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In Western countries, calcific aortic valve stenosis (CAS) is widely common, representing the third cause of death among cardiovascular diseases (CVD). The burden of CAS is high, with an increasing prevalence rate related to age. An efficient medical treatment, according to guidelines, lacks to prevent the development and to reduce the progression of CAS. In this context, due to the aging population and the lack of effective medical management, the prevalence is expected to double-triple within the next decades. In our review, we aim to provide an overview of the underlying mechanisms of pathogenesis and the current state of the art regarding pathophysiological insights and novel potential therapeutic targets. [ABSTRACT FROM AUTHOR]

We present a lattice determination of the inclusive decay rate of the process τ↦X_{us}ν_{τ} in which the τ lepton decays into a generic hadronic state X_{us} with u[over ¯]s flavor quantum numbers. Our results have been obtained in n_{f}=2+1+1 isosymmetric QCD with full nonperturbative accuracy, without any operator product expansion approximation and, except for the presently missing long-distance isospin-breaking corrections, include a solid estimate of all sources of theoretical uncertainties. This has been possible by using the Hansen-Lupo-Tantalo method [M. Hansen et al., Phys. Rev. D 99, 094508 (2019)PRVDAQ2470-001010.1103/PhysRevD.99.094508] that we have already successfully applied [A. Evangelista et al., Phys. Rev. D 108, 074513 (2023)PRVDAQ2470-001010.1103/PhysRevD.108.074513] to compute the inclusive decay rate of the process τ↦X_{ud}ν_{τ} in the u[over ¯]d flavor channel. By combining our first-principles theoretical results with the presently available experimental data, we extract the Cabibbo-Kobayashi-Maskawa matrix element |V_{us}|, the Cabibbo angle, with a 0.9% accuracy, dominated by the experimental error.

Background: Atrial fibrillation has been identified as an independent risk factor for thromboembolic events. Since 1948 different surgical techniques have described the feasibility and the rationale of left atrial surgical appendage closure. The aim of this systematic review is to evaluate the reported patency rates of different surgical techniques., Methods: This systematic review was conducted according to preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines. Two independent investigators searched the PubMed, Scopus, Web of Science, Cochrane Central Register of Controlled Trials, and OVID® (Wolters Kluwer, Alphen aan den Rijn, Netherlands) to identify relevant studies. Consecutively, a PICO (Population, Intervention, Comparison and Outcomes) strategy assessment of literature was performed to search eventual other relevant studies that may have been ignored., Results: A total of 42 studies were included in our analysis. The total number of patients who underwent surgical left atrial appendage closure was 5671, and in 61.2% an imaging follow up was performed, mostly with transesophageal echocardiographic evaluation. Success rate for the different techniques was: Clip deployment 98%; Lariat procedure 88%; Surgical amputation 91%; Endocardial suture 74.3%, Epicardial suture 65%; Left atrial appendage closure (LAAC) ligation 60.9%; Stapler technique with excision of left atrial appendage (LAA) 100%; Stapler without excision 70%., Conclusions: To date, data on surgical left atrial appendage closure are poor and not standardized, even if reported rates are acceptable and comparable to transcatheter procedures. If validated on large-scale non-retrospective and multicentric studies, these promising developments may offer a valuable alternative for patients with atrial fibrillation (AF) and ineligible for oral anticoagulation therapy., Competing Interests: The authors declare no conflict of interest. Mariangela Peruzzi is serving as Guest Editor of this journal. We declare that Mariangela Peruzzi had no involvement in the peer review of this article and has no access to information regarding its peer review. Full responsibility for the editorial process for this article was delegated to Buddhadeb Dawn., (Copyright: © 2023 The Author(s). Published by IMR Press.)

Severe tricuspid valve regurgitation has been for a long time a neglected valve disease, which has only recently attracted an increasing interest due to the notable negative impact on the prognosis of patients with cardiovascular disease. It is estimated that around 90% of tricuspid regurgitation is diagnosed as "functional" and mostly secondary to a primary left-sided heart disease and, therefore, has been usually interpreted as a benign condition that did not require a surgical management. Nevertheless, the persistence of severe tricuspid regurgitation after left-sided surgical correction of a valve disease, particularly mitral valve surgery, has been associated to adverse outcomes, worsening of the quality of life, and a significant increase in mortality rate. Similar results have been found when the impact of isolated severe tricuspid regurgitation has been studied. Current knowledge is shifting the "functional" categorization toward a more complex and detailed pathophysiological classification, identifying various phenotypes with completely different etiology, natural history and, potentially, an invasive management. The aim of this review is to offer a comprehensive guide for clinicians and surgeons with a systematic description of "functional" tricuspid regurgitation subtypes, an analysis centered on the effectiveness of existing surgical techniques and a focus on the emergent percutaneous procedures. This latter may be an attractive alternative to a standard surgical approach in patients with high-operative risk or isolated tricuspid regurgitation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Vinciguerra, Sitges, Luis Pomar, Romiti, Domenech-Ximenos, D'Abramo, Wretschko, Miraldi and Greco.)

