Arterial wall stiffness in man. On gender differences and abnormalities in insulin dependent diabetes mellitus and alpha1-antitrypsin deficiency

Abstract: The mechanical properties of major arteries may reflect early manifestations of vascular disease and are also of interest because they are important for cardiac work. Using echo-tracking sonography and blood pressure measurements, arterial stiffness and diameters were investigated in healthy individuals as well as in patients with insulin dependent diabetes mellitus (IDDM) or alpha1-antitrypsin deficiency (alpha1-AT deficiency). In healthy individuals the stiffness of the abdominal aorta (AO) and the common carotid artery (CCA) increases with age and the diameters increase. These changes are more pronounced in the AO than in the CCA. Further, there are gender differences. This may serve as a background to regional as well as gender differences in the development of vascular disease. In IDDM, stiffness was increased in both the AO and the CCA in women compared to controls. In contrast, there was no difference in stiffness between men with IDDM and controls. Thus, a marked gender-difference in changes of arterial stiffness is found in IDDM. The increased AO stiffness in IDDM women is related to the duration of diabetes. Further, independent of the duration, there is an association between increased AO stiffness and autonomic dysfunction. Increased arterial stiffness in women with IDDM may contribute to the particularly increased risk for cardiovascular complications in diabetic women. To evaluate if alpha1-AT deficiency is a pathogenetic factor in the development of abdominal aortic aneurysm (AAA), the diameter and stiffness of the AO in patients with homozygous alpha1-AT deficiency (PiZZ) were investigated. No difference in the AO diameter compared to controls was found. Men, but not women, had lower AO stiffness than controls. Further, the prevalence of alpha1-AT deficiency (PiZ) in patients with AAA was studied. There was no increase in alpha1-AT deficiency (PiZ) in the patients with AAA compared with the general population. Thus, alpha1-AT deficiency does not seem to be an important pathogenetic factor for the development of AAA.