Umbilical cord mesenchymal stem cells (UCMSCs) transplantation has been proposed as a promising treatment modality for myocardial infarction (MI), but the low retention rate remains a considerable challenge. Injectable natural polymer hydrogels with conductivity ability are highly desirable as cell delivery vehicles to repair infarct myocardium and restore the cardiac function. In this work, we developed a hydrogel system based on gelatin methacrylate (GelMA) and oxidized dextran (ODEX) as cell delivery vehicles for MI. And dopamine could be used as a reductant of graphene oxide (GO) to form reductive GO (rGO). By adjusting the amount of rGO, the conductivity of hydrogels with 0.5 mg/mL rGO concentration (≈10⁻⁴ S/cm) was similar to that of natural heart tissue. In vitro cell experiments showed that the prepared hydrogels had excellent biocompatibility and cell delivery ability of UCMSCs. More importantly, GelMA-O5/rGO hydrogel could promote UCMSCs growth and proliferation, improve the myocardial differentiation ability of UCMSCs, and up-regulate the expression of cTnI and Cx43. Further in vivo experiments demonstrated that GelMA-O5/rGO/UCMSCs Hydrogel could significantly improve the ejection fraction (EF) of rats and significantly reduce myocardial infarct area compared to PBS group, promote the survival of UCMSCs, enhance the expression level of cTnI and Cx43, and decrease the expression level of caspase-3. The findings of this study suggested that the injectable conductive GelMA-O5/rGO hydrogel encapsulating UCMSCs could improve damaged myocardial tissue and reconstruct myocardial function, which will be a promising therapeutic strategy for cardiac repair.

Background: Mutation of the ACTA2 (α-2 smooth muscle actin) gene accounts for ~15% of all cases of familial thoracic aortic aneurysms and dissections. Surprisingly, no severe vascular phenotypes were observed at baseline in mice carrying this gene mutation. Our aim was to explore whether mutation of ACTA2 promotes the development of aneurysms or dissections in the presence of angiotensin II (AngII) and to determine whether this mutation has an impact on the phenotypic modulation and apoptosis mediated by AngII in vascular smooth muscle cells (VSMCs). Methods: Mice were divided into three groups: AngII stimulated-wild-type (WT) (AngII) and ACTA2^−/− mice (ACTA2) group, in which AngII were administered subcutaneously into 8-week-old C57 mice and ACTA2^−/− mice, respectively, for 4 weeks using osmotic minipumps, and the control group (WT), in which the WT mice were infused with normal saline (NS). Ultrasound was performed to quantify lumen diameters. RT-qPCR and Western blot were used to assess gene expression, and histobiochemistry was used to evaluate the pathological changes in the thoracoabdominal aortas. TUNEL was used to assess apoptosis in VSMCs. Results: Compared with the AngII- group, the ACTA2 mice exhibited more severity of dilated lumena of the aortas, a significantly increased expression of osteopontin (OPN), an elevated ratio of Bax/Bcl-2, increased apoptosis, and a decreased expression of α-smooth muscle actin (α-SMA). Conclusions: Knockout of ACTA2 promoted AngII induced progressive lumen dilation of the aortas, apoptosis, and the phenotypic modulation in VSMCs in mice.

The cardiac microenvironment profoundly restricts the efficacy of myocardial regeneration tactics for the treatment of myocardial infarction (MI). A prospective approach for MI therapeutics encompasses the combined strategy of scavenging reactive oxygen species (ROS) to alleviate oxidative stress injury and facilitating macrophage polarization towards the regenerative M2 phenotype. In this investigation, we fabricated a ROS-sensitive hydrogel engineered to deliver our previously engineered IL-1β-VHH for myocardial restoration. In mouse and rat models of myocardial infarction, the therapeutic gel was injected into the pericardial cavity, effectively disseminated over the heart surface, forming an in situ epicardial patch. The IL-1β-VHH released from the hydrogel exhibited penetrative potential into the myocardium. Our results imply that this infarct-targeting gel can adhere to the damaged cardiac tissue and augment the quantity of anti-IL-1β antibodies. Moreover, the anti-IL-1β hydrogel safeguards cardiomyocytes from apoptosis by neutralizing IL-1β and inducing M2-type polarization within the myocardial infarction regions, thereby facilitating therapeutic cardiac repair. Our results emphasize the effectiveness of this synergistic comprehensive treatment modality in the management of MI and showcase its considerable potential for promoting recovery in infarcted hearts.

