Cardiovascular diseases (CVDs) are a group of disorders affecting the heart and the vasculature that represent the number one cause of mortality globally.1 Only in Europe, CVDs causes over 4 million deaths each year,2 accounting for 47% of all deaths in Europe. The most common underlying pathology in CVDs is atherosclerosis, which causes an ischaemia in the heart and in peripheral arteries. Atherosclerosis is defined as a chronic disease of the vasculature, whose architecture is slowly remodelled over time. This disease and remodelling process involves the interplay of numerous cell subtypes, including endothelial cells (ECs) (becoming dysfunctional), leukocytes and macrophages (triggering inflammation), and smooth muscle cells (which dedifferentiate or undergo apoptosis).3,4
Unstable atherosclerotic plaques can rupture, which results in arterial thrombosis. Thrombosis, the formation of blood clots, prevents blood flow, and triggers life-threatening clinical conditions in the arterial system, such as myocardial infarction (MI) and ischaemic forms of stroke (IS). Although MI and IS are usually acute events resulting from chronic atherosclerotic processes affecting coronary and carotid arteries, respectively, venous thromboembolism (VTE) is mainly caused by haemostatic or coagulation abnormalities.