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S T MacSweeney

Publications and source records attributed to S T MacSweeney.

25 records · Page 2Linked to original sources
PubMed1994

Pathogenesis of abdominal aortic aneurysm.

The pathogenesis of abdominal aortic aneurysm involves many factors acting over time. However, destruction of elastin in the aortic wall is a key event that shifts the load produced by blood pressure on to collagen. This is exacerbated in the presence of hypertension. Smoking and age are further important factors, as is the site; elastic lamellae are relatively less common in the abdominal aorta. Once the shielding effect of elastin is lost, further dilatation and rupture of the aorta depend on the physical properties of the collagen present.

Age Factors↗
PubMed1993

High prevalence of unsuspected abdominal aortic aneurysm in patients with confirmed symptomatic peripheral or cerebral arterial disease.

A group of 561 consecutive patients with proven symptomatic peripheral or cerebral arterial disease attending a vascular clinic was screened for abdominal aortic aneurysm (AAA) using B-mode ultrasonography. An aneurysm was present in 40 of 358 men (11.2 per cent) and 13 of 203 women (6.4 per cent), a total prevalence of 9.4 per cent. Thirty-three aneurysms were 3-4 cm in diameter. The prevalence of AAA was similar in patients referred with lower-limb and with cerebral ischaemia. Physical examination for AAA was performed in 200 patients before ultrasonography. The sensitivity of physical examination in the detection of aneurysm was 43 per cent (57 per cent for AAA > or = 4 cm in diameter, 29 per cent for AAA < 4 cm in diameter). Physical examination was an inadequate method of screening. Initial follow-up showed a mean aneurysm expansion rate of 0.20 cm/year. Patients with arterial disease have a high risk of AAA; routine ultrasonographic screening should be considered.

Aortic Aneurysm, Abdominal↗
PubMed1993

Influence of type III collagen genotype on aortic diameter and disease.

Type III collagen contributes to the tensile strength of the aortic wall, and mutations in the type III collagen gene have been suggested as the basis for the familial tendency to abdominal aortic aneurysm (AAA). Variation in this gene was investigated in 153 patients with AAA, 87 with aortoiliac stenosis and 98 age-matched controls. The rare mutation at amino acid 619 of Gly-->Arg, previously associated with AAA in a single family, was not found in any of the patients with aneurysm. For the Ala-->Thr variation at amino acid 531, the frequency of the threonine allele was 0.25 in patients with AAA and stenosis, compared with 0.35 in controls. The frequency of the rare allele in the region 3' to the gene demonstrated by Ava II digestion (0.27 in the general population) was found to be 0.29 in the AAA group and 0.19 in the stenosis group (P = 0.023). In the AAA group the presence of the Ava II rare allele was associated with a significant increase in aneurysm diameter (P = 0.044). Non-invasive assessment of aortic distensibility was available in 25 patients: those carrying the Ava II rare allele had less distensible aortas than those not carrying this allele (median pressure-strain elastic modulus 42.0 and 23.9 N/cm2 respectively, P = 0.008). Variation in the type III collagen gene may influence the mechanical properties of the ageing aorta and hence its susceptibility to disease and dilatation. In contrast, there is no evidence for a single common founder mutation in type III collagen predisposing to AAA.

Aged↗
PubMed1992

Mechanical properties of the aneurysmal aorta.

The mechanical properties of the abdominal aorta were investigated non-invasively in 30 patients with aortic aneurysm and 11 with peripheral arterial disease. The distensibility of the aorta was measured using M-mode ultrasonography, permitting non-invasive assessment of the pressure--strain elastic modulus or aortic stiffness, Ep. The median Ep value increased from 4.0 N/cm2 in control subjects in their third decade of life (n = 10) to 10.4 N/cm2 in middle age (n = 11) to 14.0 N/cm2 in the elderly (n = 13). In the presence of a normal diameter, peripheral arterial disease with aortic atherosclerosis had little effect on aortic stiffness, median Ep being 16.0 N/cm2. Aneurysmal dilatation was associated with a significant increase in aortic stiffness, median Ep being 31.3 N/cm2 (P < 0.001). For aortas of normal diameter, Ep was at all ages dependent on mean arterial pressure. In patients with aortic aneurysms there was no clear relationship between Ep and mean arterial pressure or aortic diameter. Of the patients studied, 15 underwent aortic reconstruction; increasing aortic stiffness (log Ep) was associated with a decreased medial elastin content of the aortic biopsy (r = -0.63, P < 0.02). This study demonstrates the marked stiffness or inelasticity of dilated or aneurysmal vessels, part of which is attributable to the loss of elastin.

Adult↗
PubMed1991

Genetic variants of collagen III and abdominal aortic aneurysm.

Collagens provide the tensile strength of the aortic wall. Variations in collagen structure are recognised in Ehlers Danlos syndrome type IV and could also be associated with a predisposition to aortic aneurysm. The frequency of some minor genetic variants of type III collagen, present in the normal population, can be detected by restriction enzyme digestion of genomic DNA from peripheral leucocytes. The frequency of a minor collagen type III allele demonstrated with the restriction enzyme Ava II was compared in patients with abdominal aortic aneurysm (n = 70) and aortoiliac stenosis (n = 47). The frequency of the minor allele was significantly higher in aneurysm patients (0.30) compared with patients with aortoiliac stenosis (0.17), p less than 0.05. The presence of the minor allele was associated with a less elastic aneurysm wall (median pressure strain elastic modulus 4575, n = 7), compared with patients homozygous for the common allele (median pressure strain elastic modulus 1990, n = 6), p less than 0.05. These results indicate that genetic variants of type III collagen may influence the extensile properties of the aortic wall and that mutations in the type III collagen gene may be associated with aortic aneurysms.

Aged↗