Resultados alcanzados con la puesta en marcha del circuito “Código Ictus” en un gran hospital: papel de urgencias y análisis de la curva de aprendizaje / Stroke code implementation in a large hospital: outcomes, the role of the emergency department, and analysis of the learning curve

Objetivo: Analizar el desarrollo y los resultados obtenidos con la puesta en marcha del circuito “Código Ictus” (CI), tanto en su fase de implementación intrahospitalaria, en un primer periodo, como en la fase de implementación intra y extrahospitalaria, en un segundo periodo. Método: Se definieron 2 periodos: un primer periodo A de 8 meses con circuito CI intrahospitalario y un segundo periodo B de 12 meses con circuito CI intra y extrahospitalario. De cada periodo se contabilizaron el número de ictus con criterio de CI, los CI activados, los CI con estudio completado y aquéllos que acabaron recibiendo tratamiento fibrinolítico. Finalmente se compararon los 2 periodos descritos (..) (AU)

Conclusiones: Estos resultados reflejan que la puesta en marcha de una atención protocolizaday consensuada entre los dispositivos extra e intrahospitalarios para los pacientescon ictus de menos de 3 horas de evolución consigue un porcentaje final de ictus fibrinolizadosdel 6%, lo cual no supone un incremento porcentual de tratamiento fibrinolíticorespecto al periodo de protocolo exclusivamente intrahospitalario. De este estudio seextrae, además, que las principales causas por las que no se consigue aumentar esteporcentaje son por una parte la tardanza en la llegada del paciente a urgencias y la presenciade diagnósticos alternativos, por otra. [Emergencias 2009;21:105-113]

Objective: To analyze the implementation of a stroke code protocol and the results obtained in an initial phase inside a hospital and in a second phase during which the stroke code was also used for attending emergencies outside thehospital. Methods: Retrospective analysis of 20 months' application of the stroke code protocol. Two periods were defined for analysis. During the first period of 8 months, the code was used inside the hospital. In a second period of 12 months the code was used both inside and outside the hospital. Data collected for analysis of each period were the numbers of strokes diagnosed according to the stroke code criteria, the number of times the protocol was activated, the number of code procedures finalized, and the number of patients who received fibrinolytic therapy. The results obtained during the2 periods were compared (..) (AU)

Increased levels of atherosclerosis markers in salt-sensitive hypertension.

BACKGROUND: Salt sensitivity in essential hypertension is associated with both endothelial dysfunction and increased cardiovascular risk. We evaluated several serum markers of atherosclerosis and endothelial function in a group of essential hypertensive patients classified on the basis of their salt sensitivity. METHODS: Forty-three patients were classified as having salt-sensitive (20 subjects) or salt-resistant (23 subjects) hypertension on the basis of their 24-h blood pressure (BP) response from low salt (50 mmol/d) to high salt (250 mmol/d) intake. Endothelium-dependent and independent responses were measured in the forearm previously to salt manipulation. High-sensitivity C-reactive protein (CRP), soluble intercellular adhesion molecule type 1 (sICAM-1), soluble vascular cell adhesion molecule type 1 (sVCAM-1), e-selectin, p-selectin, interleukin-6 (IL-6), monocyte chemotactic protein type 1 (MCP-1), matrix metalloproteinases types 1, 2, and 9 (MMP-1, MMP-2, and MMP-9), and the tissue inhibitor of metalloproteinases type 1 (TIMP-1) were measured in serum on the last day of both low salt and high salt intakes. RESULTS: Compared to salt-resistant patients, salt-sensitive hypertensives showed age-adjusted increased levels of p-selectin (P = .006), e-selectin (P = .042), and MCP-1 (P = .036), although differences in e-selectin were not maintained after adjustment for BP values. Moreover, salt-sensitive subjects exhibited decreased serum levels of MMP-9 (P = .007) and increased levels of TIMP-1 (P = .045). No differences in serum CRP, sICAM-1, sVCAM-1, or IL-6 were observed between salt-sensitive and salt-resistant patients. Finally, maximal acetylcholine-induced vasodilation (319% +/- 153% v 414% +/- 178% increase in forearm blood flow; P = .022 age-adjusted) was significantly impaired in salt-sensitive hypertensives. CONCLUSIONS: Serum markers of inflammation, especially selectins and chemokines, as well as markers of vascular remodeling, and endothelium-dependent vasodilation are altered in salt-sensitive hypertension. These alterations could help to explain the greater target organ damage and cardiovascular risk observed in salt-sensitive subjects.

