Clonidina y nifedipina oral en el tratamiento de la urgencia hipertensiva

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Abstract

Se diseña un estudio para evaluar la introducción de la clonidina en la terapéutica de la urgencia hipertensiva en nuestro país, con un estudio a doble ciegas en el que se usó la nifedipina como medicamento de control. Se trataron 60 pacientes aleatoriamente con una dosis horaria de 0,15 mg de clonidina o 10 mg de nifedipina por vía oral, en un ensayo prospectivo. No hubo diferencias estadísticamente significativas entre ambos grupos respecto a la edad, sexo y tensión arterial diastólica inicial. Se obtuvo una buena respuesta después de un período de observación de 3 horas en el 96,6 % del grupo tratado con clonidina y en el 90,0 % del grupo tratado con nifedipina. La ganancia tensional diastólica a los 120 minutos fue de 27,6 mmHg (nifedipina) y de 31,3 mmHg (clonidina). En ambos grupos la frecuencia del pulso disminuyó en el tiempo. No se apreció influencia estadísticamente significativa de las variables número de dosis recibidas, tipo de medicación o reducción de la tensión arterial sobre la disminución del pulso radial, aunque fue mayor (p = 0,06) con el uso de la clonidina. Los efectos sedantes del alfa agonista, aunque comunes, no fueron de importancia clínica.

Translated abstract

A study was designed to evaluate the introduction of clonidine for the therapy of hypertensive emergencies in our country, in a double-blind study with the use of nifedipine as control drug. A number of 60 patients were randomly treated with a dose of 0.15 mg of clonidine or 10 mg of nifedipine by oral route in a prospective assay. There were no statistically significant differences between both groups regarding age, sex and baseline diastolic blood pressure. A good response was obtained after an observational period of 3 hours in 96.6 % of patients treated with clonidine, and in 90.0 % of cases treated with nifedipine. The diastolic pressure gain at 120 minutes was 27.6 mm Hg (nifedipine) and of 31.3 mm Hg (clonidine). The pulse rate decreased with the time in both groups. No statistically significant influence was observed with respect to the variables such as the number of doses received, type of drug or reduction of blood pressure on the reduction of the radial pulse, although it was greater (P = 0.06) with the use of clonidine. The sedative effects of the alpha agonist, however bling common, were not relevant from the clinical point of view.

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Most cited references 21

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The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering.

(1984)

In the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), a 19% lower incidence of coronary heart disease (CHD) in cholestyramine-treated men was accompanied by mean falls of 8% and 12% in plasma total (TOTAL-C) and low-density lipoprotein (LDL-C) cholesterol levels relative to levels in placebo-treated men. When the cholestyramine treatment group was analyzed separately, a 19% reduction in CHD risk was also associated with each decrement of 8% in TOTAL-C or 11% in LDL-C levels (P less than .001). Moreover, CHD incidence in men sustaining a fall of 25% in TOTAL-C or 35% in LDL-C levels, typical responses to the prescribed dosage (24 g/day) of cholestyramine resin, was half that of men who remained at pretreatment levels. Adherence to medication was associated with reduced incidence of CHD only when accompanied by falls in TOTAL-C and LDL-C levels. Small increases in high-density lipoprotein cholesterol levels, which accompanied cholestyramine treatment, independently accounted for a 2% reduction in CHD risk. Thus, the reduction of CHD incidence in the cholestyramine group seems to have been mediated chiefly by reduction of TOTAL-C and LDL-C levels.