Increasing evidence supports the importance of hemodynamic forces that are directly related to the work of the heart as the primary triggering event of atherosclerosis and atherothrombosis. The factors that primarily determine the work of the heart include systolic blood pressure (BP), blood viscosity, and the volume of blood the myocardium has to pump.
The relationship between BP and viscosity is such that, given a constant systolic BP, if blood viscosity increases, then the total peripheral resistance (TPR) will necessarily increase, thereby reducing blood flow. Conversely, when viscosity decreases, blood flow and perfusion will increase. Because of the dependence of systemic arterial BP on cardiac output and TPR, if blood viscosity and TPR rise, systolic BP must then increase for cardiac output to be maintained. Consequently, blood viscosity has been established as a major determinant of the work of the heart and tissue perfusion [1]. Since increased viscosity requires a higher BP to ensure the same circulating volume of blood, both the burden on the heart and the forces acting on the vessel wall are directly modulated by changes in blood viscosity.
Three important studies helped establish the relationship between blood pressure and blood viscosity. The earliest study observed 49 normal subjects and 49 patients with untreated essential hypertension, showing a direct correlation between BP and blood viscosity among both normotensive and hypertensive subjects (p<0.001). Systolic blood viscosity was 8 to 10% higher in hypertensive patients compared with normotensive controls, and diastolic blood viscosity was 16 to 28% higher in hypertensive patients. Subgroups each comprised of 25 subjects having matched hematocrits were also compared, and viscosity remained significantly higher in hypertensive subjects (p<0.05). [2]
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