Progression of subclinical atherosclerosis in ankylosing spondylitis: a 10-year prospective study.

Chronic systemic inflammation contributes to increased CVD burden in Ankylosing Spondylitis (AS). Since long-term follow-up data on subclinical atherosclerosis acceleration are lacking, we examined its progression in contemporary AS patients during 10 years. Fifty-three (89% male, aged 50.4 (36.3-55.9) years,) non-diabetic, CVD-free AS patients and 53 age-sex-matched non-diabetic, control individuals were re-evaluated after 9.2-10.2 years by ultrasonography for carotid/femoral atheromatosis, pulse wave velocity (PWV) and intima-media thickness (IMT), performed by the same operator/protocol. New atheromatic plaque formation, PWV deterioration, and IMT increase were associated only with classical CVD risk factors, as reflected by the heartSCORE (age, gender, smoking status, blood pressure and cholesterol levels) by multivariate analysis, rather than disease presence. However, among AS patients, despite remission/low disease activity at follow-up end in 79%, atheromatosis progression was associated by multivariate analysis with higher BASDAI scores (p = 0.028), independently of biologic therapies administered in 2/3 of them. Moreover, in AS patients, but not in controls, PWV values at baseline were associated with plaque progression during the 10-year follow-up after taking into account baseline heartSCORE and plaque burden status (p = 0.033). Despite comparable prevalence of both hypertension and hypercholesterolemia at baseline between patients and controls, a lower percentage of AS patients had achieved "adequate" CVD risk factor control at follow-up end (11% vs 25% respectively, p = 0.076). Classical CVD risk factors and residual disease activity account for the progression of subclinical atherosclerosis in AS, pointing to the unmet needs in the contemporary management of these patients.

The effect of raisins on biomarkers of endothelial function and oxidant damage; an open-label and randomized controlled intervention.

Based on the existing data in grapes and wine, the aim of the present study was to investigate the probability that raisins improve clinical features and markers of oxidative stress, inflammation and arterial function in healthy smokers. Thirty-six apparently healthy smokers were recruited to an open-label and randomized, controlled, 4-week prospective intervention. All participants were reported to consume less than the recommended amount of five servings fruits and vegetables daily. Participants in the intervention were instructed to consume raisins equal to five fruit servings (90g/d). Anthropometric and blood pressure (BP) measurements, assessment of dietary intake, and fasting blood draws were conducted at baseline and at week 4. Biochemical (glucose, lipids, liver enzymes), inflammation [C-reactive protein (CRP), leptin], oxidative stress [Malondialdehyde (MDA), Advanced oxidation protein products (AOPPs)] and arterial function markers [Flow-mediated dilatation (FMD), Pulse wave velocity (PWV), Intercellular adhesion molecule-1 (ICAM-1), Nitric oxide (NO)] were assessed pre- and post-intervention. Baseline characteristics did not differ between the intervention and control arm. No effect of daily raisin consumption was observed on markers assessed between baseline and week 4 in either arm. Regarding vegetable consumption, no difference was observed in either group between baseline and post-intervention; however, as expected, a significant increase was reported in the intervention arm in fruit consumption between baseline and end point (p<0.001) and between two arms post-intervention (p<0.001). When analyzing according to age, ICAM-1 levels significantly decreased in subjects >30years (n=8) in intervention arm (390.1±17.6 to 302.2±11ng/mL, p=0.004). After analysis of the data for sex, women in intervention (n=5) decreased significantly diastolic BP (74.6±4.2 to 67.4±2.6mg/dL, p=0.043), total cholesterol (175.8±7 to 166.6±6.6mg/dL, p<0.001) and LDL-cholesterol (96.2±9.6 to 89±10.5mg/dL, p=0.012). However, due to the small sample size in the above, no safe conclusions can be exported.

Subclinical Atherosclerosis Is Not Accelerated in Patients with Ankylosing Spondylitis with Low Disease Activity: New Data and Metaanalysis of Published Studies.

