Ask your physician or your cardiologist 

Why is atherosclerosis region-specific? Why do the blockages in arteries responsible for heart attacks and strokes occur in some regions of the body and not in others? 

Why do these blockages, or lesions, form in the large vessels close to the heart, feeding the heart and brain (Region I), but not in the arteries of the arms or in a woman’s mammary arteries? 

For decades the region and site-specificity of lesions has long established that hemodynamic, or blood flow, forces were the culprit responsible for arterial plaques. 

Is the root cause of cardiovascular disease biomechanical? 

If, for instance, LDL cholesterol or some other biochemical stimulus was the primary culprit behind the blockages in arteries, wouldn’t we expect to see them form more uniformly throughout the body? 

In fact, lesions form in specific arteries, those that are close to the heart and absorb the force of blood flow pumped from the left ventricle. The exception, which happens to confirm the rule, is peripheral artery disease (PAD), where occlusions form in the arteries of the legs (Region II). In these cases, the pull of gravity causes blood flow to accelerate when a person is standing upright, elevating blood pressure in the legs and increasing friction. 

Lesion-prone sites in the vessels are those that encounter the most turbulent blood flow. This understanding allows us to zero in on vulnerable blood: blood that is too thick or sticky, which increases friction and causes mechanical abrasion, injury and inflammation at the arterial wall. Blood viscosity is the key parameter that controls the forces of blood flow including friction and strain in the vessels, as well as blood pressure. Elevated blood viscosity is the root cause of the pre-inflammatory injury setting in motion the cascade of events that result in the hardening and thickening of arterial walls. 

A simple analogy—one that patients can easily understand—is that of a gardener whose hands gradually become calloused after repeated friction and abrasion from tools, stones, and other rough materials. 


Holsworth RE, Cho YI. “Hyperviscosity Syndrome: A Nutritionally-Modifiable Cardiovascular Risk Factor.” Advancing Medicine with Food and Nutrients, Second Edition. Ed. Ingrid Kohlstadt. Boca Raton: CRC Press. 2012. 


Davies PF. Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology. Nat Clin Pract Cardiovasc Med. 2009; 6:16-26.

Malek AM, Alper SL and Izumo S. Hemodynamic shear stress and its role in atherosclerosis. JAMA 1999;282:2035-2042. 

Langille BL, O’Donnell F. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science. 1986; 231:405-407.

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