Roncalli et al., "Plaque rupture
and morphological characteristics of the culprit lesion in acute coronary syndromes without significant angiographic lesion: analysis by intravascular ultrasound," Annales de Cardiologie et d'Angeiologie, vol.
The same reason may explain why no statistical difference was found in plaque rupture
while a significant difference was found in TCFA between non-O type group and O-type group in this study.
In addition, G allele carriers were significantly more prone to myocardial infarction.12 In patients with acute myocardial infarction and unstable angina, the ones suffering from plaque rupture
have higher MMP-9 levels than those without, and the patients have more obvious 1562C-G polymorphism than the controls do.
This process is accentuated by intra-plaque hemorrhage and plaque rupture
with resultant thrombus formation.
Our work therefore suggests that reducing MMP-14 activity and increasing that of TIMP-3 could be valid therapeutic approaches to reduce plaque rupture
and myocardial infarction.
The expression of intimal neovessels is directly related to the stage of plaque development, the presence of symptomatic disease, and the risk of plaque rupture
. Angiogenesis is involved in the development of atherosclerosis and associated with clinical syndromes in the coronary circulation and in the context of symptomatic carotid occlusive disease [14-16].
The process of vascular plaque rupture
, hemorrhage, thrombosis, and healing is considered to be pathologically central to the chronic progression of plaque size and vascular obstruction.
A mechanistic analysis of the role of microcalcifications in atherosclerotic plaque stability: potential implications for plaque rupture
. Am J Physiol Heart Circ Physiol.
Indeed, it has been widely demonstrated that oxygen radicals are involved in plaque rupture
contributing to thromboembolism, thus resulting in acute coronary syndrome (ACS).
The knowledge will also lead to find the most vulnerable sites for the plaque rupture
Therefore, these cells are very well equipped for migration into inflammatory tissue such as atherosclerotic plaques where they may increase plaque instability with subsequent plaque rupture
. It is unknown whether there is true antigen-specific responsiveness involved as these cells can also be found within inflammatory tissue of the joint, gut or muscle in unrelated diseases like rheumatoid arthritis, colitis, and dermatomyositis [25-27].
and subsequent thrombosis at the site of the plaque rupture
are the most common underlying pathophysiologic mechanisms of ACS [4,5].