Pathophysiology of Acute Coronary Syndrome

Abstract

Despite improvements in interventional and pharmacological therapy for atherosclerotic disease, it is still the leading cause of death in the developed world. Hence, there is a need for further development of more effective therapeutic approaches. This requires better understanding of the molecular mechanisms and pathophysiology of the disease. Recent research in the last decade has changed our view of acute coronary syndrome (ACS): from a mere lipid deposition to an inflammatory disease; from ACS exclusively due to plaque rupture to the novel definitions of plaque erosion or calcified nodule; from the notion of a superimposed thrombus with necessary lethal consequences to the concept of healed plaques and thrombus contributing to plaque progression. In the hope of improving our understanding of ACS, all these recently discovered concepts are reviewed in this article.

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

“…At 15 days post-surgery, we observed a significant increase of plaque area, mainly due to necrotic core enlargement. Plaque necrosis is a characteristic hallmark of atherosclerotic lesions that causes acute atherothrombotic vascular disease [9][10][11] . Our finding of a post-surgery increase of necrotic core area may reflect increased plaque vulnerability and could, at least partly, explain the increased incidence of cardiovascular events after major orthopedic surgery.…”

“…Plaque instability is not only related to factors such as fibrous cap strength and intra-plaque hemorrhage, but also to the necrotic core area which, in turn, are all influenced by intraplaque inflammation [8][9][10][11] .…”

18F-sodium fluoride positron emission tomography assessed microcalcifications in culprit and non-culprit human carotid plaques

“…[6][7][8] Currently, plaque thickness and intraplaque processes, such as inflammation and microcalcification, are seen as important contributors to vulnerability. These processes have become targets of various molecular imaging techniques, as they potentially allow non-invasive risk stratification of individual patients with carotid artery stenosis.…”

Chewed ticagrelor tablets provide faster platelet inhibition compared to integral tablets

“…Following an atherosclerotic plaque rupture or erosion, platelet aggregation leads to thrombus formation and an acute ischemic event. (1) Ticagrelor is a direct acting and reversibly binding P2Y12 receptor inhibitor that is highly recommended in clinical guidelines for treatment of patients with acute coronary syndromes (ACS). (2)(3)(4) In patients with stable angina pectoris (SAP), administration of 180 mg loading dose (LD) of ticagrelor resulted in a more rapid and stronger inhibition of platelet reactivity (PR) compared to clopidogrel.…”