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Objectives: Conventional treatment for type A aortic dissection includes replacement of the ascending aorta with an open distal anastomosis in the hemiarch position. The frozen elephant trunk (FET) is a hybrid technique that extends the repair to the descending thoracic aorta. The goal is to improve resolution of malperfusion syndrome and to induce positive aortic remodelling and reduce the need for reintervention on the downstream aorta. We aim to summarize the data on the short and long-term outcomes of this technique., Methods: A thorough search of the literature was conducted isolating all articles dealing with aortic remodelling after the use of FET in case of type A acute aortic dissection. Keywords 'aortic dissection', 'frozen elephant trunk', 'aortic remodelling' and 'false lumen thrombosis' were used. Data for type B and chronic aortic dissections were excluded., Results: FET use favourably influences aortic remodelling. The main advantages lie in the exclusion of distal entry tears in either the aortic arch or descending aorta thus restoring antegrade blood flow in the true lumen and inducing false lumen thrombosis. False lumen thrombosis is not only induced at the level of the stent deployment but also lower in the distal descending aorta. Moreover, it offers an adequate landing zone in the mid-descending aorta for second-stage endovascular or open surgical aortic repair, if needed., Conclusions: FET can be advantageous in the treatment of acute type A aortic dissection dealing with extended aortic pathology., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Objective: The study objective was to assess the benefits of del Nido cardioplegia compared with cold blood cardioplegia solution in terms of myocardial protection during adult cardiac surgery., Methods: A total of 474 adult patients undergoing coronary artery bypass grafting, heart valve surgery, thoracic aortic surgery, or combined procedures were randomized to the del Nido cardioplegia group (n = 234) or the cold blood cardioplegia solution group (n = 240) after provided informed consent. The primary end points assessed inotropic support requirements, severe cardiovascular events, and troponin trend within the first 48 hours of intensive care unit stay. Reperfusion arrhythmias, aortic crossclamp and cardiopulmonary bypass times, and other clinical perioperative variables were considered as secondary end points., Results: No statistically significant differences were found regarding postoperative inotropic support requirements or the incidence of severe cardiovascular events. The del Nido cardioplegia group showed a higher return to spontaneous sinus rhythm (P< .001), a lower number of defibrillation attempts (P< .001), and an earlier peak troponin value in the postoperative period. Peak blood glucose levels and intravenous insulin requirements were significantly lower in the del Nido cardioplegia group. We found no significant differences regarding aortic crossclamp or cardiopulmonary bypass time. We did observe a lower incidence of postoperative stroke in the del Nido cardioplegia group (2.6% vs 6.7%; P= .035)., Conclusions: del Nido cardioplegia can be used safely and with comparable outcomes compared with traditional cardioplegia solutions. Additional advantages over glycemic control, reperfusion arrhythmias, and its comfortable redosing interval make del Nido an interesting alternative for myocardial protection in adult cardiac surgery. A significant decrease in postoperative stroke will require further research to shed light on the results of this study. VIDEO ABSTRACT., (Copyright © 2022 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)

