The actual Coronavirus Disease (COVID 19) pandemic is due to Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of the coronavirus family. Besides the respiratory involvement, COVID 19 patients frequently develop a pro-coagulative state caused by virus-induced endothelial dysfunction, cytokine storm and complement cascade hyperactivation. It is common to observe diffuse microvascular thrombi in multiple organs, mostly in pulmonary microvessels. Thrombotic risk seems to be directly related to disease severity and worsens patients' prognosis. Therefore, the correct understanding of the mechanisms underlying COVID-19 induced prothrombotic state can lead to a thorough assessment of the possible management strategies. Hence, we review the pathogenesis and therapy of COVID 19-related thrombosis disease, focusing on the available evidence on the possible treatment strategies and proposing an algorithm for the anticoagulation strategy based on disease severity. Keywords COVID-19 • SARS-CoV-2 • Thrombosis • Anticoagulation Highlights • SARS-CoV-2 induced complement hyperactivation, endothelial dysfunction and cytokine storm have a prothrombotic effect. • COVID 19 patients develop a pro-coagulative state directly related to disease severity. • In COVID 19 critical patients, thrombotic lesions in pulmunary microvessels have a prevalence twice higher than critical non-COVID 19 patients. • Anticoagulant treatment is associated with lower mortality. Hence, we propose an algorithm for the anticoagulation strategy based on disease severity.

Kidney injury may be a severe complication of acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and contributes to worsen the prognosis. Various pathophysiological mechanisms can contribute to organ damage and impair renal function, proving the complexity of the virus activity and the resulting immunity response. We summarized the evidence of the literature on the prevalence of kidney involvement, on the pathogenic pathways and on its management.

As of January 2020, a new pandemic has spread from Wuhan and caused thousands of deaths worldwide. Several studies have observed a relationship between coronavirus disease (COVID-19) infection and the cardiovascular system with the appearance of myocardial damage, myocarditis, pericarditis, heart failure and various arrhythmic manifestations, as well as an increase in thromboembolic risk. Cardiovascular manifestations have been highlighted especially in older and more fragile patients and in those with multiple cardiovascular risk factors such as cancer, diabetes, obesity and hypertension. In this review, we will examine the cardiac involvement associated with SARS-CoV-2 infection, focusing on the pathophysiological mechanism underlying manifestations and their clinical implication, taking into account the main scientific papers published to date.

Background: Coronary artery disease (CAD) and chronic kidney disease (CKD) may reciprocally influence each other. Patients with CAD and CKD have an increased risk of both ischemic and hemorrhagic events. Methods: In the present review, we summarize the existing literature focusing on the relationship between kidney dysfunction and acute coronary syndromes (ACS) in terms of risk factors, complications, and prognosis. We discuss also about the best evidence-based strategies to prevent deterioration of renal function in patients with CAD. Results: Patients with CKD less frequently receive an invasive management (percutaneous or surgical revascularization) and potent antithrombotic drugs. Nevertheless, recent evidence suggests they would benefit from a selective invasive management, especially in case of ACS. Conclusion: Patients with CKD and CAD represent a challenging population, more randomized controlled trials and meta-analyses are needed to better define the best therapeutic strategy during an ACS episode.

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