Exemplos de uso de Plaque rupture em Inglês e suas traduções para o Português
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Have plaque rupture, while the remaining 25% have.
However, in some patients, plaque rupture was not detected.
Emotional stress andextenuating exercise might cause plaque rupture.
The presence of plaque rupture, however, was prevalent in only 40% of cases.
Figure 1 illustrates a classical example of an acute thrombus overlying plaque rupture.
The presence of plaque rupture, plaque hemorrhage or thrombus was assessed.
It is known that inflammation mediates all stages of atherosclerosis from initiation to progression, and eventually plaque rupture.
Taking into account sex and age, plaque rupture is more likely for older women.
In t2dm, the matrix metalloproteinase 9(mmp-9) present high levels andparticipate in atherosclerotic plaque rupture, altering its stability.
In acute coronary syndromes, plaque rupture is induced by the inflammatory process in the atherosclerotic tissue.
The chronic inflammatory process can develop into an acute clinical event by the induction of plaque rupture, leading to acute coronary syndromes.
Unabated atherosclerosis may lead to plaque rupture and introduction of vascular wall constituents to the bloodstream.
In the right coronary artery, there was a thrombus undergoing organization in the distal bed, and a recent,occlusive thrombosis with plaque rupture at the 2nd, 3rd, and 6th centimeters Figure 6.
There were also areas of plaque rupture and hemorrhage, with acute thrombosis in the first and second centimeters of that artery Figs. 4 and 5.
Of the 25 culprit lesions analyzed in this study, plaque rupture was identified in 9 36% Figure 2.
Although most, if not all plaque ruptures originate from TCFAs, plaque rupture is not the only mechanism of coronary thrombosis.
However, the time interval between surgery and death in patients with plaque rupture was longer 7.8± 4.4 days versus 4.4± 4.8 days; p 0.047.
Qualitative analysis: plaque rupture was defined as an intraplaque cavity in communication with the lumen, in the presence of the fibrous-cap residues or fragments.
Autopsy studies show that 75% of the fatal infarctions have plaque rupture, while the remaining 25% have endothelial erosion.
The information about the size of the plaque is not enough to differentiate between unstable and stable plaques and, therefore,it is unable to predict the risk of plaque rupture.
Coronary thrombosis, usually occlusive andsecondary to atherosclerosis plaque rupture, is the most common myocardial infarction cause.
The increases in fibrinogen, fibrin and products of fibrinogen degradation can lead to sclerosis of the vessel walls and to narrowing of the lumen,in addition to contributing to plaque rupture.
Moreover, F-FDG PET could be used to predict the risk of future plaque rupture and to monitor the effects of atheroma-modifying therapies.
The silent onset ofcardiovascular diseases occurs on arterial walls and progressesthrough well-known mechanisms including endothelial dysfunction, inflammation, plaque formation and vascular remodeling,lateratherosclerotic plaque rupture, andthrombosis6.
Histological analysis indicates that plaque rupture, fibrous cap atheroma,plaque erosion and calcified nodules generate major cvd fatalities.
In relation to the event triggering the thrombosis and subsequent coronary-artery occlusion,it is well established in the literature that plaque rupture is responsible for most cases 60.
These clinical entities are the consequence of atherosclerotic plaque rupture or significant fissure, with platelet aggregation and the formation of subocclusive or occlusive thrombi 1,2.
Inflammatory processes have been shown to play a role in all aspects of acute coronary syndrome,from the pathogenesis of atherosclerosis to plaque rupture and death of myocardial cells.
It was determined that the cap thickness of TCFA associated with plaque rupture was under 65 micron, well under the resolution capacity of IVUS.
Kramer et al15, in 2009,reported that the time between plaque rupture and thrombi formation is still unpredictable, and Rittersma et al12 have also demonstrated a discrepancy between thrombotic process and onset of infarction symptoms.