INFLUENCE OF PLAQUE CONFIGURATION AND STRESS DISTRIBUTION ON FISSURING OF CORONARY ATHEROSCLEROTIC PLAQUES

To find out the types of atherosclerotic plaques that fissure and where they fissure, plaques from 85 patients who had died from coronary thrombosis were examined histologically. 67 of the plaques contained an eccentric pool of extracellular lipid in the intima; 42 (63%) of these plaques had fissured at the junction of the plaque cap with the more normal intima, and the other 25 (37%) had torn through the centre of the cap. Computer modelling of different forms of plaque showed that at systole eccentric pools of lipid concentrated stress on the plaque cap, especially near the edge of the plaque. When the lipid pool occupied less than 15% of the vessel circumference, and when the plaque cap was less stiff than the adjacent normal intima, the point of maximum stress was over the centre of the plaque. Computer modelling also showed that the distribution of circumferential tensile stress across the intima was radically altered by atherosclerotic plaques. Regions of high circumferential stress correlated well with the site of intimal tears found at necropsy. The histological findings showed that site of tearing was influenced by variation in the mechanical strength of cap tissue due to focal accumulation of foam cells. Focal weak points in the cap would explain tears which were not at the point of maximum stress.

[1]  F Litvack,et al.  A perspective of coronary disease seen through the arteries of living man. , 1987, Circulation.

[2]  Louis E. Teichholz,et al.  Angiographie morphology and the pathogenesis of unstable angina pectoris , 1985 .

[3]  H. N. Magoun Thomas, Springfield, Illinois , 1965 .

[4]  A. Chandler Mechanisms and frequency of thrombosis in the coronary circulation. , 1974, Thrombosis research.

[5]  W. F. Fulton,et al.  The coronary arteries : Arteriography, microanatomy, and pathogenesis of obliterative coronary artery disease , 1965 .

[6]  V. Fuster,et al.  Angiographic progression of coronary artery disease and the development of myocardial infarction. , 1988, Journal of the American College of Cardiology.

[7]  M J Davies,et al.  Plaque fissuring--the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. , 1985, British heart journal.

[8]  K. Carstairs The identification of platelets and platelet antigens in histological sections. , 1965, The Journal of pathology and bacteriology.

[9]  C. Swerdlow,et al.  Angiographic coronary morphology in survivors of cardiac arrest. , 1988, American heart journal.

[10]  M. J. Mitchinson,et al.  MACROPHAGES AND ATHEROGENESIS , 1987, The Lancet.

[11]  M. Davies,et al.  The pathological basis and microanatomy of occlusive thrombus formation in human coronary arteries. , 1981, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.

[12]  D C Levin,et al.  Significance of the Angiographic Morphology of Localized Coronary Stenoses: Histopathologic Correlations , 1982, Circulation.

[13]  V. Fuster,et al.  Angiographic evolution of coronary artery morphology in unstable angina. , 1986, Journal of the American College of Cardiology.

[14]  L Morgenstern,et al.  Coronary angioscopy in patients with unstable angina pectoris. , 1986, The New England journal of medicine.