Pulse Pressure, Blood Flow, and Atherosclerosis

Abstract

See Original cOntributiOn page 1055B lood vessels are exposed to two kinds of dynamic mechanical forces. One of them is shear stress and the other is the cyclic strain of the vascular wall, which, according to the Laplace's law, is mainly determined by cyclic change of blood pressure (BP). While shear stress directly affects endothelial cells, BP changes (and the resulting changes in arterial wall strain) influence all structures of the arterial wall. Arteries are permanently exposed to a basal stretch, which is related to mean BP, and to a pulsatile stretch owing to pulse pressure (PP). Cyclic changes in the intramural tension have recently been recognized an important factor in the pathogenesis of atherosclerosis and acute coronary syndromes. 1 The study by Khoueiry et al. 2 fits well into list of recent research investigating the relation between BP, arterial stiffness, and atherosclerosis. 3,4 Nowadays, there is no doubt about the presence of significant relation between the pulsatile BP component and atherosclerosis, but these links are in fact bidirectional. On one hand, diffused atherosclerotic plaques impair the elastic properties of the arterial wall (although unstable, soft, and lipid-rich plaques do not impair arterial compliance), whereas on the other hand, an increased stiffness enhances the pulsatile component of BP, leading to the progression of atherosclerotic alterations. Taken together, these relations are responsible for a vicious circle. 5 It should be, however, emphasized that low values of PP are required for the development of a differentiated and fully functional phenotype of vascular wall cells, as well as for the regulation of migratory properties, proliferation, and matrix turnover. 1 A number of studies have shown the correlation between central PP and the extent of coronary atherosclerosis. 5 In the population studied by Khoueiry et al. 2 aortic PP was higher in subjects with right coronary artery (RCA) stenosis compared to those with stenosis in the left coronary artery (LCA). This could be due to the difference in blood flow pattern between LCA and RCA (as suggested by Khoueiry et al. 2 ) or earlier (at lower level of BP) atherosclerotic plaque development in LCA compared to RCA. Although the former explanation cannot be fully excluded due to crosssectional nature of the study it should be underscored that systolic, diastolic, and mean pressure were similar in the study groups as was the mean number of antihypertensive drugs used per one participant (unfortunately the doses of drugs are unknown). Another elucidation could be stiffer aorta in RCA diseased patients as opposed to subjects with stenosed LCA, which, however, could not be explained on the basis of the current knowledge. Although the authors performed multivariate analysis the reader should remember that the study groups differed in respect of several important variables, including heart rate, which in turn is one of major determinants of PP. The selection bias or an unrecognized difference in the studied groups should be ...

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“…Obesity is related with hypertension [5,6,7,8].Obesity will trigger the occurrence of hypertension because if a person's body weight increases then the volume of blood also increases so the burden of the heart to pump blood also increases [9]. Fat accumulation due to obesity raises plaque that will clog the blood flow so that blood pressure increases [4,10].…”

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