The mechanistic relationships between hemorheological characteristics and cardiovascular disease.

Historically, the approach to atherogenesis research has been focused on factors that primarily include vessel wall histology, blood and vessel wall biochemistry, clotting factors and platelets. This approach can be referred to as the 'biochemical' approach. We now recognize that atherosclerosis is an ongoing sterile process that starts with functional impairment of the arterial endothelium. However, the cause of the endothelial injury that initiates this process has not yet been identified. This commentary article proposes that the vasculature is a dynamic organ in which the initiating event leading to atherosclerosis is a protective, adaptive response of the endothelium to a mechanical injury related to the work of the heart (WOH). Evidence is presented that this mechanical injury is readily explained by changes in blood rheology. This represents a paradigm shift from a strictly biochemical approach to our understanding of the atherogenic process to a biomechanical one. Elevated whole blood viscosity (WBV) has been independently correlated with increased carotid intima media thickness and major cardiovascular disease risk factors, including hypertension, smoking, diabetes, advanced age, elevated low density lipoprotein cholesterol, and decreased high density lipoprotein cholesterol. These associations have led several authors to propose increased WBV as a unifying factor linking major cardiovascular risk factors and atherosclerosis. Blood rheology has been more difficult to accurately study than other risk factors for cardiovascular disease, explaining why it may be an overlooked factor in our understanding of cardiovascular disease. The science of rheology is now entering a new phase of acceptance with the development of a new scanning capillary rheometer which, unlike conventional rheometers, easily and accurately determines whole blood viscosity as a function of shear rate.