Key result
Modest mural thickening due to disease may act as a lever translating physiologic medial smooth muscle shortening into critical luminal obstructions, potentially causing acute luminal occlusion.
Theoretical modeling demonstrates that structural wall thickening in diseased coronary arteries can amplify normal physiologic vasomotion into critical luminal obstruction, offering an alternative explanation to true arterial spasm.
May link modest stenosis to acute events via amplified vasomotion; leaves open in vivo validation.
Available estimates of the ratio of wall thickness to luminal radius of human coronary arteries and certain geometrical assumptions were used to calculate the amounts of vascular smooth muscle shortening required to produce specific changes in luminal diameter for hypothetical "normal" and stenotic arteries. The results indicate that even modest mural thickening due to disease may act as a "lever" in translating physiologic degrees of medial smooth muscle shortening into critical luminal obstructions, providing the diseased segment maintains some pliability. The possibility of acute luminal occlusion occurring at stenotic sites as the result of "normal" vasomotion is illustrated. The appropriate use of the term coronary arterial "spasm" is discussed in light of these observations.
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R.N. MacAlpin (1980) studied Coronary arterial constriction. Dynamic vascular wall thickening was evaluated on Amount of vascular smooth muscle shortening required to produce specific changes in luminal diameter. Modest mural thickening due to disease may act as a lever translating physiologic medial smooth muscle shortening into critical luminal obstructions, potentially causing acute luminal occlusion.
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