Background: Coronary malperfusion (CM) secondary to acute type A aortic dissection (ATAAD) is considered rare but has a high mortality rate. This study examined the incidence, management, and outcomes of patients with CM secondary to ATAAD and proposes a modified Neri classification. Methods: Between 2015 and 2020, out of 1018 patients who underwent surgical repair for ATAAD, 137 presented with CM, including 68 (49.6%), 43 (31.3%), and 15 (10.9%) with Neri types A, B, and C, respectively, and 11 (8.0%) with coronary orifice intimal tear (COIT), which we consider a novel category. Results: The occurrence rate of CM was 13.4%. CM was associated with higher in-hospital mortality (18.2% vs. 7.8%, p < 0.001). For Neri type A (98.5%) and most type B lesions (72.1%), coronary repair was adequate. Coronary artery bypass grafting (CABG) was necessary for type B patients unsuited for repair (23.2%) and for all type C patients (100%). Repair of COIT was possible (45.5%). The in-hospital mortality rates differed significantly among the four lesion groups (p = 0.006). Conclusions: The occurrence of CM secondary to ATAAD may be more frequent than previously reported. Surgical management based on lesion classification achieved acceptable outcomes. Repair was adequate for Neri type A and most type B lesions. Other type B and type C lesions could be treated by CABG. Coronary orifice intimal tear is a unique set of lesions, for which orifice repair was also possible.

Objective: This meta-analysis and systematic review investigated whether partial thrombosed false lumen was a predictor for adverse events in uncomplicated Type B aortic dissection (TBAD).Methods: We performed the current systematic review of the medical literature according to the 2009 Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. The Newcastle-Ottawa Scale was used to evaluate the quality of individual studies. Search terms based on the MEDLINE database included “type B aortic dissection,” “false lumen” and “thrombosis.” The primary outcomes included mortality, intervention, and aortic growth.Results: Six studies were included in this systematic review, with a total number of 692 patients, including 197 patency (28.5%), 214 partial thrombosis (30.9%), and 281 complete thrombosis (40.6%). Due to the insufficient data for quantitative analysis, we only conducted a scoping review for mortality and intervention. For aortic growth, we conducted a meta-analysis based on Standardized Mean Difference (SMD). The SMD of PT vs. P by random effect model was −0.05 (random effect model) [95% confidence interval (CI), −0.39 to 0.29]. The 95% CI crossed with the null line of 0, indicating no significant difference. The SMD was 0.37 (fixed effects model) (95% CI, 0.03–0.71) and 0.70 (fixed effects model) (95% CI, 0.37–1.04) for PT vs. CT, and P vs. CT, respectively.Conclusions: Current researches on partial thrombosis of TBAD are inconsistent. Partial thrombosis is not associated with a faster aortic growth rate. Until more solid evidence is available, we do not recommend partial thrombosis as a surgical indication or high-risk profile for TBAD.Systematic Review Registration: Unique Identifier: CRD42019121912.

Background: To evaluate the safety and efficacy of femoral artery cannulation as an alternative to axillary artery cannulation, we retrospectively compared outcomes between patients with axillary or femoral artery cannulation during open aortic arch repair for type A aortic dissection (TAAD). Methods: Between January 2014 and January 2019, 646 patients underwent open aortic arch repair with circulatory arrest for TAAD using antegrade selective cerebral perfusion (SACP) and were divided into two groups according to the site of arterial cannulation: an axillary artery group (axillary group, n=558) or a femoral artery group (femoral group, n=88). The axillary artery was considered as the primary cannulation site, and the femoral artery was used as an alternative when axillary artery cannulation was deemed unsuitable or had failed. Propensity score matching was performed to correct baseline differences. Results: After propensity score matching, the patients’ characteristics were comparable between groups (n=85 in each). The incidence of in-hospital mortality (10.6% vs. 14.1%; P=0.642) and stroke (3.5% vs. 5.9%; P=0.720) were comparable between the axillary and femoral groups. The incidence of newly required dialysis was lower in the femoral group, but the difference was not statistically significant (34.1% vs. 20.0%; P=0.050). Other outcomes and major adverse events were comparable. Conclusions: Femoral artery cannulation produced similar perioperative outcomes to axillary cannulation after open arch repair for TAAD. The femoral artery can be used as a safe and effective alternative to the axillary artery for arterial cannulation in TAAD patients undergoing open arch repair.