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Journal Article

Prevención y tratamiento de la hipertensión arterial sistémica en el paciente con enfermedad arterial coronaria

TL;DR: La asociacion entre hipertension arterial sistemica (HAS) y enfermedad arterial coronaria esta bien demostrada a traves de diversos estudios epidemiologicos.
Abstract: La asociacion entre hipertension arterial sistemica (HAS) y enfermedad arterial coronaria esta bien demostrada a traves de diversos estudios epidemiologicos. La hipertension arterial es un factor de riesgo independiente importante para el desarrollo de coronariopatia, enfermedad vascular cerebral y nefropatia. Existen avances importantes en el conocimiento de factores neurohumorales y hemodinamicos que confluyen en la fisiopatologia de la hipertension y en el desarrollo de enfermedad coronaria que permiten establecer mejores estrategias no solo de tratamiento sino tambien de prevencion, con la finalidad de disminuir la mortalidad cardiovascular. El espectro de la cardiopatia aterosclerosa es amplio y las estrategias de tratamiento de la hipertension deben adecuarse a la forma de manifestacion de la enfermedad coronaria que se presente. El tratamiento de ambas condiciones requiere de lineamientos especificos de acuerdo a las condiciones del paciente y la forma de presentacion de cada una de estas patologias
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TL;DR: Estudio casi experimental pre and postest sin grupo de control, cuyo objetivo fue analizar los beneficios de un programa de ejercicio fisico con ritmo en personas con hipertension arterial dirigido por enfermeria en un municipio del Estado de Mexico.
Abstract: Estudio casi experimental pre y postest sin grupo de control, cuyo objetivo fue analizar los beneficios de un programa de ejercicio fisico con ritmo en personas con hipertension arterial dirigido por enfermeria en un municipio del Estado de Mexico. Se realizo un programa de intervencion en 110 pacientes con hipertension arterial, en 20 sesiones de ejercicio fisico con ritmo habiendo aceptado participar del estudio mediante la firma de consentimiento informado. Para el analisis de datos se utilizo como prueba de significacion x² con valor de p=0.05. Dentro del estudio intervinieron 99 mujeres; de ellas, 81.8% son amas de casa. Despues de la intervencion, la presion arterial sistolica mostro disminucion significativa en 8.28 mmHg y la presion diastolica 4.72 mmHg. El programa de ejercicio fisico con ritmo provoco efectos favorables sobre la presion arterial, como una actividad de enfermeria en su rol de educador.

8 citations

Journal Article
TL;DR: This study aims to analyze the behavior of HRD mortality in Mexico between 1998 and 2009 and analyzes the specific rates by age and sex and standardized mortality ratio (SMR) by states and regions.
Abstract: espanolintroduccion: La hipertension arterial sistemica (HAS) es un factor de riesgo para las enfermedades cronicas. En el mundo, un 20-25% de los adultos presentan HAS, de los que el 70% vive en paises en desarrollo. La enfermedad renal cronica hipertensiva (ERCH) es una complicacion de la hipertension arterial mal controlada. El presente estudio pretende analizar el comportamiento de la mortalidad por ERCH en Mexico entre 1998-2009. Material y metodos: Estudio longitudinal, con analisis de registros secundarios a ERCH procedentes de las bases de datos suministradas por el Instituto Nacional de Estadistica, Geografia e Informatica (INEGI), donde se analizan las tasas especificas por edad y sexo, y razones estandarizadas de mortalidad (REM) por estados y regiones. Se emplean metodos de georreferenciacion estatal. Resultados: En Mexico, entre 1998 y 2009 hubo 48,823 muertes por ERCH. La tasa de mortalidad estandarizada ascendio desde 3.35/100,000 habitantes a 6.74 (p Englishintroduction: High blood pressure (HBP) is a risk factor for chronic diseases. Worldwide, 20-25% of adults have hypertension, with 70% of them living in developing countries. Hypertensive renal disease (HRD) is a complication of insufficiently controlled hypertension. This study aims to analyze the behavior of HRD mortality in Mexico between 1998 and 2009. Methods: Longitudinal study with secondary analysis of HRD records from the databases provided by INEGI, which analyzes the specific rates by age and sex and standardized mortality ratio (SMR) by states and regions. Georeferencing methods are used statewide. Results: In Mexico from 1998 to 2009 there were 48,823 deaths from HRD. The standardized mortality rate rose from 3.35/100,000 inhabitants to 6.74 (p

