The morphodynamic changes of the umbilical artery from full distension to total occlusion within 45 seconds of delivery is very striking. On gross examination, the constricted artery shows a small, round, outer contour and reduced external diameter. On microscopic examination, it shows a small, compressed or completely obliterated lumen with an irregular wavy luminal outline, plump endothelial cells with ovoid nuclei, remodeling of the inner muscle layer with smooth muscle cells reoriented towards the luminal center, wrinkled elastic fibrils dispersed in the inner muscle layer and/or wrinkled thick internal elastic lamina, contracted smooth muscle cells with plump cellular outline and squeezed nuclear deformity, and thickened muscle bundles. A total occlusion of the umbilical arterial lumen is accomplished by maximal contraction of smooth muscle cells in the outer muscle layer. This contraction creates thick muscle bundles, generates a constrictive force to reduce the outer circumference and external diameter, and then causes the inward projection of the inner muscle layer to obliterate the lumen. The morphological changes of smooth muscle cells and the remodeling of the arterial wall by muscle contraction and constriction can also be found in the coronary arteries of patients who died of occlusive coronary artery disease. Coronary artery constriction or spasm can cause (1) remodeling of soft atheromatous plaques, resulting in nonthrombotic occlusion; (2) volcano-like eruption of soft atheromatous plaques, resulting in thrombus formation; and (3) tearing of the nonatherosclerotic arterial wall, resulting in dissection and compressive hematoma in the arterial wall.