OBJECTIVE: Chronic inflammatory rheumatic diseases are associated with accelerated atherosclerosis, but data in ankylosing spondylitis (AS) are limited and the relative contribution of inflammation versus classical cardiovascular (CV) risk factors remains a matter of controversy. We addressed this in an original study and a metaanalysis of previous studies. METHODS: Atheromatic plaques in carotid and femoral arteries, carotid hypertrophy [intima-media thickness (IMT), cross-sectional area], and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity, were examined in consecutive nondiabetic, CV disease (CVD)-free patients with AS. Healthy individuals carefully matched 1:1 with patients for age, sex, smoking habits, hyperlipidemia, and hypertension served as controls. A metaanalysis of original studies that examined subclinical atherosclerosis in patients with AS versus controls with comparable CVD risk factors was also performed. RESULTS: Carotid and femoral atheromatic plaques were slightly less prevalent compared with controls in a contemporary cohort consisting of 67 patients with AS (82% men), aged 47.5 ± 12.5 years (mean ± SD), with a median disease duration of 12 years and a Bath AS Disease Activity Index (BASDAI) of 1.8 (interquartile range 0.4-3.6), of whom 66% were receiving anti-tumor necrosis factor (TNF) treatment. Carotid hypertrophy and stiffness, as well as aortic stiffness, were similar between patients and their matched controls. Metaanalysis of all published studies revealed a significantly increased carotid IMT, but not plaque burden, in AS versus controls. Notably, however, increased IMT was not evident in studies involving patients with low disease activity (mean BASDAI < 4) or in those studies that included > 50% of patients treated with anti-TNF. CONCLUSION: Low AS disease activity is not associated with accelerated atherosclerosis.

Early microvascular and macrovascular dysfunction is not accompanied by structural arterial injury in polycystic ovary syndrome.

OBJECTIVE: During the last decade cardiovascular risk factors and endothelial dysfunction have been shown to be present early in life in women with Polycystic Ovary Syndrome (PCOS). The aim of the present study was a global assessment of abnormalities in the arterial bed of young women with PCOS by non-invasive, reproducible methods. DESIGN: 27 women with PCOS and 27 control women of comparable age, body mass index and waist-to-hip ratio were studied. Macrovascular function was assessed by flow-mediated dilatation (FMD) on the brachial artery. Nitrate-induced dilatation (NID) was performed to exclude a vascular smooth muscle cells injury. Microvascular function was assessed by venous occlusion plethysmography studying forearm blood flow. Arterial structure was evaluated by ultrasonographic assessment of intima-media thickness (IMT) of the carotid artery. RESULTS: FMD values were lower in women with PCOS compared to controls (PCOS: 3.84+/-0.74% vs. controls: 9.83+/-0.97%, P<0.001), but no difference was observed in NID (PCOS: 16.59+/-1.84% vs. controls: 16.64+/-2.05%, P=0.98) values. The time required for reactive hyperemia to reach peak value, a plethysmography parameter, was longer in PCOS women (PCOS: 20.63+/-4.67 sec vs. controls: 10.38+/-5.11 sec, P=0.02). No difference was observed in the combined IMT among the studied groups (PCOS: 0.49+/-0.01 mm v.s. controls: 0.51+/-0.02 mm, P=0.19). CONCLUSIONS: Using non invasive methodologies endothelial dysfunction in the macrocirculation and early impairment in the microcirculation were demonstrated in young women with PCOS who had normal profile of glycemia, lipidemia and blood pressure, and no evidence of structural arterial impairment.

Tamoxifen improves endothelial function and reduces carotid intima-media thickness in postmenopausal women.

BACKGROUND: Tamoxifen is a selective estrogen-receptor modulator shown to improve several cardiovascular risk factors in postmenopausal women with breast cancer. In animal studies tamoxifen inhibits the progression of atherosclerosis. Although the presence of a history with tamoxifen treatment is related to a lower intima-media thickness (IMT) of the common carotid artery, data from controlled follow-up studies are lacking to support this observation. METHODS: We examined 14 postmenopausal women with early stage breast cancer with indication for tamoxifen treatment (20 mg/d) and 13 healthy postmenopausal women. Flow-mediated dilatation (FMD) of the brachial artery, combined carotid IMT, and aortic pulse wave were measured before and 6 months after treatment in the tamoxifen group and at the same times in the control group. RESULTS: FMD and IMT were significantly increased and decreased, respectively, in the treatment group compared to the control group (FMD: +2.2% +/- 0.9% vs +0.085% +/- 1%, P =.012; IMT: -0.088 +/- 0.03 mm vs +0.04 +/- 0.03 mm, P =.018, mean +/- standard error of the mean, treatment vs control group). These differences remained significant even when adjusted for age, duration of menopause, and cardiovascular risk factors. Low-density lipoprotein cholesterol was also significantly reduced after tamoxifen treatment. CONCLUSIONS: Tamoxifen treatment slows the progression of atherosclerosis in postmenopausal women with breast cancer as assessed by changes in carotid IMT. An improvement in endothelial function and blood lipid profile may be the reason for this beneficial effect.