Atherosclerosis, platelets and thrombosis in acute ischaemic heart disease

Abstract

Atherosclerosis is the underlying reason for nearly all causes of coronary artery disease and peripheral arterial disease and many cases of stroke. Atherosclerosis is a systemic inflammatory process characterised by the accumulation of lipids and macrophages/lymphocytes within the intima of large arteries. The deposition of these blood borne materials and the subsequent thickening of the wall often significantly compromise the residual lumen leading to ischaemic events distal to the arterial stenosis. However, these initial fatty streak lesions may also evolve into vulnerable plaques susceptible to rupture or erosion. Plaque disruption initiates both platelet adhesion and aggregation on the exposed vascular surface and the activation of the clotting cascade leading to the so-called atherothrombotic process. Yet, platelets have also been shown to be transporters of regulatory molecules (micro-RNA), to drive the inflammatory response and mediate atherosclerosis progression. Here we discuss our current understanding of the pathophysiological mechanisms involved in atherogenesis - from fatty streaks to complex and vulnerable atheromas - and highlight the molecular machinery used by platelets to regulate the atherogenic process, thrombosis and its clinical implications.

2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation

“…Stan zapalny odgrywa kluczową rolę w destabilizacji blaszki miażdżycowej. Wciąż jednak nie wiadomo, co jest bodźcem wywołującym ostry stan zapalny [14,15]. Akywacja płytek krwi i ich agregacja na eksponowanej, trombogennej powierzchni pękniętej blaszki stanowią wczesny, istotny etap w patogenezie ACS [15,16].…”

“…Wciąż jednak nie wiadomo, co jest bodźcem wywołującym ostry stan zapalny [14,15]. Akywacja płytek krwi i ich agregacja na eksponowanej, trombogennej powierzchni pękniętej blaszki stanowią wczesny, istotny etap w patogenezie ACS [15,16]. Aktywowane płytki uwalniają substancje prozapalne i mitogeny do mikrośrodowiska, przede wszystkim powodując zmianę wła-ściwości chemotaktycznych, adhezyjnych i proteolitycznych w obrębie śródbłonka [16].…”

The Clinical Value of Copeptin in Acute Coronary Syndrome

“…Atherosclerosis is a systemic inflammatory process characterized by the accumulation of lipids and macrophages/lymphocytes within the intima of large arteries [2].…”

CXCL16 in Vascular Pathology Research: from Macro Effects to microRNAs

“…Although angiogenesis in the early stages of plaque formation has atheroprotective effects because it prevents the apoptosis of vascular smooth muscle cells and formation of lipid rich core, in advanced atherosclerosis, it could have a completely different effect. In advanced atherosclerosis, angiogenesis results in blood vessels becoming more fragile and susceptible to burst 92) . However, the simple prediction of miR-221 role in vascular pathology is not possible due to cell-specific functions.…”