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.

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.

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.

The coronavirus disease 2019 (COVID-19) pandemic outbreak, caused by severe acute respiratory syndrome coronavirus-2 (SARS-Cov-2) is affecting people worldwide representing a public health emergency. The effect of concomitant COVID-19 on patients who underwent cardiac surgery using cardiopulmonary bypass (CPB) is still undefined. Both SARS-Cov-2 infection and CPB can develop a cytokines storm and haemostatic disarrangements leading to acute respiratory distress syndrome (ARDS) and post-perfusion lung syndrome, respectively. SARS-Cov-2 infection may trigger and exacerbate post-inflammatory state after CPB resulting in higher risk of post-surgical adverse outcomes. International guidelines lack to provide standard management protocols for pre-operative COVID-19 patients requiring non-deferrable cardiac surgery intervention. We present a report of a successful coronary artery bypass grafting (CABG) emergency operation in a COVID-19 patient, who presented unstable angina and coronary artery dissection during cardiac catheterization and percutaneous transluminal coronary angioplasty (PTCA).

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.

Streptococcus bovis/Streptococcus equinus complex (SBSEC) is a group of non-enterococcal group D Streptococci that colonizes both humans and animals. Due to gastrointestinal disease, they can switch in opportunistic pathogens passing through intestinal mucosal barrier and may cause bacteremia and distant organs damage. Despite infective endocarditis (IE), extra-cardiac manifestations of organs damage include osteoarticular infections, meningitis, and biliary infections among others; moreover, the association with colonic pathological lesions has been largely described. Streptococcus alactolyticus as a species included in SBSEC may share pathophysiological similarities, although it represents an extremely rare cause of distant organ infections, being reported in literature as causative agent of IE in only two other cases. We describe a case of 69-year-old male admitted to our institution due to mild–moderate dyspnea and fever, affected by cervico-brachialgia for 3 weeks. Streptococcus alactolyticus was identified as causative agent of IE on the mitral valve, causing severe regurgitation.