In this study the authors assessed the effectiveness and safety of isosorbide dinitrate aerosol administered through the oral mucosa in 30 adult patients who presented with a hypertensive crisis (mean arterial pressure > 130 mm Hg and evidence of target organ damage). The patients were given a first dose of 1.25 mg of aerosol when they were admitted to the hospital; a second dose was administered 15 minutes later if the mean arterial pressure had not decreased by > 15%. An electrocardiogram (ECG) was obtained for every patient immediately prior to and 30 minutes after administration of the medication. Nine patients (30%) had a good response with one dose, whereas 21 patients (70%) required a second dose. All 30 patients had a significant reduction of the arterial blood pressure (187+/-13 / 121+/-6.6 to 153+/-15.3 / 92.3+/-7.6 mm Hg; p<0.005) as well as of the mean arterial pressure (136.6+/-8 to 109.5+/-7 mm Hg; p<0.005) in a period of 30 minutes. No adverse effects, rebound hypertension, or severe hypotension were observed. These figures remained under control for 6 hours. Two of the patients had angina pectoris at admission and their ECG showed subepicardial ischemia, both of which disappeared with the medication. A second ECG appeared normal. A reduction of 14% in heart rate was obtained (95+/-15 to 82+/-14 beats per minute; p<0.005). These observations suggest that isosorbide dinitrate aerosol is an effective and safe alternative for the treatment of patients with hypertensive crises.

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Sixty patients with a hypertensive emergency (mean arterial pressure >130 mm Hg and evidence of target organ damage) were randomly divided into two groups of 30 patients each. Group A received 1.25 mg of isosorbide dinitrate aerosol upon arrival and a second dose 15 minutes later when the mean arterial pressure reduction was < 15%. Group B received a single 5 mg tablet of sublingual isosorbide dinitrate. Electrocardiography was performed in both groups prior to and 30 minutes after the medication. Blood pressure was monitored for 6 hours. Blood pressure in Group A patients decreased in an average time of 10 minutes from 191 +/- 12/122.3 +/- 5 to 151.5 +/- 9.2/93 +/- 4 mm Hg, p < 0.005. Mean arterial pressure decreased by 22.8%: 145 +/- 7 to 112 +/- 7.5 mm Hg, p < 0.005. No adverse effects occurred. Five patients in Group B did not respond; in the rest of the group blood pressure decreased 45 minutes after receiving the medication from 194 +/- 8/125 +/- 5.5 to 160 +/- 11/98 +/- 6 mm Hg; p < 0.005. Mean arterial pressure decreased by 20.1%: 148.3 +/- 12 to 118.6 +/- 9 mm Hg, p < 0.002; ten patients suffered headache. Three patients in Group A had a subepicardial lesion in the first electrocardiograph, which disappeared with the use of the aerosol. In Group B, electrocardiography results were normal. These results seem to indicate that isosorbide dinitrate aerosol is better than tablets for the treatment of patients with a hypertensive emergencies.

La rigidez de la pared arterial es un predictor independiente de mortalidad cardiovascular. Se evalúa midiendo la velocidad de la onda del pulso (VOP), un procedimiento no invasivo y validado. El exceso de ácido úrico genera disfunción endotelial y daño vascular, lo que favorece la fibrosis y remodelación vascular, y con ello rigidez arterial. Objetivo: Evaluar si hay correlación entre los niveles de ácido úrico y la VOP en sujetos con síndrome metabólico. Método: Se evaluaron 165 pacientes con síndrome metabólico, en quienes se determinó la VOP usando un equipo Arteriograph. Se consideró normal una VOP ≤ 9 m/s. En todos ellos se realizó la determinación de ácido úrico (método enzimático). Los métodos estadísticos usados fueron coeficiente de correlación de Pearson y razón de momios. Resultados: Encontramos una correlación significativa (r = 0.41, r 2 = 0.16; p < 0.00001) entre la VOP y los niveles séricos de ácido úrico, la razón de momios para presentar VOP aumentada en sujetos con hiperuricemia fue . Conclusión: Nuestros resultados sugieren que el ácido úrico tiene un papel sobre los mecanismos que llevan a la rigidez arterial. Estudios posteriores determinarán si disminuir sus niveles séricos mejorarían la rigidez arterial.

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