Dynamics of coronary occlusion in the pathogenesis of myocardial infarction.
In most coronary artery stenoses in humans, lumen size decreases in response to acute vasoconstriction, reduced aortic pressure or passive collapse. Because the effects of vasoconstriction and plaque rupture with thrombus formation are additive, in some cases total cessation of flow may result from only minimal obstruction by thrombus. This hypothesis was investigated with use of a previously developed model of the coronary circulation in which the pressure drop across and flow through an arterial stenosis were determined by standard hemodynamic equations. The vessel wall was assumed to be composed of pliable and rigid sections, as is the case in most arterial stenoses in humans. The computer analysis was conducted for a rigid stenosis and for a dynamic stenosis in which proximal artery constriction and distal collapse were simulated. Plaque rupture with subsequent thrombus formation was simulated as a decrease in lumen area without effect on the arterial wall. Compared with a dynamic stenosis, a rigid stenosis required a significantly larger thrombus for vessel occlusion. Thrombus formation equal to the nonobstructed area of the lumen was required to occlude a rigid vessel; a 60% stenotic vessel required a 40% plaque rupture with thrombus formation for occlusion. However, for a dynamic stenosis, if vasoconstriction and passive collapse were simulated, small plaque ruptures led to vessel occlusion: a 60% stenotic vessel required only a 12% plaque rupture with thrombus formation for occlusion. This analysis indicates that even mild coronary lesions may be responsible for myocardial infarction, suggesting that vasomotion may be a very important element in the pathogenesis of most myocardial infarcts.
Philadelphia Heart Institute, Presbyterian Medical Center, Pennsylvania 19104.
W P
WP
Santamore
B W
BW
Yelton
J D
JD
Ogilby
D003198:Computer Simulation; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000150:complications* / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000209:etiology*; D014661:Vasoconstriction / Q000502:physiology