Objectives: The goal of this study was to analyse early- and long-term outcomes of aortic valve reimplantation (David operation) in patients with heritable thoracic aortic disease., Methods: This is a retrospective observational analysis using data from a prospectively maintained surgical database from March 2004 to April 2021. Patients with heritable thoracic aortic disease were included in the study., Results: A total of 157 patients with aortic root aneurysm with the diagnosis of heritable thoracic aortic disease received the David procedure. Marfan syndrome was found in 143 (91.1%) patients, Loeys-Dietz in 13 and Ehler-Danlos in 1 patient. The median age was 35.0 (IQR: 17.5) years and the median ascending aorta diameter in the Valsalva sinuses was 48 mm (IQR: 4). A Valsalva graft was used in 8 patients; the David V technique was performed in the rest of the cases. The median follow-up time was 7.3 years [standard deviation: 0.58, 95% confidence interval (CI): 6.12-8.05]. Only 2 patients died during the follow-up period. The overall survival was 99% (95% CI: 95%; 99%); 98% (95% CI: 92%; 99%); and 98% (95% CI: 92%; 99%) at 5, 10 and 15 years. Freedom from significant aortic regurgitation (AR> II), reintervention and postoperative type-B dissection was 90% (95% CI: 77%; 95%), 96% (95% CI: 91%; 99%) and 87% (95% CI: 68%; 95%) at 15 years, respectively. No differences were found in any outcome between Marfan syndrome and Loeys-Dietz syndrome. No statistically significant differences in survival were found when we compared expected gender- and age-specific population survival values., Conclusions: The David operation is an excellent option for the treatment of patients with heritable thoracic aortic disease and dilatated aortic root. Surgical expertise in referral centres is essential to achieve the best long-term results., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Pathological vascular remodeling is the underlying cause of atherosclerosis and abdominal aortic aneurysm (AAA). Here, we analyzed the role of galectin-1 (Gal-1), a β-galactoside-binding protein, as a therapeutic target for atherosclerosis and AAA. Mice lacking Gal-1 ( Lgals1 -/- ) developed severe atherosclerosis induced by pAAV/D377Y-mPCSK9 adenovirus and displayed higher lipid levels and lower expression of contractile markers of vascular smooth muscle cells (VSMCs) in plaques than wild-type mice. Proteomic analysis of Lgals1 -/- aortas showed changes in markers of VSMC phenotypic switch and altered composition of mitochondrial proteins. Mechanistically, Gal-1 silencing resulted in increased foam cell formation and mitochondrial dysfunction in VSMCs, while treatment with recombinant Gal-1 (rGal-1) prevented these effects. Furthermore, rGal-1 treatment attenuated atherosclerosis and elastase-induced AAA, leading to higher contractile VSMCs in aortic tissues. Gal-1 expression decreased in human atheroma and AAA compared to control tissue. Thus, Gal-1-driven circuits emerge as potential therapeutic strategies in atherosclerosis and AAA.

Left atrial appendage occlusion has become an alternative for long-term anticoagulation for patients with non-valvular atrial fibrillation. Although the procedure is safe, life-threatening complications such as embolization of the device or cardiac tamponade might occur. We present a case of a LAmbre device that migrated 4 days after being implanted and remained trapped in the mitral valve. Secondary massive mitral regurgitation with severe stenosis and haemodynamic instability required emergency surgery. The device was successfully removed, but severe damage in the anterior leaflet and chords forced a valve replacement., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Cervical necrotizing fasciitis represents an aggressive form of deep neck space infection with a high mortality rate. The origin is generally odontogenic, in most cases, resulting from a dental abscess. A series of three cases developed after local application of herbal medicine in patients with no co-morbidities and with a history of a toothache in the lower quadrants for >2 weeks is presented. All patients were managed with antibiotics, extraction of offending tooth and serial wound debridement. Two patients recovered with a resultant skin defect on the neck and one died due to multiple organ failure. This case series demonstrated that early diagnosis, prompt surgical intervention and appropriate medical treatment are very important to increase patient survival. Late report to hospital because of financial constraints and over-reliance on herbal preparation could lead to the development of serious complication in patients with dental infections and could even lead to death of the patient., (Published by Oxford University Press and JSCR Publishing Ltd. © The Author(s) 2021.)

Cardiac paragangliomas are extremely rare. Sometimes surgical resection is a challenge owing to the proximity of vital structures and coronary arteries involvement. We report a case of a 34-year-old man with cardiac paragangliomas located between right atrium and right ventricle with a feeding blood supply from collaterals of the right coronary artery. In this case, we implanted a covered single stent (PK Papyrus®) in the right coronary artery with the objective of embolizing collateral branches and to reinforce the coronary artery wall. Although tumour mass was not reduced, vascularization was minimized, and this hybrid strategy made the surgery easier and safer., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery.)

Cardiovascular disease (CVD) is the leading cause of mortality in the world, with most CVD-related deaths resulting from myocardial infarction or stroke. The main underlying cause of thrombosis and cardiovascular events is atherosclerosis, an inflammatory disease that can remain asymptomatic for long periods. There is an urgent need for therapeutic and diagnostic options in this area. Atherosclerotic plaques contain autoantibodies 1,2 , and there is a connection between atherosclerosis and autoimmunity 3 . However, the immunogenic trigger and the effects of the autoantibody response during atherosclerosis are not well understood 3-5 . Here we performed high-throughput single-cell analysis of the atherosclerosis-associated antibody repertoire. Antibody gene sequencing of more than 1,700 B cells from atherogenic Ldlr -/- and control mice identified 56 antibodies expressed by in-vivo-expanded clones of B lymphocytes in the context of atherosclerosis. One-third of the expanded antibodies were reactive against atherosclerotic plaques, indicating that various antigens in the lesion can trigger antibody responses. Deep proteomics analysis identified ALDH4A1, a mitochondrial dehydrogenase involved in proline metabolism, as a target antigen of one of these autoantibodies, A12. ALDH4A1 distribution is altered during atherosclerosis, and circulating ALDH4A1 is increased in mice and humans with atherosclerosis, supporting the potential use of ALDH4A1 as a disease biomarker. Infusion of A12 antibodies into Ldlr -/- mice delayed plaque formation and reduced circulating free cholesterol and LDL, suggesting that anti-ALDH4A1 antibodies can protect against atherosclerosis progression and might have therapeutic potential in CVD.

Objectives: The impact of inflammatory rheumatic diseases on COVID-19 severity is poorly known. Here, we compare the outcomes of a cohort of patients with rheumatic diseases with a matched control cohort to identify potential risk factors for severe illness., Methods: In this comparative cohort study, we identified hospital PCR+COVID-19 rheumatic patients with chronic inflammatory arthritis (IA) or connective tissue diseases (CTDs). Non-rheumatic controls were randomly sampled 1:1 and matched by age, sex and PCR date. The main outcome was severe COVID-19, defined as death, invasive ventilation, intensive care unit admission or serious complications. We assessed the association between the outcome and the potential prognostic variables, adjusted by COVID-19 treatment, using logistic regression., Results: The cohorts were composed of 456 rheumatic and non-rheumatic patients, in equal numbers. Mean age was 63 (IQR 53-78) years and male sex 41% in both cohorts. Rheumatic diseases were IA (60%) and CTD (40%). Most patients (74%) had been hospitalised, and the risk of severe COVID-19 was 31.6% in the rheumatic and 28.1% in the non-rheumatic cohort. Ageing, male sex and previous comorbidity (obesity, diabetes, hypertension, cardiovascular or lung disease) increased the risk in the rheumatic cohort by bivariate analysis. In logistic regression analysis, independent factors associated with severe COVID-19 were increased age (OR 4.83; 95% CI 2.78 to 8.36), male sex (1.93; CI 1.21 to 3.07) and having a CTD (OR 1.82; CI 1.00 to 3.30)., Conclusion: In hospitalised patients with chronic inflammatory rheumatic diseases, having a CTD but not IA nor previous immunosuppressive therapies was associated with severe COVID-19., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: The use of cardioplegia solutions as a myocardial protection technique is essential during cardiac surgery with cardiopulmonary bypass. The del Nido cardioplegia solution (DNS) has been widely used as a myocardial preservation technique for pediatric patients undergoing cardiac surgery with cardiopulmonary bypass. Its unique pharmacological features have created growing interest for adult cardiac surgery, especially for elderly patients or those with ventricular dysfunction who are more prone to ischemia-reperfusion injury. Ever since its implementation, several retrospective studies have been published to validate the efficacy, safety, and efficiency of DNS in adult patients undergoing coronary revascularization, valve replacement, or combined procedures. Recently, a meta-analysis based on nine retrospective studies was published claiming the noninferiority of DNS compared to other conventional cardioplegia solutions. Few prospective randomized studies have been conducted whose primary outcome was the assessment of DNS clinical efficacy compared to other solutions commonly used in adult patients., Objective: The aim of this randomized clinical trial is to assess the benefits of DNS compared to Cardi-Braun blood cardioplegia solution in clinical and biochemical terms regarding myocardial protection during adult cardiac surgery., Methods: This is the protocol of a controlled, randomized, single-center clinical trial carried out at the Puerta de Hierro Majadahonda University Hospital in Spain. A total of 474 participants over the age of 18 years undergoing elective cardiac surgery with cardiopulmonary bypass will be assigned to groups by simple randomization to receive either DNS or Cardi-Braun blood cardioplegia solution. The primary outcome will be the differences between groups in myocardial protection in biochemical terms (ie, perioperative troponin levels) and clinical terms (ie, presence of the composite variable acute cardiovascular event). The clinical trial will be carried out under conditions of respect for the fundamental rights of the person and the ethical principles that affect biomedical research with human beings, as well as in accordance with international recommendations contained in the Declaration of Helsinki and its subsequent revisions., Results: The inclusion process started in 2018. Data cleaning and analyses are expected to take place in the fall of 2020 and the results are expected in January 2021., Conclusions: This study is particularly relevant as it will be one of the first to analyze the clinical effects of del Nido cardioplegia on the basis of direct myocardial protection parameters. In light of published studies, carrying out prospective studies based on primary clinical objectives with a larger sample, high-risk patients, and longer cardiopulmonary bypass times continues to be necessary. We believe that our study addresses an important gap in the knowledge of del Nido cardioplegia in adult patient cardiac surgery and will be able to clarify the possible benefits of this method in a large population of patients undergoing these procedures., Trial Registration: European Union Drug Regulating Authorities Clinical Trials Database (EudraCT) 2017-005144-14; https://www.clinicaltrialsregister.eu/ctr-search/search?query=2017-005144-14+; ClinicalTrials.gov NCT04094168; https://clinicaltrials.gov/ct2/show/NCT04094168., International Registered Report Identifier (irrid): DERR1-10.2196/17826., (©Jessica Garcia-Suarez, Javier Garcia Fernandez, Sergio Sanz, Daniel Martinez Lopez, Leticia Reques, Alberto Forteza Gil. Originally published in JMIR Research Protocols (http://www.researchprotocols.org), 14.07.2020.)

Cardiovascular diseases (CVD) remain the major cause of morbidity and mortality in Europe. The clinical complications associated to arterial wall rupture involve intimal cap rupture in complicated atherosclerotic plaques and medial rupture in abdominal aortic aneurysm (AAA). The mechanisms underlying pathological vascular remodeling include lipid accumulation, cell proliferation, redox imbalance, proteolysis, leukocyte infiltration, cell death, and eventually, thrombosis. The complement system could participate in vascular remodeling by several mechanisms, from an initial protective response that aims in the clearing of cell debris to a potential deleterious role participating in leukocyte chemotaxis and cell activation and bridging innate and adaptive immunity. We have reviewed the presence and distribution of complement components, as well as the triggers of complement activation in atherosclerotic plaques and AAA, to later assess the functional consequences of complement modulation in experimental models of pathological vascular remodeling and the potential role of complement components as potential circulating biomarkers of CVD. On the whole, complement system is a key mechanism involved in vascular remodelling, which could be useful in the diagnostic/prognostic setting, as well as a potential therapeutic target, of CVD., (Copyright © 2019. Published by Elsevier Ltd.)

Abdominal aortic aneurysm (AAA) is a vascular pathology with a high rate of morbidity and mortality and a prevalence that, in men over 65 years, can reach around 8%. In this disease, usually asymptomatic, there is a progressive dilatation of the vascular wall that can lead to its rupture, a fatal phenomenon in more than 80% of cases. The treatment of patients with asymptomatic aneurysms is limited to periodic monitoring with imaging tests, control of cardiovascular risk factors and treatment with statins and antiplatelet therapy. There is no effective pharmacological treatment capable of limiting AAA progression or avoiding their rupture. At present, the aortic diameter is the only marker of risk of rupture and determines the need for surgical repair when it reaches values greater than 5.5cm. This review addresses the main aspects related to epidemiology, risk factors, diagnosis and clinical management of AAA, exposes the difficulties to have good biomarkers of this pathology and describes the strategies for the identification of new therapeutic targets and biomarkers in AAA., (Copyright © 2018 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.)

Background: Animal models support dietary omega-3 fatty acids protection against abdominal aortic aneurysm (AAA), but clinical data are scarce. The sum of red blood cell proportions of the omega-3 eicosapentaenoic and docosahexaenoic acids, known as omega-3 index, is a valid surrogate for long-term omega-3 intake. We investigated the association between the omega-3 index and the prevalence and progression of AAA. We also investigated associations between AAA and arachidonic acid, an omega-6 fatty acid that is a substrate for proinflammatory lipid mediators., Methods and Results: We obtained blood samples from 498 AAA patients (maximal aortic diameter ≥30 mm) within a population-based ultrasound-screening trial in men and from 199 age-matched controls who screened negative. We determined the fatty acids of red blood cells by gas chromatography. During a median follow-up of 4.85 years, 141 AAA patients reached criteria for vascular surgical repair. Participants were high consumers of omega-3 (average omega-3 index: 7.6%). No significant associations were found for omega-3 index. In contrast, arachidonic acid in AAA patients was higher than in controls ( P <0.001), and individuals in the upper tertile of arachidonic acid at baseline had higher probability of having AAA (odds ratio: 1.309; 95% confidence interval, 1.021-1.678; P =0.033). AAA patients at the upper tertile of arachidonic acid at baseline had a 54% higher risk of needing surgical repair during follow-up (hazard ratio: 1.544; 95% confidence interval, 1.127-2.114; P =0.007)., Conclusions: Omega-3 index is unrelated to men with AAA from a country in which fish consumption is customarily high. Arachidonic acid is associated with AAA presence and progression., Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT00662480., (© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)

