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Arterial stress from intraluminal pressure modified by tissue pressure offers a complete explanation for the distribution of atherosclerosis.

Pressure-induced arterial stress is probably the principle factor in the localization of atherosclerotic disease. The occurrence of lesions at the bifurcations and ostia of arteries seems to be caused by the concentration of stress at these locations. Other puzzles and paradoxes regarding the distribution of atherosclerosis can be explained by dynamic extra-arterial pressure (DEAP): fluctuations in tissue pressure that occur with movement, body position, and the beating of the heart. These tissue pressures, both above and below atmospheric pressure, change the transmural pressures in arteries and thereby either retard or accelerate atherogenesis. The DEAP hypothesis predicts that physical fitness increases extra-arterial tissue pressure, which protects important arteries from high transmural pressure. Deconditioning is expected to have the exact opposite effect, producing the equivalent of localized hypertension in the cerebral, internal carotid, coronary, abdominal aorta, and lower extremity arteries.