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Blood Viscosity in Myocardial Perfusion

Blood viscosity represents the thickness and stickiness of blood and is defined as its inherent resistance to flow. In hemodynamic theory, arterial blood pressure should decrease due to increases in flow resistance caused by blood viscosity. However, as long as the coronary artery is not significantly blocked (i.e., < 50% stenosis), blood pressure distal to the coronaries will be almost identical to that of the aorta, even with elevated blood viscosity. This can be mathematically proved using the Bernoulli and Poiseuille equations [1].  In other words, even though elevated blood viscosity worsens shear stress and chronic inflammation, all things held equal, thicker blood does not immediately reduce blood flow at the coronaries.

Without existing coronary atherosclerosis, the real and hidden cardiac risk of elevated blood viscosity arises in the flow of capillaries buried in the myocardium. Blood flow in the capillaries is characterized by extremely slow velocity (i.e., < 0.01 cm/s) [2], profoundly increasing the tendency of red blood cells to aggregate. Since the diameter of erythrocytes (approximately 5-8 microns) is comparable with or slightly less than the diameters of capillary vessels [3], stagnation of blood flow can occur at the smallest vessels if red blood cell aggregation is excessive [4].

Blood Flow Regimes

When blood is flowing slowly through arterioles and capillaries, blood viscosity necessarily increases as the aggregated erythrocytes increase friction at the vessel walls. In contrast, systolic flows through large arteries are characterized by well-separated and dispersed erythrocytes, making the blood thin by comparison. When compared to coronary flows, blood viscosity in the microvasculature is approximately three to eightfold higher which results primarily from the aggregation behavior of erythrocytes [5, 6].

There are a number of variables that affect the aggregation of erythrocytes in microvessels, including hematocrit, plasma protein concentrations (i.e., fibrinogen and immunoglobulins), and low-density lipoprotein [4]. Naturally, these are among the principal determinants of blood viscosity [4, 7-9]. 

The microvasculature can act as a bottleneck for oxygen delivery to the myocardium. In asymptomatic coronary disease, for example, patients without significant atherosclerotic plaques in the coronary artery can experience angina, which is known to be caused by inadequate microvascular perfusion to the myocardium [10, 11].

Clinical Evidence

In a 10-year prospective study to assess the clinical usefulness of blood viscosity for cardiovascular risk assessment in hypertensive males, 331 middle-aged men with newly diagnosed essential hypertension (age at entry 40-64 years, average blood pressure 151/95 mmHg) were assessed for blood viscosity at low and high shear rates. After taking into account several established cardiovascular risk factors in a Cox survival analysis, elevated low-shear blood viscosity conferred an increased risk for cardiovascular events (top vs. bottom tertile hazard ratio = 3.42, 95% confidence interval = 1.4-8.4, p = 0.006; middle vs. bottom tertile hazard ratio = 2.25, 95% confidence interval = 0.9-5.6, p = 0.09) [12].

Figure 1 shows that the event-free survival rate was significantly lower in adult males recently diagnosed with essential hypertension having elevated low shear-rate blood viscosity, compared to those with normal low shear-rate blood viscosity. In hypertensive men, an increased blood viscosity at low shear rate was shown to be an independent predictor of cardiovascular events. Accordingly, assessments of low-shear blood viscosity may enable earlier intervention and reduce the risk of angina and future cardiovascular events.

March 2014 CommentaryFigure 1. Cardiovascular event-free survival curves in 331 middle-aged hypertensive men divided by tertiles of the distribution of whole-blood viscosity at low shear rate  [12].


1.  B. Munson, T. H. Okiishi, W. Huebsch, and D. Young, "Fundamentals of Fluid Mechanics," ed: New York: John Wiley & Sons Inc, 2013.

2.  U. Dinnar, Cardiovascular fluid dynamics vol. 264: CRC Press Boca Raton, FL, 1981.

3.  J. E. Hall, Guyton and Hall Textbook of Medical Physiology, 12th ed. Philadelphia: Saunders, 2011.

4.  O. K. Baskurt and H. J. Meiselman, "Erythrocyte aggregation: Basic aspects and clinical importance," Clinical Hemorheology and Microcirculation, vol. 53, pp. 23-37, 2013.

5.  E. W. Merrill, E. R. Gilliland, G. Cokelet, H. Shin, A. Britten, and R. E. Wells, Jr., "Rheology of human blood, near and at zero flow. Effects of temperature and hematocrit level," Biophys J, vol. 3, pp. 199-213, May 1963.

6.  S. Chien, "Blood rheology in myocardial infarction and hypertension," Biorheology vol. 23, pp. 633-53, 1986.

7.  J. F. Stoltz, M. Singh, and P. Riha, Hemorheology in Practice. Washington DC: IOS Press, 1999.

8.  H. C. Kwaan, "Role of plasma proteins in whole blood viscosity: a brief clinical review," Clin Hemorheol Microcirc, vol. 44, pp. 167-76, 2010.

9.  S. Chien, "Determinants of blood viscosity and red cell deformability," Scandinavian Journal of Clinical & Laboratory Investigation, vol. 41, pp. 7-12, 1981.

10.  K. M. Kent, D. R. Rosing, C. J. Ewels, L. Lipson, R. Bonow, and S. E. Epstein, "Prognosis of asymptomatic or mildly symptomatic patients with coronary artery disease," The American journal of cardiology, vol. 49, pp. 1823-1831, 1982.

11.  R. Hachamovitch, "Prognostic characterization of patients with mild coronary artery disease with myocardial perfusion single photon emission computed tomography: Validation of an outcomes-based strategy," Journal of Nuclear Cardiology, vol. 5, pp. 90-95, 1998.

12.  G. Ciuffetti, G. Schillaci, R. Lombardini, M. Pirro, G. Vaudo, and E. Mannarino, "Prognostic impact of low-shear whole blood viscosity in hypertensive men," Eur J Clin Invest, vol. 35, pp. 93-8, Feb 2005.


LAST UPDATED: 2014-12-30 


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