Background: The rupture of the fibrous cap overlying the lipid pool of atherosclerotic plaques is the leading cause of acute myocardial infarction. Plaque rupture often occurs at the location of stress concentration and in stress levels much lower than those required for plaque disruption with monotonic tension. Based on these observations, it has been hypothesized that mechanical fatigue caused by pulsatile blood pressure is the main mechanism underlying atherosclerotic plaque rupture. Aim: To quantify the effect of mean and pulse pressure on the fatigue process and subsequent plaque rupture in realistic models of human coronary atherosclerotic plaques. Methods: Eight samples of left anterior descending coronary artery with type V plaques were obtained by endarterectomy surgery. Based on histological examination, the different components of the atherosclerotic plaques were located (fibrous cap; lipid pool; calcification). The plaque geometry was constructed (Abaqus software) and the stiffness of different components of the atherosclerotic plaque was allocated based on published data. Pulsatile blood pressure was applied as the external load. Stress distribution within each model was estimated using finite element method. The initial crack was located at the highest stress concentration and its propagation was modelled in a stable way until it reached the lipid pool or arterial wall. The number of fatigue cycles required for plaque rupture was calculated for different pulse and mean pressures based on fracture mechanic rules. Results: The effect of blood pressure was consistent for different models and various tissue properties tested. The location of initial crack formation and the direction of crack propagation were not affected by blood pressure variation. However, the rate of crack propagation changed significantly in response to alteration of pulse and mean pressure. For the same pulse pressure of 60 mmHg, decreasing the mean pressure from 120 to 100 mmHg (17% decrease) increased the cycles to rupture by 27±6% (1.6% increase per % decrease in mean pressure, or 1.4 %/mmHg). Decreasing the pulse pressure from 80 to 60 mmHg (25% decrease) increased the fatigue life by 154±18% (6.2% increase per % decrease in pulse pressure, or 7.7 %/mmHg). Further reduction of pulse pressure to 40 mmHg resulted in 275±29 % increase in fatigue life (5.5% increase per % decrease in pulse pressure, or 6.9 %/mmHg). Conclusions: Modelling showed that pulse pressure has greater influence than mean pressure on the rate of crack propagation in atherosclerotic plaques. Reduced pulse pressure potentially prolongs time for plaque rupture.
|Number of pages||1|
|Publication status||Published - Nov 2018|
|Event||High Blood Pressure Research Council of Australia Abstracts from the Joint HBPRCA, AAS and AVBS Meeting 2018 - Glenelg, Australia|
Duration: 27 Nov 2018 → 30 Nov 2018
|Conference||High Blood Pressure Research Council of Australia Abstracts from the Joint HBPRCA, AAS and AVBS Meeting 2018|
|Period||27/11/18 → 30/11/18|