Once-daily fixed-combination irbesartan 300 mg/ hydrochlorothiazide 25 mg and circadian blood pressure profile in patients with essential hypertension.

BACKGROUND: More than 60% of patients with hypertension included in morbidity and mortality trials needed >or=2 drugs to achieve a substantial, sustained reduction in blood pressure. Tolerable combinations using higher doses of antihypertensive drugs are frequently required to control blood pressure. OBJECTIVE: The goal of this study was to assess the effect of a once-daily fixed combination of irbesartan 300 mg/hydrochlorothiazide (HCTZ) 25 mg on the circadian blood pressure profile in patients with essential hypertension that was not controlled with full-dose single therapy or low-dose combined therapy. METHODS: Study patients were recruited consecutively from the outpatient hypertension clinics of 3 university hospitals in Spain. After a 1-week washout period, patients with a mean daytime blood pressure >135/85 mm Hg were treated with irbesartan 300 mg/HCTZ 25 mg once daily for 12 weeks. Twenty-four-hour ambulatory blood pressure monitoring was performed at the end of the washout period and during the last week of treatment. RESULTS: Fifty-seven patients with essential hypertension (28 men, 29 women) were enrolled; their mean (SD) age was 60.4 (7.2) years (range, 45-78 years). After treatment, a significant reduction in both clinic and ambulatory mean (SD) blood pressure values was observed in the whole group of 57 patients (from 146.0 [11.0] mm Hg to 123.3 [13.3] mm Hg, P < 0.001 for 24-hour systolic blood pressure [SBP]; from 89.9 [8.2] mm Hg to 76.5 [9.4] mm Hg, P < 0.001 for 24-hour diastolic blood pressure [DBP]. The mean lowering of ambulatory SBP and DBP at peak was 25.2 (14.5) mm Hg and 14.7 (9.5) mm Hg, respectively, and at trough, 22.3 (18.3) mm Hg and 12.3 (10.9) mm Hg. The trough-to-peak ratio of the group was 0.92 for SBP (0.97 in responders) and 0.84 for DBP (0.89 in responders). The smoothness index, calculated as the mean of all individual values, was 1.7 (1.0) for SBP (1.8 [0.9] in responders) and 1.3 (0.8) for DBP (1.5 [0.6] in responders). Seven side effects in 6 patients were reported. No metabolic changes were observed, and no patient discontinued the study because of treatment-related adverse effects. CONCLUSIONS: The fixed combination of irbesartan 300 mg/HCTZ 25 administered once daily produced a crude meaningful effect in reducing 24-hour blood pressure and was well tolerated. The circadian profile was preserved, as shown by trough-to-peak ratios and smoothness index values for both SBP and DBP.

[Impact of components and methods of measurement of blood pressure on damage of target organs and cardiovascular complications in arterial hypertension]. / Impacto de los componentes y sistemas de medición de la presión arterial sobre la lesión de órgano diana y las complicaciones cardiovasculares en la hipertensión arterial.

BACKGROUND: The goal of this study was to evaluate the relative association of several components of blood pressure (BP), as measured in the office and by ambulatory monitoring (ABPM), with clinically useful indicators of target organ damage and cardiovascular events (CE) in essential hypertensive patients. PATIENTS AND METHOD: We retrospectively included 390 hypertensives (55% men; mean age: 56 years) between 1989 and 1998. All them had a baseline office BP measurement and a valid 24-hour ABPM record, both performed while the patient was free of antihypertensive therapy. Estimates of target organ damage included electrocardiographic indexes of left ventricular hypertrophy (Cornell and Sokolow-Lyon), serum creatinine, 24-hour urine protein excretion and creatinine clearance. Multiple linear regression and logistic regression analyses were used to evaluate the relationship between BP and target organ damage or CE. RESULTS: Forty-nine patients had CE (26 stroke, 18 myocardial infarction and 5 both). The BP parameter correlating better with cardiovascular events was office pulse pressure (multivariate odds ratio: 1.03; CI 95%: 1.00-1.05; p = 0.0095). Nevertheless, cardiac growth indexes correlated better with ABPM measurements. In fact, Cornell index correlated with night-time systolic BP (standardized regression coefficient beta: 0.260; p < 0.001) and Sokolow-Lyon index correlated with day-time systolic BP ( beta: 0.257; p < 0.001). Creatinine clearance inversely correlated with night-time pulse pressure ( beta: 0.122; p = 0.017) while proteinuria correlated better with 24-hour systolic BP ( beta: 0.390; p < 0.001). CONCLUSIONS: Whereas office BP (especially pulse pressure) is associated with the development of CE, ABPM estimates show a better association with target organ damage, especially systolic and pulse pressures.

