Screening for IAD of BP is important but the measurement methodology has a major influence on IAD results. To prevent overestimation and observer bias IAD should be assessed simultaneously at both arms, with one or two automatic devices and multiple readings should be taken.

The ability to predict severity of the post-thrombotic syndrome (PTS) early after acute deep-vein thrombosis (DVT) is limited. The aim of our study was to examine the incidence of PTS prospectively and to evaluate the predictive value of non-invasive venous examinations shortly after DVT for the development of PTS. In 93 patients with DVT thrombosis score (TS), reflux, venous outflow resistance (VOR) and calf muscle pump dysfunction (CMP) were examined prospectively. After one, two and six years patients were evaluated for PTS using the clinical scale of the CEAP-classification (PTS present > or = 3 on a scale from 0 to 6). Area under the curves (AUC) were used to evaluate the predictive value of the non-invasive examinations at one and three months after diagnosis of DVT for future PTS. The cumulative incidence of PTS increased from 49% (32/65) after one year to 55% (36/65) and 56% (27/48) after two and six years, whereas the incidence of patients with PTS class 4 progressed from 20% after two years to 33% after six years. The prognostic value to predict PTS was highest for the combination of TS, VOR and reflux measured three months after diagnosis and showed an AUC of 0.77 (0.65-0.90) for PTS after one year. In conclusion, the incidence of PTS after DVT did not increase significantly after one year, whereas during longer follow-up the severity of PTS rose in patients with PTS. Moreover, measurement of TS, VOR and reflux three months after DVT could predict, with reasonable accuracy, the risk of PTS after one year of follow-up.

Abstract-It is still uncertain whether one can safely base treatment decisions on self-measurement of blood pressure. In the present study, we investigated whether antihypertensive treatment based on self-measurement of blood pressure leads to the use of less medication without the loss of blood pressure control. We randomly assigned 430 hypertensive patients to receive treatment either on the basis of self-measured pressures (nϭ216) or office pressures (OPs; nϭ214). During 1-year follow-up, blood pressure was measured by office measurement (10 visits), ambulatory monitoring (start and end), and self-measurement (8 times, self-pressure group only). In addition, drug use, associated costs, and degree of target organ damage (echocardiography and microalbuminuria) were assessed. Key Words: blood pressure Ⅲ hypertension Ⅲ self-measurements Ⅲ home monitoring Ⅲ ambulatory blood pressure measurement Ⅲ treatment A s indications for lowering blood pressure (BP) become increasingly stringent, the associated medication use and costs rise markedly. 1 This calls for proper diagnosis and careful selection of patients in whom treatment is really indicated. In this respect, conventional office BP measurements (OBPMs) have disadvantages, because they can easily elicit a white-coat effect, overestimation of a patient's BP, 2 and unnecessary drug prescription. Self-BP measurements (SBPMs) are less liable to the white-coat effect 3 and may provide a more reliable estimate of a patient's "true" BP. In addition, SBPM correlates better with the development of target organ damage (TOD) than OBPM 4 -6 and for the occurrence of cardiovascular complications. 7,8 Therefore, SBPM has the potential to identify subjects that may not need treatment. This could reduce drug use and lead to considerable costs savings. The Home versus Office Measurement, Reduction of Unnecessary treatment Study (HOMERUS) was designed to determine whether treatment based on SBPM leads to a decreased drug prescription without an impaired BP control and TOD as compared with treatment based on OBPM. MethodsThe design of the HOMERUS has been described in detail elsewhere. 9 Briefly, HOMERUS is a multicenter, prospective, randomContinuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz.

-Hydrochlorothiazide and indapamide are thought to exert their hypotensive efficacy through a combined vasodilator and diuretic effect, but in vivo evidence for a direct vascular effect is lacking. The presence and mechanism of a direct vascular action of hydrochlorothiazide in vivo in humans were examined and compared with those of the thiazide-like drug indapamide. Forearm vasodilator responses to infusion of placebo and increasing doses of hydrochlorothiazide (8, 25, and 75 microg. min-1. dL-1) into the brachial artery were recorded by venous occlusion plethysmography. Dose-response curves were repeated after local tetraethylammonium (TEA) administration to determine the role of potassium channel activation and, in patients with the Gitelman syndrome, to determine the role of the thiazide-sensitive Na-Cl cotransporter in the vasodilator effect of hydrochlorothiazide. Vascular effects of hydrochlorothiazide were compared with those of indapamide in both normotensive (mean arterial pressure, 85+/-7 mm Hg) and hypertensive (mean arterial pressure, 124+/-16 mm Hg) subjects. At the highest infusion rate, local plasma concentrations of hydrochlorothiazide averaged 11.0+/-1.6 microg/mL, and those of indapamide averaged 7. 2+/-1.5 microg/mL. In contrast to indapamide, hydrochlorothiazide showed a direct vascular effect (maximal vasodilation, 55+/-14%; P=0. 013), which was inhibited by TEA (maximal vasodilation after TEA, 13+/-10%; P=0.02). The response was not dependent on blood pressure and was similar in patients with Gitelman syndrome, indicating that absence of the Na-Cl cotransporter does not alter the vasodilatory effect of hydrochlorothiazide. The vasodilator effect of hydrochlorothiazide in the human forearm is small and only occurs at high concentrations. The mechanism of action is not mediated by inhibition of vascular Na-Cl cotransport but involves vascular potassium channel activation. In contrast, indapamide does not exert any direct vasoactivity in the forearm vascular bed.