Abdominal aortic aneurysm (AAA) evolution is unpredictable and no specific treatment exists for AAA, except surgery to prevent aortic rupture. Galectin-3 has been previously associated with CVD, but its potential role in AAA has not been addressed. Galectin-3 levels were increased in the plasma of AAA patients ( n =225) compared with the control group ( n =100). In addition, galectin-3 concentrations were associated with the need for surgical repair, independently of potential confounding factors. Galectin-3 mRNA and protein expression were increased in human AAA samples compared with healthy aortas. Experimental AAA in mice was induced via aortic elastase perfusion. Mice were treated intravenously with the galectin-3 inhibitor modified citrus pectin (MCP, 10 mg/kg, every other day) or saline. Similar to humans, galectin-3 serum and aortic mRNA levels were also increased in elastase-induced AAA mice compared with control mice. Mice treated with MCP showed decreased aortic dilation, as well as elastin degradation, vascular smooth muscle cell (VSMC) loss, and macrophage content at day 14 postelastase perfusion compared with control mice. The underlying mechanism(s) of the protective effect of MCP was associated with a decrease in galectin-3 and cytokine (mainly CCL5) mRNA and protein expression. Interestingly, galectin-3 induced CCL5 expression by a mechanism involving STAT3 activation in VSMC. Accordingly, MCP treatment decreased STAT3 phosphorylation in elastase-induced AAA. In conclusion, increased galectin-3 levels are associated with AAA progression, while galectin-3 inhibition decreased experimental AAA development. Our data suggest the potential role of galectin-3 as a therapeutic target in AAA., (© 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Atherothrombosis remains one of the main causes of morbidity and mortality worldwide. The underlying pathology is a chronic pathological vascular remodeling of the arterial wall involving several pathways, including oxidative stress. Cellular and animal studies have provided compelling evidence of the direct role of oxidative stress in atherothrombosis, but such a relationship is not clearly established in humans and, to date, clinical trials on the possible beneficial effects of antioxidant therapy have provided equivocal results. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is one of the main sources of reactive oxygen species (ROS) in human atherothrombosis. Moreover, leukocyte-derived myeloperoxidase (MPO) and red blood cell-derived iron could be involved in the oxidative modification of lipids/lipoproteins (LDL/HDL) in the arterial wall. Interestingly, oxidized lipoproteins, and antioxidants, have been analyzed as potential markers of oxidative stress in the plasma of patients with atherothrombosis. In this review, we will revise sources of ROS, focusing on NADPH oxidase, but also on MPO and iron. We will also discuss the impact of these oxidative systems on LDL and HDL, as well as the value of these modified lipoproteins as circulating markers of oxidative stress in atherothrombosis. We will finish by reviewing some antioxidant systems and compounds as therapeutic strategies to prevent pathological vascular remodeling., Competing Interests: The authors declare no conflict of interest.

Abdominal aortic aneurysm (AAA) is a permanent dilation of the aorta due to excessive proteolytic, oxidative and inflammatory injury of the aortic wall. We aimed to identify novel mediators involved in AAA pathophysiology, which could lead to novel therapeutic approaches. For that purpose, plasma from four AAA patients and four controls were analysed by a label-free proteomic approach. Among identified proteins, paraoxonase-1 (PON1) was decreased in plasma of AAA patients compared with controls, which was further validated in a bigger cohort of samples by ELISA. The phenylesterase enzymatic activity of PON1 was also decreased in serum of AAA patients compared with controls. To address the potential role of PON1 as a mediator of AAA, experimental AAA was induced by aortic elastase perfusion in wild-type (WT) mice and human transgenic PON1 (HuTgPON1) mice. Similar to humans, PON1 activity was also decreased in serum of elastase-induced AAA mice compared with healthy mice. Interestingly, overexpression of PON1 was accompanied by smaller aortic dilation and higher elastin and vascular smooth muscle cell (VSMC) content in the AAA of HuTgPON1 compared with WT mice. Moreover, HuTgPON1 mice display decreased oxidative stress and apoptosis, as well as macrophage infiltration and monocyte chemoattractant protein-1 (MCP1) expression, in elastase-induced AAA. In conclusion, decreased circulating PON1 activity is associated with human and experimental AAA. PON1 overexpression in mice protects against AAA progression by reducing oxidative stress, apoptosis and inflammation, suggesting that strategies aimed at increasing PON1 activity could prevent AAA., (© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society.)