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Pathophysiology and mechanisms of Acute Coronary Syndromes: atherothrombosis, immune-inflammation, and beyond

ABSTRACT Introduction The pathophysiology of atherosclerosis and its acute complications, such as the Acute Coronary Syndromes (ACS), is continuously under investigation. Immunity and inflammation seem to play a pivotal role in promoting formation and grow of atherosclerotic plaques. At the same time, plaque rupture followed by both platelets’ activation and coagulation cascade induction lead to intracoronary thrombus formation. Although these phenomena might be considered responsible of about 90% of ACS, in up to 5–10% of acute syndromes, a non-obstructive coronary artery disease (MINOCA) might be documented. This paper gives an overview on atherothrombosis and immuno-inflammation processes involved in ACS pathophysiology, also emphasizing the pathological mechanisms potentially involved in MINOCA. Areas covered The relationship between immuno-inflammation and atherothrombosis is continuously updated by recent findings. At the same time, pathophysiology of MINOCA still remains a partially unexplored field, stimulating the research of potential links between these two aspects of ACS pathophysiology. Expert opinion Pathophysiology of ACS has been extensively investigated; however, several gray areas still remain. MINOCA represents one of these areas. At the same time, many aspects of immune-inflammation processes are still unknown. Thus, research should be continued to shed a brighter light on both these sides of “ACS” moon.