Papel de la espironolactona en el tratamiento de la hipertensión arterial resistente / Role of spironolactone in the treatment of resistant hypertension

Resumen Este artículo aporta herramientas útiles para el diagnóstico y el diagnóstico diferencial de la hipertensión arterial resistente. En él, se refieren las recomendaciones de las principales guías internacionales de tratamiento respecto de las cifras meta de presión arterial, la incapacidad o falla del tratamiento triple en un amplio porcentaje de pacientes y los factores para la elección racional del cuarto agente para la institución de un tratamiento cuádruple. Esta elección se basa en la capacidad de la espironolactona -antagonista de los receptores de aldosterona- para inhibir los efectos nocivos de la aldosterona que dificultan el control de la presión arterial e incrementan el riesgo cardiovascular en un alto porcentaje de pacientes.

Abstract This article provides useful tools for the diagnosis and differential diagnosis of resistant hypertension. Here, we refer the recommendations of the main international guidelines of management respect to the target goals of the blood pressure, the failure of triple therapy in a large percentage of patients and the factors for the rational choice of the fourth agent for the institution of a quadruple therapy. This choice is based on the ability of spironolactone, antagonist of aldosterone receptors, to inhibit the deleterious effects of aldosterone that difficult the control of blood pressure and increase the cardiovascular risk in a high percentage of patients.

Relationship Between Nocturnal Dip, Carotid Artery Blood Flow, Brain Ischemic Change in Open Angle Glaucoma

PURPOSE: To investigate the effect of nocturnal dip, carotid artery blood flow, and brain ischemic change on the progression of glaucomatous visual field defect in open-angle glaucoma (OAG) when IOP is less than the target pressure. METHODS: We classified OAG patients (74 patients, 148 eyes) who maintained IOP less than the target pressure as normal tension glaucoma (NTG; 52 patients, 104 eyes) or primary OAG (POAG; 22 patients, 44 eyes). Additionally, we performed 24-hr ambulatory blood pressure monitoring (24-hr ABPM), carotid artery color Doppler U/S (CAD), brain MRI, and visual field (V/F) tests on the patients. Nocturnal dips less than 10% were classified as non-dippers, and dips greater than 10% as dippers. The relationships among nocturnal dip, carotid artery blood flow, brain ischemic change, and progression of glaucomatous V/F defect were examined. RESULTS: In the case of dippers, glaucomatous V/F defects were aggravated, with a relative risk of approximately 1.74 (NTG) and 2.91 (POAG) times that of non-dippers. In NTG, decreased carotid artery blood flow and brain ischemic change furthered glaucomatous V/F defects, with a relative risk of approximately 2.40 and 2.54 times that of normal carotid artery blood flow and brain MRI findings, respectively. However, in POAG, decreased carotid artery blood flow and brain ischemic change were not influenced by the progression of glaucomatous V/F defects. CONCLUSIONS: In dippers, decreased carotid artery blood flow and brain ischemic change caused a progression of glaucomatous V/F defects in NTG and POAG patients. Thus, performing 24-hr ABPM, CAD, and brain MRI should be helpful for glaucoma patients with progression of glaucomatous V/F defects even when the IOP is less than the target pressure. In addition, this analysis provides useful information regarding glaucoma diagnosis and treatment.

Correlation Between Nocturnal Dip and Progression of Glaucoma

PURPOSE: To investigate the effect of nocturnal dip influence on the progression of glaucomatous visual field defect. METHODS: We performed 24hr ABPM and V/F tests on patients diagnosed with NTG (140 patients, 280 eyes) and POAG (84 patients, 168 eyes). Nocturnal dips below 10% were classified as non-dippers, and those above 10% were noted as dippers. The correlations among nocturnal dip, progression of glaucomatous visual field defect, and hypertension treatment were examined. RESULTS: In NTG, dippers in both systolic and diastolic blood pressure furthered glaucomatous visual field defects, with a relative risk of approximately three times that of non-dippers. Hypertension treatment was not influenced by the progression of glaucomatous visual field defect but was influenced by dips in the systolic and diastolic pressures in NTG and in diastolic pressure in POAG. