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The association between thrombosis, cancer and inflammation is well-established. Platelets play a major role in atherosclerosis, inflammation and immune response. Furthermore, growing evidence suggests that they are also significantly involved in tumor development and progression so that anti-platelet agents may prevent cancer and improve outcomes in oncological patients. In this review, we aimed at analyzing the relationship between platelets, cardiovascular diseases and cancer. A comprehensive study in the main educational platforms was performed and high-quality original articles and reviews were included.This review will focus on the role of platelets in cardiovascular disease and in cancer genesis and progression, analyzing their function as immune cells that link inflammation to thrombosis. Finally, it will examine the recent controversies on the use of anti-platelet agents as cancer medications, in particular the already known anti-tumor properties of aspirin, as well as the new perspectives regarding P2Y12 inhibitors.Platelet-cancer crosstalk generates a vicious feed-back loop involving tumor cells and secreting molecules that activate platelets, which in turn promote cancer-associated inflammation, proliferation, spreading and immune system evasion. Therefore, platelets inhibition may represent an innovative therapeutical strategy offered to cancer patients, in the perspective of personalized medicine.

Aims Randomized trials support the safety and efficacy of direct oral anticoagulants (DOACs) vs. vitamin K antagonists (VKA) in patients with nonvalvular atrial fibrillation (AF), leading to increased use of these compounds. Crushed forms of DOACs have shown to be reliable, but evidence supporting percutaneous endoscopic gastrostomy (PEG) delivery is lacking. PEG is a long-term option for enteral food and drug delivery in patients unable to maintain oral intake, bypassing the risks and disadvantages of parenteral nutrition. We investigate the safety and efficacy of Edoxaban administered via PEG in patients with atrial fibrillation and a clinical indication for a long-term anticoagulation. Methods and results In this prospective, single centre observational study, 12 PEG-treated patients with indication to anticoagulation will receive edoxaban via PEG and will be followed-up to 6 months. Plasma anti-Factor Xa activity and edoxaban concentrations will be assessed. Thromboembolic (ischaemic stroke, systemic embolism, venous thromboembolism) and bleeding events (Bleeding Academic Research Consortium and Thrombolysis in Myocardial Infarction) will be recorded at 1 and 6 months. A retrospective analysis of 5 AF cases undergoing PEG-implantation at our Institution, who received edoxaban via PEG, showed plasma anti-FXa levels at steady state of 146 ± 15 ng/ml, without major adverse event at a mean follow-up of 6 months. Conclusion We prospectively investigate PEG-administration of edoxaban in PEG-treated patients requiring long term anticoagulation. Our preliminary retrospective data support this route of DOAC administration.

Heart failure is the cardiovascular epidemic of the twenty-first century, with poor prognosis and quality of life despite optimized medical treatment. Despite over the last decade significant improvements, with a major impact on morbidity and mortality, have been made in therapy for heart failure with reduced ejection fraction, little progress was made in the development of devices, with the implantable defibrillator indicated for patients with left ventricle ejection fraction ≤ 35% and cardiac resynchronization therapy for those with QRS ≥ 130 ms and evidence of left bundle branch block. Nevertheless, only a third of patients meet these criteria and a high percentage of patients are non-responders in terms of improving symptoms. Nowadays, in patients with symptomatic heart failure with ejection fraction between 25% and 45% and QRS

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged in Wuhan, Hubei-China, as responsible for the coronavirus disease 2019 (COVID-19) and then spread rapidly worldwide. While most individuals remain asymptomatic or develop only mild symptoms, approximately 5% develop severe forms of COVID-19 characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF) that usually require intensive-care support and often yield a poor prognosis. Summary: The pathophysiology of COVID-19 is far from being completely understood, and the lack of effective treatments leads to a sense of urgency to develop new therapeutic strategies based on pathophysiological assumptions. The exaggerated cytokine release in response to viral infection, a condition known as cytokine release syndrome (CRS) or cytokine storm, is emerging as the mechanism leading to ARDS and MOF in COVID-19, thus endorsing the hypothesis that properly timed anti-inflammatory therapeutic strategies could improve patients’ clinical outcomes and prognosis. Key Messages: The objective of this article is to explore and comment on the potential role of the promising immunomodulatory therapies using pharmacological and nonpharmacological approaches to overcome the dysregulated proinflammatory response in COVID-19.

From first cases reported on December 31, 2019, in Wuhan, Hubei-China, SARS-CoV2 has spread worldwide and finally the World Health Organization declared the pandemic status. We summarize what makes SARS-CoV2 different from previous highly pathogenic coronaviruses and why it is so contagious, with focus on its clinical presentation and diagnosis, which is mandatory to start the appropriate management and reduce the transmission. As far as infection pathophysiology is still not completely clarified, this review focuses also on the cardiovascular (CV) implication of COVID-19 and the capability of this virus to cause direct myocardial injury, myocarditis and other CV manifestations. Furthermore, we highlight the relationship between the virus, enzyme ACE2 and ACE inhibitors. Clinical management involves the intensive care approach with intubation and mechanical ventilation in the most serious cases and drug therapy with several apparently promising old and new molecules. Aim of this review is then to summarize what is actually known about the SARS-CoV2 and its cardiovascular implications.

From December 31th, 2019, a novel highly pathogenic coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread worldwide, reaching at present the dimension of a pandemic. In addition to damaging the lungs, SARS-CoV-2 may also damage the heart and this is corroborated by the evidence that cardiovascular comorbidities are associated with a higher mortality and poor clinical outcomes in patient infected by the virus. During the infection myocardial injury, myocarditis and arrhythmias have also been reported, but the pathophysiological mechanisms of these complications are yet to be understood. Great attention is also being posed on the potential beneficial/harmful role of angiotensin converting enzyme (ACE) inhibitors, as far as the virus binds to angiotensin converting enzyme 2 (ACE2) to infect cells, but evidences lack. Furthermore, SARS-CoV-2 can also affect the aspect of acute coronary syndromes, not only because these two distinct pathological entities share pathogenic aspects (such as the systemic inflammatory state and cytokine release), but also and above all for the consequences that the need to contain the infection has on the management of cardiological urgencies. Aim of this review is therefore to summarize the relationship between the virus and the cardiovascular system.

