Abstract
BackgroundAtherosclerotic plaque is subjected to a repetitive deformation due to arterial pulsatility during each cardiac cycle and damage may be accumulated over a time period causing fibrous cap (FC) fatigue, which may ultimately lead to rupture. In this study, we investigate the fatigue process in human carotid plaques using in vivo carotid magnetic resonance (MR) imaging.MethodTwenty seven patients with atherosclerotic carotid artery disease were included in this study. Multi-sequence, high-resolution MR imaging was performed to depict the plaque structure. Twenty patients were found with ruptured FC or ulceration and 7 without. Modified Paris law was used to govern crack propagation and the propagation direction was perpendicular to the maximum principal stress at the element node located at the vulnerable site.ResultsThe predicted crack initiations from 20 patients with FC defect all matched with the locations of the in vivo observed FC defect. Crack length increased rapidly with numerical steps. The natural logarithm of fatigue life decreased linearly with the local FC thickness (R2 = 0.67). Plaques (n=7) without FC defect had a longer fatigue life compared with those with FC defect (p = 0.03).ConclusionFatigue process seems to explain the development of cracks in FC, which ultimately lead to plaque rupture.
Highlights
Rupture of atherosclerotic plaque with resulting thromboembolism is a predominant cause of ischemic events such as myocardial infarction and cerebrovascular accidents [1]
Fatigue process seems to explain the development of cracks in fibrous cap (FC), which lead to plaque rupture
Angiography identifies only those lesions encroaching significantly upon the lumen, and there is a poor correlation between the angiographic appearance and subsequent risk of plaque rupture, e.g. more than 80% of rupture events occur in lesions that cause less than 70% luminal stenosis in coronaries [2]
Summary
In total 27 MR slices (one from each patient) were used in this study, 20 with FC rupture or ulceration and 7 without any FC defect. This indicated that once the fatigue crack was initiated, it developed exponentially during further loading cycles. It is impossible to observe the in vivo crack propagation with current imaging technique, comparing the fatigue life of plaques with and without FC rupture or ulceration might provide indirect support for this hypothesis. With this consideration, the fatigue simulation was performed with the MR slice at the most stenotic site of 7 randomly-chosen patients with no shown rupture.
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