[This corrects the article DOI 10.3389/fcvm.2021.650191.].We recently treated a 36-year-old previously healthy male with a prolonged hypothermic (lowest temperature 22.3°C) cardiac arrest after an alcohol intoxication with a return of spontaneous circulation after 230min of mechanical cardiopulmonary resuscitation and rewarming by veno-arterial ECMO with femoral cannulation and retrograde perfusion of the aortic arch. Despite functional veno-arterial ECMO, we continued mechanical cardiopulmonary resuscitation (Auto Pulse™ device, ZOLL Medical Corporation, Chelmsford, USA) until return of spontaneous circulation to prevent left ventricular distention from persistent ventricular fibrillation. The case was further complicated by extensive trauma caused by mechanical cardiopulmonary resuscitation (multiple rib fractures, significant hemothorax, and a liver laceration requiring massive transfusion), lung failure necessitating a secondary switch to veno-venous ECMO, and acute kidney injury with the need for renal replacement therapy. Shortly after return of spontaneous circulation, the patient was already following commands and could be discharged 3 weeks later without neurologic, cardiac, or renal sequelae and being entirely well. Prolonged accidental hypothermic cardiac arrest might present with excellent outcomes when supported with veno-arterial ECMO. Until return of spontaneous circulation, one might consider continuing with mechanical cardiopulmonary resuscitation in addition to ECMO to allow some left ventricular unloading. However, the clinician should keep in mind that prolonged mechanical cardiopulmonary resuscitation may cause severe injuries.Background The metabolic syndrome (MS) is significantly associated with the risk of incident heart failure (HF). However, there are still great controversies about the impact of MS on the prognosis in patients with established HF. This meta-analysis aimed to ascertain the effect of MS on the prognosis in patients with HF. Methods We searched multiple electronic databases, including PubMed, Opengrey, EMBASE, and Cochran Library, for potential studies up to February 15, 2021. Observational studies that reported the impact of MS on the prognosis in patients with established HF were included for meta-analysis. Results Ten studies comprising 18,590 patients with HF were included for meta-analysis. The median follow-up duration of the included studies was 2.4 years. Compared with HF patients without MS, the risk of all-cause mortality and cardiovascular mortality was not increased in HF with MS (HR = 1.04, 95% CI = 0.88-1.23 for all-cause mortality; HR = 1.66, 95% CI = 0.56-4.88 for cardiovascular mortality, respectively). However, there was a significant increase in composited cardiovascular events in the HF patients with MS compared with those without MS (HR = 1.73, 95% CI = 1.23-2.45). Conclusions In patients with established HF, the presence of MS did not show an association on the risk of all-cause mortality or cardiovascular mortality, while it may increase the risk of composite cardiovascular events.Cardiac remodeling occurs after the heart is exposed to stress, which is manifested by pathological processes such as cardiomyocyte hypertrophy and apoptosis, dendritic cells activation and cytokine secretion, proliferation and activation of fibroblasts, and finally leads to heart failure. Circular RNAs (circRNAs) are recently recognized as a specific type of non-coding RNAs that are expressed in different species, in different stages of development, and in different pathological conditions. Growing evidences have implicated that circRNAs play important regulatory roles in the pathogenesis of a variety of cardiovascular diseases. In this review, we summarize the biological origin, characteristics, functional classification of circRNAs and their regulatory functions in cardiomyocytes, endothelial cells, fibroblasts, immune cells, and exosomes in the pathogenesis of cardiac remodeling.Lymphatic vessels are necessary for maintaining tissue fluid balance, trafficking of immune cells, and transport of dietary lipids. Growing evidence suggest that lymphatic functions are limited under hypercholesterolemic conditions, which is closely related to atherosclerotic development involving the coronary and other large arteries. Indeed, ablation of lymphatic systems by Chy-mutation as well as depletion of lymphangiogenic factors, including vascular endothelial growth factor-C and -D, in mice perturbs lipoprotein composition to augment hypercholesterolemia. Several investigations have reported that periarterial microlymphatics were attracted by atheroma-derived lymphangiogenic factors, which facilitated lymphatic invasion into the intima of atherosclerotic lesions, thereby modifying immune cell trafficking. In contrast to the lipomodulatory and immunomodulatory roles of the lymphatic systems, the critical drivers of lymphangiogenesis and the details of lymphatic insults under hypercholesterolemic conditions have not been fully elucidated. Interestingly, cholesterol-lowering trials enable hypercholesterolemic prevention of lymphatic drainage in mice; however, a causal relationship between hypercholesterolemia and lymphatic defects remains elusive. In this review, the contribution of aberrant lymphangiogenesis and lymphatic cholesterol transport to hypercholesterolemic atherosclerosis was highlighted. The causal relationship between hypercholesterolemia and lymphatic insults as well as the current achievements in the field were discussed.Background While a small number of studies suggest that oxidative stress has an influential role in fibrocalcific aortic valve disease (FCAVD), the roles of specific antioxidant enzymes in progression of this disease remain poorly understood. Here, we focused on selectively altering mitochondrial-derived oxidative stress-which has been shown to alter progression of a myriad of age-associated diseases-on the progression of molecular and phenotypic drivers of FCAVD. Methods We generated low-density lipoprotein receptor-deficient, Apolipoprotein B100-only mice (LA) that were either haploinsufficient for MnSOD (LA-MnSOD +/-) or genetically overexpressing MnSOD (LA-MnSOD Tg/0). After 6 months of Western diet feeding, mice underwent echocardiography to assess valvular and cardiac function and tissues were harvested.  https://www.selleckchem.com/products/vo-ohpic.html  Quantitative-RT PCR, immunohistochemistry, and histopathology were used to measure changes in molecular pathways related to oxidative stress, calcification, and fibrosis. Results While reductions in MnSOD increased oxidative stress, there was not an overt phenotypic effect of MnSOD deficiency on valvular and cardiac function in LA-MnSOD +/- mice.