Dear Colleagues,

Atherosclerotic disease and its thrombotic complication are the pathophysiological substrate underlying several clinical conditions, such as acute and chronic coronary syndrome (ACS and CCS, respectively), stroke, and peripheral artery disease. Activation of coagulation cascade as well as platelet aggregation are key steps of the thrombotic process. Vessel injury results in exposure of the glycoprotein tissue factor (TF) to the flowing blood. Once exposed, TF binds factor VII/VIIa (FVII/FVIIa), and in presence of calcium ions, it forms a tertiary complex able to activate FX to FXa, FIX to FIXa, and FVIIa itself. The final step is thrombin formation at the site of vessel injury with subsequent platelet activation, fibrinogen to fibrin conversion, and ultimately thrombus formation. Platelets are crucial cells in primary hemostasis. For years, they have been considered only as cell fragments participating in primary hemostasis. However, recent advances in platelet pathophysiology have shown that these cells are able to regulate their gene and protein expression, make de novo protein synthesis, and release different mediators with paracrine effects that may interfere with different cell function. Pharmacological modulation of both components of thrombosis, the coagulation cascade and platelet activation, is of great clinical importance. Several clinical trials have clearly shown the efficacy of anticoagulation and/or antiplatelet aggregation in different thrombotic disorders, even in the context of aortic valve replacement, mitral valve repair through the MITRACLIP system, and left atrial appendix occlusion. However, real world practice has clearly indicated that antithrombotic strategies need to be personalized according to patient characteristics, such as age, concomitant diseases already requiring antithrombotic drugs or at risk for bleeding. In this regard, the combination of multiple antithrombotic drugs represents a challenging scenario and was therefore the focus for multiple recent randomized controlled trials, and more are still to come. As the knowledge about platelets and the coagulation system has substantially evolved within the last few years, so should our approach to antithrombotic treatment. Finally, the ongoing global pandemic of coronavirus disease 2019 (COVID‑19) has also modified our antithrombotic strategies of acute ischemic events.

This issue will focus on current hurdles of antithrombotic treatments in patients with cardiovascular disease, proposing practical solutions to compelling clinical scenarios using a pathophysiology-oriented approach on the basis of current clinical evidence.

Prof. Giovanni Cimmino
Prof. Salvatore De Rosa
Guest Editors

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• Tissue factor
• Coagulation cascade
• Platelets
• Aggregation
• Thrombosis
• Acute coronary syndrome
• Stroke
• Peripheral artery disease
• COVID-19 pandemic