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Cardiovascular disease risk increases in women after the menopausal transition; why this inflection point occurs remains uncertain. We aimed to characterize the influence of menopause on vascular aging by prospective assessment of change in indexes of subclinical atherosclerosis across the menopausal transition. We evaluated 411 healthy women from SWAN Heart, an ancillary study of SWAN (Study of Women's Health Across the Nation), for subclinical atherosclerosis at baseline and again after an average of 2.3 years. Carotid intima-media thickness and aortic pulse wave velocity were measured by ultrasound. Coronary artery calcium scores were obtained by computed tomography. Women were grouped by menopausal status as premenopausal, postmenopausal, or having undergone the transition during follow-up. Analyses of changes were adjusted for age at baseline and time between scans. Mean age at baseline was 51 ± 3 years; 93 (23%) subjects transitioned to menopause (Pre-Post), 147 (36%) remained premenopausal (Pre-Pre), while 171 (41%) were postmenopausal at baseline (Post-Post). Blood pressure readings did not differ between groups with similar increase noted in carotid intima-media thickness and log coronary artery calcium + 1 from baseline to follow-up. Change in aortic pulse wave velocity from baseline to follow-up was higher in Pre-Post (121 ± 23 cm/s) compared with Pre-Pre (38 ± 250 cm/s, p = 0.029) and Post-Post (41 ± 228 cm/s, p = 0.045). In conclusion, changes in aortic stiffness were more sensitive measures of perimenopausal vascular aging than morphologic indexes of subclinical atherosclerosis in women undergoing the menopausal transition. Serial assessment of such changes could potentially elucidate mechanisms of disease and identify women to target for aggressive lifestyle risk factor modification.

Background. The goal of this study was to evaluate the role of the fibrinolytic system in patients with unstable angina at rest associated with transient electrocardiographic changes.Methods and Results. Tissue plasminogen activator activity in plasma was comparable among patients with unstable angina (n = 17), patients with stable exertional angina (n = 10), and control patients with normal coronary arteriograms (n=8). In contrast, plasminogen activator inhibitor-1 (PAI-1) activity in plasma was elevated in the unstable angina group (21.67±+9.52 AU/mi) as compared with either the stable angina group (12.01±+7.06 AU/mil, p<0.02) or the controls (12.49±8.54 AU/mil, p<0.02). Coronary angiography performed within 24 hours after the last anginal episode showed a similar extent of coronary artery disease in the unstable and stable angina groups. However, intracoronary thrombi were observed in eight patients in the unstable

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