Pathophysiology of arterial aneurysms.

Studies were performed to evaluate the contributions of elastin and collagen to the formation of arterial aneurysms. Dog carotid arteries and human external and internal iliac arteries were excised, mounted horizontally in a tissue bath, and were pressurized. Vessel diameter and longitudinal force were measured. the vessels were treated with elastase or collagenase. Those treated with elastase dilated, but never ruptured. Those treated with collagenase dilated still more and, in every case, ruptured. Circumferential stability resulted from recruitment of previously non-loaded collagen fibers, and from a change in geometry from a cylinder to a sphere. The laminated thrombus lining the lumen has little intrinsic strength and therefore does not confer strength to the aneurysmal wall. Treatment with elastase also reduces the retractive force exerted by the vessel in the longitudinal direction. Therefore loss of elastin permits the vessel to elongate and to become tortuous. In aged human arteries collagen also contributes a small portion of the retractive force. Progressive enlargement of aneurysms results from continued failure of wall connective tissues reflecting a) genetically defective collagen and or b) activity of the immune system.