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Background: Fibromuscular dysplasia (FD) is a non-atherosclerotic, non-inflammatory arterial disease of unknown cause, and most frequently affects the renal and internal carotid arteries. Our objectives were to determine whether quantitative and qualitative lesions could be detected by high-resolution echotracking techniques at two arterial sites generally considered as free of echographic lesions: the common carotid and the radial arteries, and to compare their frequency with a control population., Methods and Results: We studied 70 patients with renal FD and 70 control subjects matched for age, sex and systolic blood pressure. Arterial parameters were determined using non-invasive high-resolution echotracking systems. Carotid B-mode scans and radiofrequency signals were analysed and quoted by three observers blinded to diagnosis. FD patients had thicker carotid (+12%, P < 0.001) and radial arteries (+10%, P < 0.05) than controls. Abnormal echographic patterns of the carotid artery, including supernumerary interfaces and/or interruption of the blood-intima acoustic interfaces, were frequently observed in FD patients and rarely in control subjects. These abnormalities were quantified with a phenotypic score ranging from 2 to 7, and their sensitivity and specificity were 73 and 81%, respectively, as markers of FD. Having a phenotypic score > 3 conferred an odds ratio of 12.9 (95% CI 5.7-29.3) of having renal FD., Conclusion: We defined a new carotid phenotype in FD patients using a non-invasive echotracking system, and showed an increased wall thickness and distensibility of the radial artery. These data indicate the presence of subclinical lesions at arterial sites distant from the renal arteries, suggesting that renal FD is not a focal but a systemic arterial disease.

Background: Previous genomic studies with human tissues have compared differential gene expression between 2 conditions (ie, normal versus diseased) to identify altered gene expression in a binary manner; however, a potentially more informative approach is to correlate the levels of gene expression with quantitative physiological parameters., Methods and Results: In this study, we have used this approach to examine genes whose expression correlates with arterial stiffness in human aortic specimens. Our data identify 2 distinct groups of genes, those associated with cell signaling and those associated with the mechanical regulation of vascular structure (cytoskeletal-cell membrane-extracellular matrix). Although previous studies have concentrated on the contribution of the latter group toward arterial stiffness, our data suggest that changes in expression of signaling molecules play an equally important role. Alterations in the profiles of signaling molecules could be involved in the regulation of cell cytoskeletal organization, cell-matrix interactions, or the contractile state of the cell., Conclusions: Although the influence of smooth muscle contraction/relaxation on arterial stiffness could be controversial, our provocative data would suggest that further studies on this subject are indicated.

Objectives: In the present study, we describe the characteristics and examine the anticoagulation levels and safety of subcutaneous enoxaparin in unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI) patients who would not have been eligible in the Efficacy Safety Subcutaneous Enoxaparin in Non-Q-wave Coronary Events (ESSENCE) and Thrombolysis In Myocardial Infarction (TIMI)-11B trials., Background: It is not known whether the benefit shown with enoxaparin in the selected population of pivotal trials can be extended to the real world., Methods: In our center, all patients with UA/NSTEMI are anticoagulated with subcutaneous enoxaparin adjusted to creatinine clearance. Among 515 consecutive patients, we identified 174 who would not have been eligible for ESSENCE or TIMI-11B ("EP" group for excluded patients). We evaluated cardiovascular death or non-fatal myocardial infarction (MI), as well as major and minor bleeding events, at 30 days in the EP group and in patients without any of the exclusion criteria ("NEP" group for non-excluded patients)., Results: This EP group was older, had a higher female/male ratio, and more frequently had a history of MI or a diagnosis of non-Q MI on admission than the NEP group. The distribution of the anti-Xa activity was similar in both groups. The bleeding rates (major and minor) at 30 days were similar in the EP and NEP groups (2.3% vs. 2.9%, respectively, P = NS). On multivariate analysis, the use of glycoprotein IIb/IIIa inhibitors and the presence of hypertension were the only independent predictors of bleeding found in the whole population. Compared with the NEP group, the EP group had a fourfold increased rate of death or MI at 30 days (15.5% vs. 4.1%, p < 0.01). On multivariate analysis, the independent predictors of death or MI at 30 days were NSTEMI on admission, creatinine clearance, and heart failure., Conclusions: Patients who do not fit the enrollment criteria of ESSENCE/TIMI-11B have higher risk baseline characteristics for both bleeding and ischemic events. In these patients, enoxaparin with dose adjustment to creatinine clearance provides adequate anti-Xa levels and no excess of bleeding.