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In patients with ACVD, acute mesenteric ischemia results from either plaque rupture and in-situ complete thrombosis, or occlusive thromboembolism from proximal plaque.
The chain of reasoning is as follows: The biomarker of plaque instability is found in atherosclerotic plaques and is more abundant in plaques with unstable characteristics than in plaques with stable characteristics an increased concentration of the biomarker in the circulation signals that the patient has plaques with unstable characteristics that are more prone to rupture; and plaque rupture leads to unstable angina or AMI.
Two main cell types are involved in plaque rupture, smooth muscle cells and inflammatory white blood cells, called macrophages.
Only 1 in 500 LDL particles may be associated with Lp-PLA2, and LDL may be elevated for decades before Lp-PLA2 rises, signaling a change from chronic atherosclerosis to acute risk for plaque rupture.
Smaller plaques susceptible to plaque rupture can cause occlusive events.
This risk is the result of increased inflammation in atherosclerotic plaques, contributing to plaque rupture.
In the first-of-its-kind study, ultrasound tests to assess plaque rupture were performed on 174 consecutive heart attack patients.
However, regular exercise both protects against plaque rupture and improves basal vagal tone.
One might ask what triggers the plaque rupture because, if we know the reason(s) that precipitate it, we would be able to take measures to prevent a rupture and, thus, the heart attack.
Researchers identified proteins associated with the biological processes underlying vulnerable plaque development and showed they could be measured in a patient's blood up to 5 years prior to a plaque rupture and the ensuing heart attack.
Quertermous and team demonstrated that these proteins could be measured, analyzed and used to assess the risk of plaque rupture and heart attack as early as five years prior to the event.
Plaque rupture is the usual cause of most heart attacks and many strokes.