From first cases reported on December 31, 2019, in Wuhan, Hubei-China, SARS-CoV2 has spread worldwide and finally the World Health Organization declared the pandemic status. We summarize what makes SARS-CoV2 different from previous highly pathogenic coronaviruses and why it is so contagious, with focus on its clinical presentation and diagnosis, which is mandatory to start the appropriate management and reduce the transmission. As far as infection pathophysiology is still not completely clarified, this review focuses also on the cardiovascular (CV) implication of COVID-19 and the capability of this virus to cause direct myocardial injury, myocarditis and other CV manifestations. Furthermore, we highlight the relationship between the virus, enzyme ACE2 and ACE inhibitors. Clinical management involves the intensive care approach with intubation and mechanical ventilation in the most serious cases and drug therapy with several apparently promising old and new molecules. Aim of this review is then to summarize what is actually known about the SARS-CoV2 and its cardiovascular implications.

Aims The ORal anticoagulants In fraGile patients with percutAneous endoscopic gastrostoMy and atrIal fibrillation (ORIGAMI) study investigates the safety and efficacy of Edoxaban administered via PEG in patients with atrial fibrillation and a clinical indication for a long-term anticoagulation. Design In this prospective, single-centre observational study, 12 PEG-treated patients with indication to anticoagulation will receive edoxaban via PEG and will be followed up to 6 months. Plasma antifactor Xa activity and edoxaban concentrations will be assessed. Thromboembolic (ischaemic stroke, systemic embolism, venous thromboembolism) and bleeding events (Bleeding Academic Research Consortium and Thrombolysis in Myocardial Infarction) will be recorded at 1 and 6 months. Preliminary results A retrospective analysis of five atrial fibrillation cases undergoing PEG implantation at our Institution who received edoxaban via PEG showed plasma anti-FXa levels at a steady state of 146 ± 15 ng/ml, without major adverse event at a mean follow-up of 6 months. Conclusion ORIGAMI prospectively investigates PEG-administration of edoxaban in PEG-treated patients requiring long-term anticoagulation. Our preliminary retrospective data support this route of DOAC administration. Clinicaltrialsgov identifier NCT04271293.

Over the last several decades, clinicians and clinical scientists have had growing interest in heart failure (HF) diagnosis and treatment. While HF with reduced ejection fraction (EF) is a well-known clinical entity with several therapeutic strategies proven to be successful, HF with preserved ejection fraction is a more heterogenous syndrome with a prevalence that has increased in the last two decades, without effective therapeutic strategies. Great strides have been made in the detection of predisposing risk factors and pathological mechanisms; however, pharmacological therapies have shown to be ineffective in reducing cardiovascular mortality in the HF with preserved EF (HFpEF) population, opening the way to the necessity of developing new precision medicine based approaches. On the other hand, novel therapies and device interventions still require refinements with the ultimate goal of offering new clinically treatments for the HFpEF population. The aim of the present review is to provide insights into the HFpEF pathophysiology, diagnostic pathways and the latest updates on treatment strategies and their potential future application in routine clinical practice.

Background: Sex and gender-related factors have been under-investigated as relevant determinants of health outcomes across non-communicable chronic diseases. Poor medication adherence results in adverse clinical outcomes and sex differences have been reported among patients at high cardiovascular risk, such as diabetics. The effect of diabetes and gender-related factors on medication adherence among women and men at high risk for ischemic heart disease (IHD) has not yet been fully investigated. Aim: To explore the role of sex, gender-related factors, and diabetes in pre-admission medication adherence among patients hospitalized for IHD. Materials and Methods: Data were obtained from the Endocrine Vascular disease Approach (EVA) (ClinicalTrials.gov Identifier: NCT02737982), a prospective cohort of patients admitted for IHD. We selected patients with baseline information regarding the presence of diabetes, cardiovascular risk factors, and gender-related variables (i.e., gender identity, gender role, gender relations, institutionalized gender). Our primary outcome was the proportion of pre-admission medication adherence defined through a self-reported questionnaire. We performed a sex-stratified analysis of clinical and gender-related factors associated with pre-admission medication adherence. Results: Two-hundred eighty patients admitted for IHD (35% women, mean age 70), were included. Around one-fourth of the patients were low-adherent to therapy before hospitalization, regardless of sex. Low-adherent patients were more likely diabetic (40%) and employed (40%). Sex-stratified analysis showed that low-adherent men were more likely to be employed (58 vs. 33%) and not primary earners (73 vs. 54%), with more masculine traits of personality, as compared with medium-high adherent men. Interestingly, women reporting medication low-adherence were similar for clinical and gender-related factors to those with medium-high adherence, except for diabetes (42 vs. 20%, p = 0.004). In a multivariate adjusted model only employed status was associated with poor medication adherence (OR 0.55, 95%CI 0.31–0.97). However, in the sex-stratified analysis, diabetes was independently associated with medication adherence only in women (OR 0.36; 95%CI 0.13–0.96), whereas a higher masculine BSRI was the only factor associated with medication adherence in men (OR 0.59, 95%CI 0.35–0.99). Conclusion: Pre-admission medication adherence is common in patients hospitalized for IHD, regardless of sex. However, patient-related factors such as diabetes, employment, and personality traits are associated with adherence in a sex-specific manner.