Mechanisms of arterial and aneurysmal tortuosity

Most arteries follow a straight course because they are stretched by longitudinal traction. However, aneurysms and arteries in aged, hypertensive patients often exhibit tortuosity. This study was undertaken to examine mechanisms of tortuosity and the role of the arterial wall connective tissues. Experiments were performed in vitro on 48 dog carotid arteries before and after treatment with elastase or collagenase. Degradation of wall elastin caused aneurysmal dilatation and a marked decrease in longitudinal retractive force (p less than 0.05). This permitted the development of tortuosity. Degradation of wall collagen caused minimal dilatation but did cause vessel rupture; however, degradation of collagen produced no decrease in longitudinal retractive force (p = NS). These data demonstrate that failure of elastin permits vessels to (1) dilate aneurysmally and (2) elongate sufficiently to become tortuous. Failure of elastin plays a role in the tortuosity seen with age and hypertension, congenital kinking of arteries, aneurysms, and ectasias (arteriomegaly). Failure of collagen causes vessels to rupture but does not facilitate the development of tortuosity.