Impaired LV early diastolic relaxation, detected by pulsed Doppler echocardiography, identifies hypertensive patients at increased cardiovascular risk. Such association is independent of LV mass and ambulatory BP.

No abstract

Systolic blood pressure and pulse pressure, but not diastolic blood pressure, are predictors of plasma C-reactive protein concentrations in patients with newly diagnosed, never-treated hypertension, irrespective of the potential proinflammatory action of traditional cardiovascular risk factors.

Early identification of causative pathogen in sepsis patients is pivotal to improve clinical outcome. SeptiFast (SF), a commercially available system for molecular diagnosis of sepsis based on PCR, has been mostly used in patients hospitalized in hematology and intensive care units. We evaluated the diagnostic accuracy and clinical usefulness of SF, compared to blood culture (BC), in 391 patients with suspected sepsis, hospitalized in a department of internal medicine. A causative pathogen was identified in 85 patients (22%). Sixty pathogens were detected by SF and 57 by BC. No significant differences were found between the two methods in the rates of pathogen detection (P ‫؍‬ 0.74), even after excluding 9 pathogens which were isolated by BC and were not included in the SF master list (P ‫؍‬ 0.096). The combination of SF and BC significantly improved the diagnostic yield in comparison to BC alone (P < 0.001). Compared to BC, SF showed a significantly lower contamination rate (0 versus 19 cases; P < 0.001) with a higher specificity for pathogen identification (1.00, 95% confidence interval [CI] of 0.99 to 1.00, versus 0.94, 95% CI of 0.90 to 0.96; P ‫؍‬ 0.005) and a higher positive predictive value (1.00, 95% CI of 1.00 to 0.92%, versus 0.75, 95% CI of 0.63 to 0.83; P ‫؍‬ 0.005). In the subgroup of patients (n ‫؍‬ 191) who had been receiving antibiotic treatment for >24 h, SF identified more pathogens (16 versus 6; P ‫؍‬ 0.049) compared to BC. These results suggest that, in patients with suspected sepsis, hospitalized in an internal medicine ward, SF could be a highly valuable adjunct to conventional BC, particularly in patients under antibiotic treatment.

The impact of hypertension on vascular structure at different arterial sites and the relation of vascular hypertrophy with left ventricular (LV) hypertrophy in the early stages of essential hypertension are unclear. In 96 newly diagnosed, never-treated, uncomplicated hypertensive subjects aged < 55 years (43 +/- 9 years, 68 men, clinic blood pressure 152/99 mm Hg, 24-h blood pressure 135/89 mm Hg), we measured LV mass (M-mode echocardiography) and intima-media thickness (IMT) of the carotid and femoral arteries (high-resolution B-mode ultrasound). The average of 24 carotid and 24 femoral IMT readings (common and internal carotid or common and superficial femoral, right and left side, far and near wall, three sampling points per segment) was analyzed. Carotid and femoral IMT were strongly related to each other (r = 0.77). Subjects with LV hypertrophy (n = 33) had a greater IMT at the carotid (0.84 +/- 0.2 v 0.71 +/- 0.2 mm, P < .0001) and femoral (0.77 +/- 0.1 v 0.64 +/- 0.1 mm, P < .0001) level. Carotid IMT showed a positive correlation with LV mass (r = 0.46) and age (r = 0.38), and an inverse one with high-density lipoprotein (HDL) cholesterol (r = -0.26). Femoral IMT was associated positively to LV mass (r = 0.50), age (r = 0.33) and triglycerides (r = 0.29), and inversely to HDL-cholesterol (r = -0.33). The association between IMT (both carotid and femoral) and LV mass held after controlling for age and other confounders in a multiple regression analysis. In summary, in the early stages of hypertension arterial wall thickening appears to be a diffuse process, which occurs in parallel at the carotid and femoral level and shows a positive association with LV hypertrophy.

Low HDL-cholesterol is an independent predictor of LV mass in untreated hypertensive subjects. Common hormonal and metabolic mechanisms, including insulin resistance, could explain this association, which may contribute to the adverse prognostic significance of low HDL-cholesterol levels.

No abstract

Endothelial progenitor cells maintain endothelium integrity by replacing injured endothelial cells. Cholesterol-lowering promotes either endothelial progenitor cells mobilization or improves endothelial function. It is unknown whether improving endothelial function with statin is associated with a parallel increased endothelial progenitor cells availability. Thirty-two hypercholesterolemic patients were assigned to 4-week rosuvastatin (10 mg daily) and 16 hypercholesterolemic served as controls. Circulating endothelial progenitor cells, brachial artery flow-mediated vasodilatation, an index of endothelial function, and the lipid profile were measured before and after the 4-week statin therapy. At baseline, we found a correlation between circulating endothelial progenitor cells and flow-mediated vasodilatation (r = .31, P = .029). At the end of the 4-week intervention with rosuvastatin there was a 37% reduction in low-density lipoprotein cholesterol (P < .001) and a significant 72% increase in the number of endothelial progenitor cells and flow-mediated vasodilatation (4.7 + 0.7% to 8.8 + 0.4%, P < .001). Endothelial progenitor cells and flow-mediated vasodilatation were unchanged at the end of the study in patients not taking statin. A correlation emerged between endothelial progenitor cells and flow-mediated vasodilatation variations (r = .52, P < .001), this correlation being still significant after controlling for blood cholesterol reduction. In conclusion, short-term rosuvastatin therapy contributes in hyperchoelsterolemic patients to improving endothelial function by lowering cholesterol and increasing the number of circulating endothelial progenitor cells; the latter effect appears to be partly independent from reduction in plasma cholesterol.