Impacto de los componentes y sistemas de medición de la presión arterial sobre la lesión de órgano diana y las complicaciones cardiovasculares en la hipertensión arterial / Impact of components and methods of measurement of blood pressure on damage of target organs and cardiovascular complications in arterial hypertension

FUNDAMENTO: Evaluar el impacto de los diferentes componentes de la presión arterial (PA), determinados tanto en la consulta como por monitorización ambulatoria de la PA (MAPA), sobre el desarrollo de la lesión de órgano diana y los episodios cardiovasculares (ECV) de la hipertensión arterial (HTA).PACIENTES Y MÉTODO: Estudio retrospectivo llevado a cabo en 390 pacientes (55 per cent varones; edad media de 56 años) atendidos en una unidad de HTA entre 1989 y 1998. En todos los pacientes se disponía de las determinaciones iniciales de la PA clínica mediante esfigmomanómetro de mercurio y de MAPA de 24 h, con el paciente libre de tratamiento antihipertensivo. Se obtuvieron los índices de Cornell y Sokolow del ECG como reflejo de la afección cardíaca hipertensiva y la creatinina sérica, aclaramiento de creatinina y excreción urinaria de proteínas en 24 h, como medida del daño renal. La metodología estadística empleada fue la regresión lineal múltiple y la regresión logística. RESULTADOS: Cuarenta y nueve pacientes desarrollaron ECV (26 accidentes cerebrovasculares, 18 infartos de miocardio y 5 pacientes con ambos episodios). De todas las mediciones de PA, fue el aumento de la presión de pulso (PP) en la clínica el factor independiente mejor relacionado con la aparición de ECV (odds ratio multivariado = 1,03; intervalo de confianza [IC] del 95 per cent, 1,00-1,05; p = 0,0095).Respecto a la correlación con los diferentes indicadores de lesión del órgano diana, los análisis de regresión lineal múltiple pusieron de manifiesto una asociación del índice de Cornell del ECG con la PAS nocturna obtenida en MAPA (coeficiente estandarizado Beta = 0,260; p < 0,001), del índice de Sokolow con la PAS diurna (Beta = 0,257; p < 0,001), del aclaramiento de creatinina con la PP nocturna (correlación inversa Beta = -0,122; p = 0,017) y de la proteinuria con la PAS de 24 h (Beta = 0,390; p < 0,001).CONCLUSIONES: El desarrollo de ECV en la HTA se correlaciona con las cifras de PA clínica (especialmente con la PP), mientras que los indicadores de la lesión del órgano diana (hipertrofia cardíaca, lesión renal) se correlacionan mejor con la PA obtenida mediante MAPA (especialmente con la PAS y PP) (AU)

Salt intake, endothelial dysfunction, and salt-sensitive hypertension.

Numerous epidemiologic and clinical studies have demonstrated a clear relationship between high salt intake and blood pressure. However, the mechanisms of a salt-induced increase in blood pressure--a phenomenon known as salt sensitivity--and the heterogeneity of this effect are far from being completely understood. Endothelial dysfunction, and especially the nitric oxide system, is implicated in both experimental and clinical hypertension. Animal studies indicate that endogenous nitric oxide plays an important role in renal hemodynamics and sodium homeostasis, inducing renal vasodilation and natriuresis. Studies of essential hypertensive patients have also suggested that both high salt intake and salt sensitivity are associated with impaired endothelial function. Although there are many hypotheses concerning the nature of salt sensitivity, clinical data indicate that salt-sensitive patients may be unable to up-regulate the production of nitric oxide in response to salt intake. This endothelial dysfunction, which is more frequent in salt-sensitive than in salt-resistant essential hypertensive patients, may partially explain the blood pressure increase in response to salt intake and may underlie the more pronounced target organ damage and cardiovascular risk in salt-sensitive patients.