we detected the presence of ADAMTS7 within and around smooth muscle cells in the plaques, particularly in areas near the border between the intima and media (Figure 1A). In studies of primary cultures of vascular smooth muscle cells (VSMCs) from different individuals, we found that VSMCs of the G/G genotype had a lower migratory ability than VSMCs of the A/A genotype (Figure 1B). We also found that conditioned media of VSMCs of the G/G genotype contained less of the cleaved form of thrombospondin-5 (Figure 1C), an ADAMTS7 substrate that had been shown to be produced by VSMCs and inhibit VSMC migration. Furthermore, we found that media conditioned by VSMCs of the G/G genotype had lower amounts of cleaved ADAMTS7 propeptide (Figure 1D). To further assess the effect of the Ser-to-Pro substitution on ADAMTS7 propeptide domain cleavage, we transfected cultured HEK293 cells with a plasmid for expressing either ADAMTS7-214Ser or ADAMTS7-214Pro, and then determined the relative amounts of the cleaved and uncleaved forms of ADAMTS7 propeptide in conditioned media. In these experiments, we found that media conditioned by cells transfected with the ADAMTS7-214Pro plasmid had less cleaved ADAMTS7 propeptide than media conditioned by cells transfected with the ADAMTS7-214Ser plasmid. Conclusion The results of our study indicate that the CAD-associated SNP rs3825807 has a functional effect on ADAMTS7 maturation, thrombospondin-5 cleavage and VSMC migration, with the G allele associated with protection from atherosclerosis and CAD rendering a reduction in ADAMTS7 function.