The ischemic impairment of the left ventricular contractility, followed by an adverse remodeling leading to the displacement of the papillary muscles (PMs), increased tethering forces and loss of valve competence has been the long-term accepted definition of ischemic mitral regurgitation (IMR). Over the years, different approaches of management have attempted to address valve regurgitation, nevertheless failing to achieve satisfactory outcomes. Recent studies have observed some structural and molecular changes of the mitral valve (MV), challenging the concept of a bystander passive to the subvalvular involvement. Indeed, the solely mechanical stretch of the PMs, as in the dilated left ventricle because of the aortic valve regurgitation, is not enough in causing relevant MV regurgitation. This setting triggers a series of structural changes called "mitral plasticity," leaflets increase in their size among others, ensuring an adequate systolic area closure. In contrast, the ischemic injury not only triggers the mechanical stretch on the subvalvular apparatus but is also a powerful promotor of profibrotic processes, with an upregulation of the transforming growth factor (TGF)-β signaling pathway, leading to a MV with exuberant leaflet thickness and impaired mobility. In this article, we revise the concept of IMR, particularly focusing on the new evidence that supports dynamic changes in the MV apparatus, discussing the consequent clinical insights of "mitral plasticity" and the potential therapeutic implications., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Vinciguerra, Romiti, Wretschko, D'Abramo, Rose, Miraldi and Greco.)

At the beginning of the COVID-19 pandemic, the lung was recognized as the main target organ; now, new evidence suggests that SARS-CoV-2 infection leads to vascular disease. In a previous review, we supposed a bidirectional link between endothelial dysfunction and COVID-19, identifying atherosclerosis as having a crucial role in its pathogenesis. Atherosclerosis with an existing endothelial dysfunction may worsen COVID-19 manifestations, leading to adverse outcomes, as largely reported. However, COVID-19 may be the trigger factor in the progression of the atherosclerotic process up to making it clinically manifest. The thrombotic complications can involve not only the atherosclerotic plaque, but also the durability of the surgical device implanted to treat a pre-existing coronary artery disease as recently reported. The burden of the disease makes necessary a long-term stratification of patients, revising drastically targeted therapy among others.

Background: Acute type A aortic dissection (AAAD) is a pathological process that implicates the ascending aorta and represents a surgical emergency burdened by high mortality if not promptly treated in the first hours of onset. Despite best efforts, the annual incidence rates of aortic dissection has remained stable over the past decades. We measured aortic dimensions (aortic diameters, area, length and volume) using 3D multiplanar reconstruction imaging with the purpose of refining the risk- morphology for AAAD., Methods: Computerized tomography angiography studies of three groups were compared retrospectively: patients affected by AAAD (AAAD group; n=71), patients affected by aortic aneurysm and subsequently subjected to ascending aorta replacement (Aneurysm, n=77) and a healthy aorta's group (Control, n=75)., Results: Mean diameters of AAAD (4.9 cm) and Aneurysm (5.1 cm) aortas were significantly larger than those of the control group (3.4 cm). In AAAD patients, an ascending aorta diameter greater than 5.5 cm was observed in 18% of patients. Multiple comparisons showed statistically significant differences among mean of the ratio of aortic root area to height between the three groups (P<0.001). In frontal and sagittal planes, the length of the ascending aorta was significantly greater in patients affected by aortic pathology (AAAD and aneurysm) than in the control group (P<0.001). Significant differences were confirmed when indexing the aortic length to patient's height and BSA, and the aortic volume to patient's BSA., Conclusions: Maximum transverse diameter, considered separately, is not the best predictor of aortic dissection. In our opinion, the introduction into clinical practice of measurements of the area, length, and volume of the aorta, as absolute or indexed values, could improve the selection of patients who would benefit from preventive surgical aortic replacement., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/jtd-21-119). The authors have no conflicts of interest to declare., (2021 Journal of Thoracic Disease. All rights reserved.)

Dysfunction of the left ventricle (LV) with impaired contractility following chronic ischemia or acute myocardial infarction (AMI) is the main cause of ischemic mitral regurgitation (IMR), leading to moderate and moderate-to-severe mitral regurgitation (MR). The site of AMI exerts a specific influence determining different patterns of adverse LV remodeling. In general, inferior-posterior AMI is more frequently associated with regional structural changes than the anterolateral one, which is associated with global adverse LV remodeling, ultimately leading to different phenotypes of IMR. In this narrative review, starting from the aforementioned categorization, we proceed to describe current knowledge regarding surgical approaches in the management of IMR.

The severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) outbreak is a public health emergency affecting different regions around the world. The lungs are often damaged due to the presence of Sars-CoV-2 binding receptor ACE2 on epithelial alveolar cells. Severity of infection varies from complete absence of symptomatology to more aggressive symptoms, characterized by sudden acute respiratory distress syndrome (ARDS), multiorgan failure, and sepsis, requiring treatment in intensive care unit (ICU). It is not still clear why the immune system is not able to efficiently suppress viral replication in a small percentage of patients. It has been documented as pathological conditions affecting the cardiovascular system, strongly associated to atherosclerotic progression, such as heart failure (HF), coronary heart disease (CHD), hypertension (HTN) and diabetes mellitus (DM), could serve as predictive factors for severity and susceptibility during Sars-CoV-2 infection. Atherosclerotic progression, as a chronic inflammation process, is characterized by immune system dysregulation leading to pro-inflammatory patterns, including interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and IL-1β. Reviewing immune system and inflammation profiles in atherosclerosis and laboratory results reported in severe COVID-19 infections, we hypothesized a pathogenetic correlation. Atherosclerosis may be an ideal pathogenetic substrate for high viral replication ability, leading to adverse outcomes, as reported in patients with cardiovascular factors. The level of atherosclerotic progression may affect a different degree of severe infection; in a vicious circle, feeding itself, Sars-CoV-2 may exacerbate atherosclerotic evolution due to excessive and aberrant plasmatic concentration of cytokines.

Cardiovascular disease (CVD), despite the significant advances in the diagnosis and treatments, still represents the leading cause of morbidity and mortality worldwide. In order to improve and optimize CVD outcomes, artificial intelligence techniques have the potential to radically change the way we practice cardiology, especially in imaging, offering us novel tools to interpret data and make clinical decisions. AI techniques such as machine learning and deep learning can also improve medical knowledge due to the increase of the volume and complexity of the data, unlocking clinically relevant information. Likewise, the use of emerging communication and information technologies is becoming pivotal to create a pervasive healthcare service through which elderly and chronic disease patients can receive medical care at their home, reducing hospitalizations and improving quality of life. The aim of this review is to describe the contemporary state of artificial intelligence and digital health applied to cardiovascular medicine as well as to provide physicians with their potential not only in cardiac imaging but most of all in clinical practice., Competing Interests: The authors declare no potential conflicts of interest with respect to the research, authorship and/or publication of this article., (Copyright © 2020 Silvia Romiti et al.)

This paper discusses the reasons why evidence of clinical effectiveness is not enough to facilitate adequate adoption of robotic technologies for upper-limb neurorehabilitation. The paper also provides a short review of the state of the art technologies. In particular, the paper highlights the barriers to the adoption of these technologies by the markets in which they are, or should be, deployed. On the other hand, the paper explores how low rates of adoption may depend on communication biases between the producers of the technologies and potential adopters. Finally, it is shown that, although technology-efficacy issues are usually well-documented, barriers to adoption also originate from the lack of solid evidence of the economic implications of the new technologies.

This paper is a radiographic approach to ascertain if the hardware at the medial malleolus is intra-articular. A human tibia was removed from a skeleton and pins were placed in the medial malleolus representing pins that would be intra- and extra-articular (in the mortise). Radiographs were obtained at precise rotation intervals. Those pins that were placed intra-articularly could not be made to appear otherwise. The pin that was placed extra-articularly was visualized on a single view to be extra-articular. Therefore, if hardware can be demonstrated to be extra-articular on any one view then it is not intra-articular.

Methods are presented that describe alternative protocols for the isolation of rat liver microsomes containing the vitamin K-dependent carboxylase and the procedure in which the solubilized enzyme is assayed. The method for determining the rate of 14CO2 incorporation into low molecular weight, acid soluble substrates by the rat liver microsomal vitamin K-dependent carboxylase has been modified in order to optimize safety, accuracy and simplicity. For these studies the rat liver microsomes containing the vitamin K-dependent carboxylase were isolated by CaCl2 precipitation. These Triton X-100 solubilized microsomes were found to be equivalent to the microsomes obtained by high speed ultracentrifugation with regard to protein concentration, pentapeptide carboxylase activity, carboxylase activity, preprothrombin concentration and total carboxylatable endogenous protein substrate. This modified assay procedure requires fewer steps and pipetting transfers and is quantitatively equivalent to previously employed protocols. The described technique can be adapted for any assay where 14CO2 or H14CO3- is incorporated into non-volatile products. This newly developed assay procedure was employed to assess conditions necessary for optimal vitamin K-dependent carboxylation of the less expensive substrate, N-t-Boc-L-glutamic acid alpha-benzyl ester. The optimal conditions for the carboxylation of N-t-Boc-L-glutamic acid alpha-benzyl ester by the carboxylase were found to be 10 mM N-t-Boc-L-glutamic acid alpha-benzyl ester, 10 mM MgCl2 at 15-18 degrees C. The rate of N-t-Boc-L-glutamic acid alpha-benzyl ester carboxylation under these optimized conditions was found to be higher (1.5-fold) than the rate of carboxylation of 1 mM Phe-Leu-Glu-Glu-Ile in the presence of the cation activator, MgCl2.