Giovanni Cimmino, Francesco S. Loffredo, Alberto Morello, Saverio D’Elia, Raffaele De Palma, Plinio Cirillo and Paolo Golino* Pages 110 - 117 ( 8 )
In the last twenty years, our comprehension of the molecular mechanisms involved in the formation, progression and complication of atherosclerotic plaque has advanced significantly and the main role of inflammation and immunity in this phenomenon is now largely accepted. Accumulating evidence highlight the crucial role of different inflammatory and immune cells, such as monocytes and T-lymphocytes, in the pathophysiology of atherosclerotic lesion, particularly in contributing to its complications, such as rupture or ulceration. According to the new terminology, “vulnerable plaque” identifies an inflamed atherosclerotic lesion that is particularly prone to rupture. Once disrupted, prothrombotic material is exposed to the flowing blood, thus activating coagulation cascade and platelet aggregation, ultimately leading to acute thrombus formation within the coronary vessel. To date this is the key event underlying the clinical manifestations of acute coronary syndromes (ACS).The degree of vessel occlusion (complete vs. incomplete) and the time of blood flow cessation will define the severity of clinical picture. This phenomenon seems to be the final effect of a complex interaction between different local and systemic factors, involving the degree of inflammation, type of cells infiltration and the rheological characteristics of blood flow at the site of plaque rupture, thrombogenic substrates within the atherosclerotic lesion and different soluble mediators, already present or acutely released in the circulating blood. This article will review currently available data on the pathophysiology of ACS, emphasizing the immunological and inflammatory aspects of vulnerable plaque. We may postulate that intraplaque antigens and local microenvironment will define the immune-inflammatory response and cells phenotype, thus determining the severity of clinical manifestations.
Atherosclerosis, inflammation, immunity, coagulation, thrombosis.
Department of Cardio-Thoracic and Respiratory Sciences, Section of Cardiology, Second University of Naples, Naples, Molecular Cardiology, International Centre for Genetic Engineering and Biotechnology, Trieste, Department of Cardio-Thoracic and Respiratory Sciences, Section of Cardiology, Second University of Naples, Naples, Department of Cardio-Thoracic and Respiratory Sciences, Section of Cardiology, Second University of Naples, Naples, Department of Clinical and Experimental Medicine, Section of Immunology, Second University of Naples, Naples, Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Department of Cardio- Thoracic and Respiratory Sciences, Section of Cardiology, Second University of Naples, S. Anna e S. Sebastiano Hospital, Via Tescione, 1 81100 Caserta