These data suggest that aortic ABPM, when compared to brachial ABPM, improves the individualized assessment of the BP-associated heart damage.

To assess the differences among seven different methods for the calculation of mean arterial pressure (MAP) and to identify the formula that provides MAP values that are more closely associated with target organ deterioration as expressed by the carotid cross-sectional area (CSA), carotid-to-femoral pulse-wave velocity (cf-PWV) and left ventricular mass (LVM). The study population consisted of 1878 subjects who underwent noninvasive cardiovascular risk assessment. Blood pressure (BP) was assessed in all subjects, and MAP was calculated by direct oscillometry and six different formulas. Carotid artery ultrasound imaging was performed in 1628 subjects. The CSA of the right and left common carotid artery (CCA) were calculated and used as surrogates of arterial wall mass and hypertrophy. Aortic stiffness was evaluated in 1763 subjects by measuring the cf-PWV. Finally, 218 subjects underwent echocardiographic examination for the assessment of LVM. Among the examined methods of MAP calculation, the formula MAP1=[diastolic BP]+0.412 × [pulse pressure] yielded the strongest correlations with the LVM, cf-PWV and CSA of the right and left CCA, even after adjusting for age and gender. The MAP calculation using the 0.412 was superior compared with the traditional formula that uses the 0.33 for the discrimination of subjects with left ventricular and carotid wall hypertrophy, as well as subjects with increased aortic stiffness. MAP estimated with the 0.412 is better correlated with target organ deterioration compared with other formulas. Future studies are needed to explore the accuracy of these formulas for MAP estimation compared with direct intra-arterial BP measurement.

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Aortic blood pressure (BP) and 24-h ambulatory BP are both better associated with target organ damage than office brachial BP. However, it remains unclear whether a combination of these two techniques would be the optimal methodology to evaluate patients' BP in terms of left ventricular diastolic dysfunction (LVDD) prevention. In 230 participants, office brachial and aortic BPs were measured by a validated BP monitor and a tonometry-based device, respectively. 24-h ambulatory brachial and aortic BPs were measured by a validated ambulatory BP monitor (Mobil-O-Graph, Germany). Systematic assessment of patients' LVDD was performed. After adjustment for age, gender, hypertension and antihypertensive treatment, septum and lateral E/Ea were significantly associated with office aortic systolic BP (SBP) and pulse pressure (PP) and 24-h brachial and aortic SBP and PP (P ⩽ 0.04), but not with office brachial BP (P ⩾ 0.09). Similarly, 1 standard deviation in SBP was significantly associated with 97.8 ± 20.9, 86.4 ± 22.9, 74.1 ± 23.3 and 51.3 ± 22.6 in septum E/Ea and 68.6 ± 2 0.1, 54.2 ± 21.9, 37.9 ± 22.4 and 23.1 ± 21.4 in lateral E/Ea, for office and 24-h aortic and brachial SBP, respectively. In qualitative analysis, except for office brachial BP, office aortic and 24-h brachial and aortic BPs were all significantly associated with LVDD (P ⩽ 0.03), with the highest odds ratio in 24-h aortic SBP. Furthermore, aortic BP, no matter in the office or 24-h ambulatory setting, showed the largest area under receiver operating characteristic curves (P ⩽ 0.02). In conclusion, 24-h aortic BP is superior to other BPs in the association with LVDD.

Low AS disease activity is not associated with accelerated atherosclerosis.

IntroductionRheumatoid arthritis (RA) is associated with a high cardiovascular disease (CVD) risk, whereas arterial hypertension is a major modifiable CVD risk factor with still unclear prevalence in RA disease. We conducted a comprehensive study on hypertension characteristics evaluating for the first time out-of-office blood pressure (BP) in a typical contemporary RA cohort.MethodsAssessment of office and out-of-office BP (when office systolic/diastolic BP was >129/79) and vascular studies including evaluation of aortic stiffness, carotid hypertrophy/plaques and ankle-brachial index, were performed in 214 consecutive, consenting RA patients free of CVD (aged 58.4 ± 12.3 years, 82% women). As comparators regarding office hypertension measurements, data from 214 subjects (1:1 matched for age and gender with the RA patients) derived from a cohort designed to assess the prevalence of hypertension in the general population were used.ResultsThe prevalence of declared known hypertension in the RA population was 44%. Of the remaining RA patients, 2 in every 5 individuals had abnormal office BP (systolic/diastolic >139/89 mmHg), contributing to almost double the prevalence of declared/office hypertension compared to the general matched population (67% vs. 34%). Out-of-office (home or ambulatory 24 hour) BP measurements revealed that: (i) a 54% prevalence of actual hypertension in RA, in other words almost 10% of the patients were unaware of having hypertension and (ii) 29% of the RA patients with known hypertension were not well controlled. Actual hypertension was positively associated with age and body mass index, and inversely with the use of biologic drugs. Overall, almost 1 out of 5 presented the 'white coat’ phenomenon. An intermediately compromised vascular phenotype was evident in this “white coat” subgroup (lying between patients with sustained normotension and sustained hypertension) in terms of aortic stiffness, carotid hypertrophy and ankle-brachial index, even after adjustment for confounders.ConclusionBeyond any doubt on the basis of out-of-office evaluation, arterial hypertension in RA has a high prevalence, low awareness and poor control, as well as substantial and vascular damage-associated “white coat” phenomenon. Thus, correct diagnosis and effective treatment of hypertension is of key importance in RA for CVD risk reduction.

Plaque progression is accelerated in SLE regardless of disease activity, and is associated with antiphospholipid antibodies and the Systemic Coronary Risk Evaluation. In LLDAS, cumulative corticosteroid dose and disease duration are additional determinants of progression.

Effective disease control may abrogate any RA-specific effect on the progression of atherosclerosis regardless of treatment. Whether early and sustained RA control translates to the CVD outcomes expected in the general population should be examined in prospective studies.