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.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is affecting different regions of the world since the end of 2019, causing infection named COVID-19 by World Health Organization (WHO). Up to the date (i.e. April 28, 2020) 3,063,814 cases have been confirmed by the Center for System Science and Engineering (CSSE) at Johns Hopkins University (JHU) (https://coronavirus.jhu.edu/map. html). The infection may produce, after a period of cough, fever and thoracic pain, a severe pulmonary failure requiring in more than 15% of the patients assisted ventilation (Zhou et al., 2020). Due to the lack of specific therapy and vaccine, the consequences of hospitals overload have produced a dangerous growth of the number of deaths. Sars-CoV-2 and Sars-CoV, responsible of the outbreak in 2003, share a high homology in the structure of spike protein, which bind host cells receptor (Zhang et al., 2020). Angiotensin-converting enzyme 2 (ACE2) is the host functional receptor recognized by viral protein (spike) and allows to the Sars-CoV-2 to go into the cell (Hoffmann et al., 2020). The affinity to bind ACE2 receptor is documented as more efficiently for Sars-CoV-2 than his predecessor, explaining the higher rate of transmission. The expression of ACE2 is ubiquitous, although lung represents the target and more vulnerable organ due to the high presence of ACE2 on the type II alveolar epithelial cell allowing adhesion, translocation and facilitating replication. However, different tissues such as gastrointestinal tract and heart among others, representing a further possible entry site, may be hit by Sars-CoV-2, characterizing the clinical picture for extra-pulmonary manifestations (Zhang et al., 2020; Zheng et al., 2020; Gu et al., 2020). Moreover, the different molecular expression of ACE2, limiting the ingress of Sars-CoV-2 into the cells, seems to be crucial to track the incidence of COVID-19 in different populations and to explain their dissimilar susceptibility. Regarding the potential racial heterogeneous molecular expression of ACE2, first Zhao et al. (Zhao et al., 2020) have analyzed lung cells through single-cell RNA sequencing (scRNA-Seq) and have interestingly found higher ACE2 pulmonary levels in Asian than white and African American donors. Additional studies in literature, analyzing big datasets such as the cancer genome atlas (TCGA), have not confirmed this evidence, indicating a similar molecular expression of ACE2 in the lung cells, without difference of race (Chen et al., 2020; Cai, 2020). Evidences result controversial, although recently has been documented the highest expression of ACE2 in the upper respiratory tract, particularly in the nasal epithelial cells, explaining a possible lack in the previous studies limited only to analysis of lung tissue (Sungnak et al., 2020). However, focusing on black population, a reduced molecular

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.

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.