Atherosclerosis, and Newton, Poiseuille, Reynolds and Prandtl

Abstract

Atherosclerotic fibrous plaques typically manifest at inlets of branches and in expansions etc. of large elastic arteries. A resting man with a surface area of 1.78m2produces energy at a rate of 100 W (86kcal/h), mainly by core organs. Core blood heat is convected to arterial walls and conducted through tissues to be lost from body surfaces. High losses are compensated by an increase in the basal metabolic rate, and vice versa. In laminar flow, the fluid–tube wall heat transfer coefficient is higher close to tube inlets than downstream. Unless lipoprotein etc. suspects are exceptions from the rule that an increase in temperature speeds up chemical reactions, transfer of core heat may contribute to plaque localization. In laminar flow, heat transfer is little influenced by viscosity. Hence correlations between blood viscosity and cardiovascular disease (CVD) may reside in other mechanisms: viscosity limits flow relatively more in small than in large arteries, and viscosity-linked thixotropic properties of blood increase resistance to flow in capillaries and postcapillary venules (exchange vessels). The exchange vessels of large arteries belong to the vasa vasorum, in which reduction of flow induces diffuse parent artery wall changes found also in plaques. Correlations between blood viscosity and peripheral symptoms of CVD may be explained by reduced flow in vascular loops of symptomatic organs, even if maximum flow is limited by upstream plaques. Physiological differences in the type of blood flow and in blood–tissue exchange between vessels of different size may shed light on apparent paradoxes in research on CVD.