Day, T. K.; Newman, E.

The dynamic forces contributing to arteriosclerotic plaque separation were studied in-vitro using fresh porcine arteries and artificial plaques of different thicknesses mounted on thin ferro-magnetic strips. The arteries were subjected to pulsatile perfusion using an apparatus in which dynamic and rheological variables could be varied and controlled. The plaques were held on the inner wall of the artery by the force exerted by an externally-mounted electromagnet. The pressure retaining the artificial plaque to the wall could be regulated by varying the power supplied to the magnet. The separation of the plaque from the vessel wall, characterised by the appearance of a cleft beneath it with each pulsation, was observed with M and B mode ultrasound. In this way the critical detachment force (CDF), acting on the plaque at the moment of first separation of the plaque, could be calculated. 10 arteries were used during the study, using multiple observations in single arteries to reduce inter-artery variation. The CDF was found to correlate closely with pulse pressure (r= 0.9, p<0.001). Wall stiffness was found to determine pulse pressure when other parameters were kept constant, irrespective of whether the stiffness was induced by raising mean arterial pressure or by stiffening the artery artificially with formalin. In comparing plaques producing approximately 20% and 40% occlusion there was roughly a doubling of CDF, but no further increase between 40% and 60% (t = 4.0, p<0.001). Longitudinal tortuous movement of the artery (arc bending) had a profound effect on CDF, increasing progressively with the angle of bend (Rs 1.0, p <0.001). In this model the main dynamic contributions to plaque stress are: (i) moderate stenosis in the presence of sustained flow; (ii) high pulse pressure, to which arterial wall stiffness in distributive arteries contributes (iii) arc bending. The clinical implications of the findings of this study are discussed, and it is proposed that recurrent dynamic wall stress, in addition to its direct effects on the plaque, may also play a part in the inflammatory determinants of plaque vulnerability.