Increased prevalence of peripheral arterial disease in osteoporotic postmenopausal women.

The aim of this study was to investigate the prevalence and correlates of peripheral arterial disease (PAD) in a population of osteoporotic postmenopausal women. The presence of PAD was assessed by ankle brachial index (ABI) in 345 ambulatory osteoporotic postmenopausal women, and in 360 community-based, age- and race-matched postmenopausal women with normal bone mineral density (BMD) (control group). PAD was detected in 63/345 (18.2%) osteoporotic women and in 14/360 (3.8%) control subjects (P < 0.0001). The mean ABI values were significantly lower in the osteoporosis group than in the control group (0.98 +/- 0.09 vs. 1.04 +/- 0.06, P < 0.0001). No difference in cardiovascular risk factors was observed between osteoporotic patients and controls, or between osteoporotic patients with and without PAD. Osteoporotic patients with PAD had lower femoral neck BMD T scores than those without PAD (-4.2 +/- 0.7 vs. -2.3 +/- 0.7, P < 0.0001). Only 4 PAD patients (5.1%) had intermittent claudication. In multivariate logistic regression analysis, factors independently associated with PAD within osteoporotic patients were lower femoral neck BMD T score (odds ratio (OR) = 0.20, 95% confidence interval (CI), 0.05-0.70, P = 0.01) and systolic blood pressure (OR = 1.02, 95% CI, 1.00-1.03, P = 0.01). This study shows for the first time an increased prevalence of PAD among osteoporotic postmenopausal women, with a lower femoral neck BMD T score being a significant independent predictor. The findings suggest that vascular status evaluation should be done in osteoporotic postmenopausal women in order to identify candidate patients for preventive and therapeutic cardiovascular interventions.

Impaired cognitive performance in asymptomatic peripheral arterial disease: relation to C-reactive protein and D-dimer levels.

BACKGROUND AND PURPOSE: asymptomatic peripheral arterial disease (APAD), a highly prevalent condition in the general older population, is associated with an increased risk of cerebrovascular events because of co-existing clinical or subclinical cerebral atherosclerosis. The purpose of this study was to investigate whether cognitive function is impaired in stroke- and transient ischaemic attack-free patients with APAD, and whether inflammatory and haemostatic markers are associated independently with neuropsychological performance. METHODS: cognitive performances of 164 well-functioning, community-dwelling patients with APAD were compared with those of 164 age-, gender- and education-matched healthy control subjects on six neuropsychological tests. Levels of C-reactive protein (CRP), D-dimer and fibrinogen were also analysed in all participants. RESULTS: patients with APAD scored significantly worse (P < 0.0001) than control subjects on five cognitive tests assessing domains of verbal working memory, attention, perceptuomotor speed, mental flexibility, visuoconstructive skills and visual memory. Multiple linear regression analyses showed that CRP and D-dimer were significant, independent predictors of poorer performances on four and three cognitive tests, respectively, within patients with APAD. CONCLUSIONS: patients with APAD show cognitive impairment in a range of psychometric tests, and CRP and D-dimer appear to be independent negative predictors of some cognitive performances. These findings suggest the need for screening for APAD among at-risk subjects in order to identify patients to be treated for prevention of functional decline and dementia. They also support the hypothesis that inflammation and hypercoagulability are implicated in the pathophysiology of cognitive dysfunction associated with APAD.

Exaggerated endothelin release in response to acute mental stress in patients with intermittent claudication.

Endothelin-1 (ET-1) is an endothelial-derived 21-amino-acid peptide with potent vasoconstrictor and mitogenic properties implicated in several cardiovascular disorders. To evaluate the plasma ET-1 response to mental stress in patients with intermittent claudication, plasma endothelin concentrations were measured by radioimmunoassay in 15 claudicant outpatients (13 men and 2 women; mean age 62 +/- 4 years) and in 15 sex- and age-matched healthy control subjects (12 men and 3 women; mean age 60 +/- 8 years) before and after mental arithmetic performed for 10 minutes. Venous blood samples were drawn from an antecubital vein at baseline, at the end of the mental arithmetic, and at 10 minutes of recovery. Baseline ET-1 values were higher in patients with intermittent claudication as compared with control subjects (4.5 +/- 0.5 pmol/L and 2.2 +/- 0.3 pmol/L, respectively, p < 0.0001). At the end of mental stress, ET-1 levels rose significantly in both groups from baseline (p < 0.001) reaching a higher value in patients with intermittent claudication than in control subjects (5.6 +/- 0.7 pmol/L and 2.4 +/- 0.4 pmol/L, respectively, p < 0.0001). The percent increases (delta%) in ET-1 plasma concentrations from baseline in response to mental stress were significantly greater in claudicant patients than in control subjects (+23 +/- 9% and +9 +/- 7%, respectively, p < 0.0001). ET-1 plasma concentrations returned to baseline values similarly in both groups at minute 10 of the recovery period. These findings show that acute mental stress causes an exaggerated release of ET-1 in patients with intermittent claudication and suggest that this could be a potential pathophysiological mechanism through which mental stress may trigger adverse acute cardiac events and accelerate progression of atherosclerosis in these patients.