Thoracic endovascular aortic repair (TEVAR) has been considered as a first-choice treatment for type B aortic dissection (TBAD). However, some patients that is lack of optimal landing zones (<15 mm in dissected Z2, Z3 or the presence of a lusorian artery) still pose significant challenges for TEVAR. We utilized a surgical stent-graft implantation in the descending aorta combined with supra-aortic vessels transposition through median sternotomy for these special TBAD patients. The short- and mid-term results showed that our procedure is a good and alternative therapy for such kind patients.
I‐ κ B kinase‐ ε (IKK ε ) is a member of the IKK complex and a proinflammatory regulator that is active in many diseases. Angiotensin II (Ang II) is a vasoconstricting peptide hormone, and Ang II‐induced myocardial hypertrophy is a common cardiovascular disease that can result in heart failure. In this study, we sought to determine the role of IKK ε in the development of Ang II‐induced myocardial hypertrophy in mice. Wild‐type (WT) and IKK ε ‐knockout (IKK ε ‐KO) mice were generated and infused with saline or Ang II for 8 weeks. We found that WT mouse hearts have increased IKK ε expression after 8 weeks of Ang II infusion. Our results further indicated that IKK ε ‐KO mice have attenuated myocardial hypertrophy and alleviated heart failure compared with WT mice. Additionally, Ang II‐induced expression of proinflammatory and collagen factors was much lower in the IKK ε ‐KO mice than in the WT mice. Apoptosis and pyroptosis were also ameliorated in IKK ε ‐KO mice. Mechanistically, IKK ε bound to extracellular signal‐regulated kinase (ERK) and the mitogen‐activated protein kinase p38, resulting in MAPK/ERK kinase (MEK) phosphorylation, and IKK ε deficiency inhibited the phosphorylation of MEK‐ERK1/2 and p38 in mouse heart tissues after 8 weeks of Ang II infusion. The findings of our study reveal that IKK ε plays an important role in the development of Ang II‐induced myocardial hypertrophy and may represent a potential therapeutic target for the management of myocardial hypertrophy.
Objective
To study the expression and role of cartilage oligomeric matrix protein (COMP) in human ascending aortic aneurysm (AAA).
Methods
From January 2015 to January 2016, the ascending aorta specimens removed from AAA patients were collected as AA group [24 patients, mean age (62.70±7.56) years, 22 males and 2 females]; and the ascending aorta specimens removed from donors in heart transplantations were collected as no-AA group [18 patients, mean age (51.50±11.23) years, 14 males and 4 females]. Histological changes of the two groups were observed by hematoxylin and eosin (HE) and Masson. Comparisons of the levels of SMα-actin, SM22α, OPN in the two samples were made by Western blotting. Meanwhile, a comparison of the expression of COMP in the two groups was made by both Western blotting and immunohistochemistry (IHC).
Results
HE and Masson showed well-structured, well-colored, clear nucleus of vascular smooth muscle cells (VSMCs), and less collagen deposition in the no-AA group. Conversely, in AA-group, VSMCs lost their original fusiform and typical orderly structures, elastic fibers fractured, collagen deposited obviously. Compared with no-AA group, the expressions of SMα-actin, SM22α, decreased significantly (1.738±0.112 vs. 1.426±0.103, t=7.527, P<0.05; 1.196±0.218 vs. 0.481±0.236, t=14.640, P<0.05), while the expression of OPN increased significantly in AA group (0.773±0.312 vs. 1.457±0.419, t=8.644, P<0.05). The level of COMP was much lower in the AA group than that in no-AA group (0.395±0.109 vs. 0.128±0.085, t=9.207, P<0.05).
Conclusion
The expression of COMP is reduced in ascending aortic aneurysm, which may lead to phenotypic switching of VSMCs in ascending aortic aneurysm. The decreased expression COMP may contribute to aortic aneurysm in human.