6 citations

Journal ArticleDOI
TL;DR: The factors affecting the length of intensive care unit (ICU) stay in patients undergoing isolated on-pump coronary artery bypass (CABG) and effective factors on morbidity, mortality, and survival among patients with prolonged ICU stay were investigated.
Abstract: We aimed to investigate the factors affecting the length of intensive care unit (ICU) stay in patients undergoing isolated on-pump coronary artery bypass (CABG). We also aimed to evaluate effective factors on morbidity, mortality, and survival among patients with prolonged ICU stay. Between January 2002 and December 2009, a total of 1,657 patients underwent isolated on-pump CABG in our clinic. Prolonged ICU stay (>2 days) was present in 532 patient (32.1 %). Diabetes (OR 1.49, P = 0.006), hypertension (OR 1.37, P = 0.029), chronic obstructive pulmonary disease (OR 9.06, P 3 units) (OR 3.23, P = 0.007) were the independent predictive factors of prolonged ICU stay (>2 days). Postoperative mortality rate was 7 % (n = 37) and 2.3 % (n = 26) in patients with length of ICU stay >2 days and length of ICU stay ≤2 days (P 2 days (P < 0.0001). Postoperative mortality was higher in patients with prolonged ICU stay. Mean follow-up was shorter in patients with prolonged ICU stay.

1 citations

References
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TL;DR: Aldosterone exerts powerful effects on blood vessels, independent of actions that can be attributed to blood pressure (BP) rise mediated via regulation of salt and water balance and through rapid nongenomic pathways that may also be important in hypertension.
Abstract: Aldosterone is a steroid with mineralocorticoid activity produced mostly by the adrenal glomerulosa. Aldosterone may also be generated in the heart and blood vessels, although there is controversy on whether the amounts produced are physiologically relevant. The classical target of aldosterone is the distal convoluted tubule of the kidney, where it acts on cytosolic mineralocorticoid receptors (MRs) that translocate to the nucleus and via different mechanisms (serum and glucocorticoid-induced kinase-1 [SGK-1], neural precursor cell expressed developmentally downregulated 4 [nedd4], nedd4 isoform 2 [nedd4-2], K-Ras2A, and capsaicin)1 modulating the epithelial sodium channel and renal outer medullary potassium channels to induce increased reabsorption of sodium and excretion of potassium, thus regulating sodium, potassium, and body fluid balance. Over the past few years it has become increasingly evident that aldosterone exerts powerful effects on blood vessels,2 independent of actions that can be attributed to blood pressure (BP) rise mediated via regulation of salt and water balance. Some deleterious consequences of aldosterone and, accordingly, some benefits derived from MR antagonism, may be BP dependent.3 However, the aldosterone effects on which this review will concentrate are the direct, BP-independent ones, although these may, indeed, contribute together with salt and water retention to BP elevation. The reader should be cautioned, however, that many of the vascular actions of aldosterone mentioned in this article were obtained with large unphysiological doses of aldosterone, which may raise questions regarding their physiological significance. Aldosterone has been reported to be synthesized,4 MRs demonstrated,5 and the presence of the cortisol-inactivating enzyme 11-β-hydroxysteroid-dehydrogenase-2 identified in blood vessels.6 However, the production of aldosterone by blood vessels and the heart remains controversial (see below).7,8 In addition to its classical genomic mechanisms, aldosterone exerts effects through rapid nongenomic pathways that may also be important in hypertension.9 Some studies …

274 citations

Journal ArticleDOI
TL;DR: Hirudin reduces reocclusion compared to heparin following thrombolysis in acute myocardial infarction: results of the TIMI-5 trial.
Abstract: 117. Cannon CP, McCabe CH, Henry TD, Rogers WJ, Schweiger M, Gibson RS, Anderson JL, Williams DO, Braunwald E, for the TIMI 5 Investigators. Hirudin reduces reocclusion compared to heparin following thrombolysis in acute myocardial infarction: results of the TIMI-5 trial. J Am Coll Cardiol. 1993;21:136a.

