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Objectives: To evaluate the different internal factors influencing patient flow, effectiveness, and overcrowding in the emergency department (ED), as well as the effects of ED reorganisation on these indicators. Methods: [...]

AbstractEndothelial dysfunction plays a pivotal role in the development of essential hypertension and its complications. The purpose of this study is to assess the effect of antihypertensive treatment with the angiotensin receptor blocker irbesartan on endothelial function in a group of essential hypertensive patients. Thirty-two untreated hypertensives are examined at baseline and at the end of a six-month period of irbesartan treatment. Endothelium-dependent and -independent responses are determined by measuring changes in forearm blood flow (FBF) by strain gauge plethysmography in response to intrarterial infusions of acetylcholine (endothelium-dependent vasodilation [EDV]), sodium nitroprusside (endothelium-independent vasodilation [EIV]), with and without the addition of the nitric oxide (NO) synthase inhibitor L-NMMA. Plasma endothelin, plasma and urinary nitrates and nitrites, and cyclic GMP are measured at baseline and at the end of treatment. Irbesartan promoted a significant increase in EDV (from 433±147% to 488±75%; P=0.027) and EIV (from 442±130% to 495±104%; P=0.041). L-NMMA-induced vasoconstriction was significantly enhanced after irbesartan treatment (relative decrease of FBF from 33.4±9.5% to 39.5±5.6%; P=0.001). Plasma concentrations of endothelin fell significantly after irbesartan treatment (from 5.78±1.86 to 4.16±1.52 pg/mL; P=0.001). We concluded that long-term irbesartan treatment enhances both endothelium-dependent and -independent vascular vasodilation capacity. In addition to this non-specific effect, irbesartan restores the vasoconstriction capacity of NO synthase inhibitors, suggesting a direct effect on tonic NO release, and decreases endothelin production. These actions may play an important role in the vascular protecting effects of irbesartan.

The aim of the study was to evaluate endothelial function in essential hypertensives (EH) classified according to the presence of salt-sensitivity (SS) or salt-resistance (SR). Thirty-seven never treated EH patients without evidence of target organ damage were studied. Salt-sensitive hypertension was defined as a significant rise (p<0.05) in 24-hour mean BP, measured by means of ABPM, from a 7-day period of low-salt intake (50 mmol/day) to a 7-day period of high-salt intake (250 mmol/day). At the end of the high-salt period, endothelial function was determined by means of the forearm vascular response (by strain-gauge plethysmography) to intrabrachial infusion of increasing doses of acetylcholine, an endothelium-dependent vasodilator, or sodium nitroprusside, an endothelium-independent vasodilator, with and without the presence of the NO synthase inhibitor L-NMMA. When compared to SR hypertensives (n=16), SS patients (n=21) exhibited a significant decreased endothelium-dependent vasodilation. The maximal acetylcholine induced vasodilation was (mean±sem) 358±36% in SS hypertensives and 518±39% in SR patients (p=0.005). The addition of L-NMMA significantly reduced acetylcholine induced vasodilation in SR patients (from 518% to 318%), but not in SS patients (from 358% to 292%). The endothelium-independent vasodilation did not differ between groups (maximal response to sodium nitroprusside infusion: 411±32% in SS vs. 378±30 in SR; p=0.464), and it was unmodified with the addition of L-NMMA. In conclusion, salt sensitivity of essential hypertension is associated with a decrease in acetylcholine-induced vasodilation, indicating an impairment in endothelial L-arginine NO pathway.

The aim of the present study was to assess the relationship of 24-hour noninvasive continuous finger blood pressure variability to the presence of cerebral white matter lesions (WML) in asymptomatic middle-aged untreated hypertensive patients. Seventeen mild to moderate never treated essential hypertensive patients (11 men, 6 women), aged 50–60 years, without clinical evidence of target organ damage were studied. All patients underwent a brain-magnetic resonance imaging and a 24-hour noninvasive beat-to-beat finger blood pressure monitoring by means of a Portapres device. Systolic (SBP), diastolic (DBP) and mean (MBP) blood pressures were obtained from each single pulse wave by the FAST software. We calculated 24-hour SBP, DBP, MBP, pulse pressure (PP) as well as short-term variability (average of the standard deviations obtained for each half-hour MBP) and long-term variability (standard deviation of the average of the half-hour MBP values). Preliminary results show that middle-aged hypertensives with silent cerebral WML have a tendency towards higher values of SBP, DBP, MBP, PP, and longterm variability than hypertensives without WML. (See Table) Without WML (n = 9)With WML (n = 8)Portapres 24-h SBP135.79 (13.05)138.54 (11.21)Portapres 24-h DBP77.00 (10.02)79.84 (6.97)Portapres 24-h MBP95.71 (9.67)99.84 (6.27)Pulse pressure56.93 (13.03)58.69 (10.82)Short-term variability9.59 (1.41)9.15 (1.26)Long-term variability9.63 (2.87)10.49 (1.80) Data are mean (standard deviation). Values are expressed in mmHg. These preliminary results suggest that, in addition to the severity of BP values, long-term Bp variability may be associated with the development of cerebral white matter lesions.