Key words:
Cartilage oligomeric matrix protein; Ascending aortic aneurysm; Vascular smooth muscle cells
Abstract Objectives This single-centre, retrospective propensity score matching (PSM) study designed to study the impact of cardiopulmonary bypass (CPB) on postoperative acute kidney injury (AKI) and the relationship between AKI and long-term outcomes in elderly patients undergoing coronary artery bypass grafting (CABG). Methods After PSM, 466 pairs of patients (A group, on-pump; B group, off-pump) who were aged≥70 years undergoing first isolated CABG surgery from January 2012 to December 2016 entered the study. AKI was defined and classified according to the Acute Kidney Injury Network (AKIN) criteria. The incidence and severity of in-hospital AKI was compared. The impacts of AKI on the long-term outcomes including new onset of dialysis and mortality were analyzed. Results The two PSM groups had similar baseline and procedure except whether the CPB was used or not. In hospital and 30-day mortality was of no difference(χ2=0.051, p=0.821). AKI of any severity occurred in 40.3% of all patients, with stage 1 accounting for most cases. No difference regarding the incidence and severity of AKI could be found: AKIN stage 1: 139 (29.8%) vs 131 (28.1%); AKIN stage 2: 40 (8.6%) vs 35 (7.5%); AKIN stage 3: 18 (3.9%) vs 13 (2.8%), (u=0.543, p=0.532). No difference was observed in the in-hospital new onset of dialysis (χ2=0.312, P=0.576). The use of CPB was not found to influence long-term new onset of dialysis (χ2=0.14, p=0.708) and mortality (χ2=0.099, p=0.753). Comparing with non-AKI patients, AKI patients were associated with an increased rates of new onset of dialysis (χ2=8.153, p=0.004) and mortality (χ2=6.277, p=0.012) during the follow-up. Comparing with non-AKI patients, the HR for long-term new onset of dialysis and mortality in AKI patients was 1.83 and 1.31 respectively (95%CI 1.12-2.86, p=0.007; 95%CI 1.17-2.58, p=0.015). Conclusions For elderly CABG patients, AKI was common, but deterioration of dialysis was a seldom incidence. Comparing with on-pump, off-pump did not decrease the rates or severity of AKI, long-term new onset of dialysis or mortality. AKI was associated with an increased long-term new onset of dialysis and decreased long-term survival.
Nonalcoholic fatty liver disease (NAFLD) is an emerging driver of cardiac arrhythmias. However, the relationship between NAFLD and malignant arrhythmia in non-ST-segment elevation myocardial infarction (NSTEMI) patients is still unclear.In this study, 358 NSTEMI inpatients were enrolled. They all received 24-hour Holter monitoring after percutaneous coronary intervention. All inpatients were divided into two groups: the non-NAFLD group (236 cases, 65.9%) and the NAFLD group (122 cases, 34.1%). Compared with the non-NAFLD group, the NAFLD group had a significantly higher incidence of PVCs/hour > 5 (premature ventricular complexes, 32.0% versus 9.3%, P < 0.001), ventricular tachycardia (VT, 22.1% versus 5.9%, P < 0.001), and sinus arrest (SA, 7.4% versus 1.3%, P = 0.002). We found that NAFLD was closely associated with the occurrence of VT [unadjusted odds ratio (OR) 4.507, 95% confidence interval (CI) 2.263-8.974, P < 0.001] and SA (OR 6.186, 95%CI 1.643-23.291, P = 0.007). After adjusting for age, sex, body mass index, and other confounding factors, the above differences were still statistically significant (VT: OR 4.808, 95%CI 2.254-10.253, P < 0.001; SA: OR 9.589, 95%CI 2.027-45.367, P = 0.004).NAFLD is associated with the occurrence of VT and SA in NSTEMI patients. It indicates that NAFLD might be a risk factor for malignant arrhythmias in post-NSTEMI patients.
To identify and analyze the live proliferating cardiomyocytes is crucial for deciphering the mechanisms controlling endogenous cardiac regeneration. Traditional methods confuse cell division with multinucleation in postnatal cardiomyocytes. Recent efforts have achieved significant progress on discerning cytokinesis from only nuclear division. However, those methods were either designed to label post-cytokinesis progeny or challenging to sort the live proliferating cardiomyocytes. In this study, we highlighted an Aurora kinase B reporter-based mouse system with a tdTomato fluorescence labeling. It could efficiently identify proliferating cardiomyocytes in neonates. The analysis of sorting tdTomato+ cardiomyocytes with different ploidy indicated that mononucleated cardiomyocytes might not possess significantly higher proliferating potential than other cardiomyocytes when most cardiomyocytes have become post-mitotic. Moreover, tdTomato+ cardiomyocytes were significantly increased and enriched at injury border zone after apex resection in neonates, while there were no increased tdTomato+ cardiomyocytes after myocardial infarction in adults.
Abstract Acute myocardial infarction (MI) is one of the leading causes of death in humans. Our previous studies showed that gastrin alleviated acute myocardial ischaemia–reperfusion injury. We hypothesize that gastrin might protect against heart injury after MI by promoting angiogenesis. An MI model was simulated by ligating the anterior descending coronary artery in adult male C57BL/6J mice. Gastrin was administered twice daily by intraperitoneal injection for 2 weeks after MI. We found that gastrin reduced mortality, improved myocardial function with reduced infarct size and promoted angiogenesis. Gastrin increased HIF-1α and VEGF expression. Downregulation of HIF-1α expression by siRNA reduced the proliferation, migration and tube formation of human umbilical vein endothelial cells. These results indicate that gastrin restores cardiac function after MI by promoting angiogenesis via the HIF-1α/VEGF pathway.
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