274 citations

Journal Article
01 Jan 1986-Heart
TL;DR: It is suggested that in patients not on previous beta blockade metoprolol has a beneficial short term effect on unstable angina, that fixed combination with nifedipine provides no further gain, and that nifingipine may be detrimental.
Abstract: A multicentre, double blind, placebo controlled, randomised trial of nifedipine, metoprolol, and nifedipine and metoprolol combined was conducted in a group of 338 patients with unstable angina not pretreated with a beta blocker and of nifedipine in 177 patients pretreated with a beta blocker. The main outcome event was recurrent ischaemia or myocardial infarction within 48 hours. Trial medication effects were expressed as ratios of event rates relative to placebo. In patients not pretreated with a beta blocker the event rate ratios with associated 95% confidence intervals were 1.15 (0.83, 1.64) for nifedipine, 0.76 (0.49, 1.16) for metoprolol, and 0.80 (0.53, 1.19) for nifedipine and metoprolol combined. In patients already on a beta blocker the addition of nifedipine was beneficial (rate ratio 0.68 (0.47, 0.97). Equal numbers of patients developed myocardial infarction and reversible ischaemia. Most infarctions occurred early, within six hours of randomisation. In patients not already on a beta blocker the nifedipine rate ratio for infarction only was 1.51 (0.87, 2.74). These results suggest that in patients not on previous beta blockade metoprolol has a beneficial short term effect on unstable angina, that fixed combination with nifedipine provides no further gain, and that nifedipine may be detrimental. On the other hand, the addition of nifedipine to existing beta blockade when the patient's condition becomes unstable seems beneficial.

274 citations

Journal ArticleDOI
TL;DR: Data reveal a significant upregulation of AT1 receptor gene expression by LDL in vascular smooth muscle cells through mechanisms that involve posttranscriptional mRNA stabilization, which leads to an elevated functional response of vascular smoother muscle cells on angiotensin II stimulation.
Abstract: Background Because LDL and the angiotensin II type 1 (AT1) receptor are thought to be involved in the pathogenesis of chronic vascular disease, we studied possible interactions between these two biological systems in cultured rat vascular smooth muscle cells. Methods and Results Incubation of vascular smooth muscle cells with 100 μg/mL LDL profoundly increased AT1 receptor mRNA to ≈250% of control levels as assessed by Northern hybridization analysis. This effect is maximal 12 hours after addition of LDL to the culture medium and is sustained for up to 24 hours. The LDL-induced upregulation is dose dependent, with a maximal effect obtained with 100 μg/mL LDL. There is a correlative increase of cell surface–associated AT1 receptors as assessed by saturation radioligand binding assays. The half-life of AT1 receptor mRNA is increased substantially by LDL compared with that of cells treated only with 5,6-dichlorobenzimidazole to block transcription. Angiotensin II–induced elevation of cytosolic calcium concen...

272 citations

Journal ArticleDOI
TL;DR: It is demonstrated that hypercholesterolemia-induced stimulation of angiotensin peptide production provides a basis for the marked effect of AT1A receptor deficiency in reducing atherosclerosis.
Abstract: Background— Hypercholesterolemia-induced atherosclerosis is attenuated by either pharmacological antagonism of AT1 receptors or AT1A receptor deficiency. However, the mechanism underlying the pronounced responses to angiotensin II (Ang II) antagonism has not been determined. We hypothesized that hypercholesterolemia stimulates the production of angiotensin peptides to provide a rationale for the profound effect of AT1A receptor deficiency on atherogenesis. Methods and Results— Atherosclerotic lesions were analyzed in LDL receptor–deficient mice. Immunocytochemical analysis demonstrated that atherosclerotic lesions contained all the components of the conventional pathway for Ang II synthesis. AT1A receptor deficiency caused a marked decrease in atherosclerotic lesion size in both the aortic root and arch of male and female mice, without a discernible effect on composition. AT1A receptor deficiency–induced reductions in atherosclerosis were independent of systolic blood pressure and measurements of oxidatio...

258 citations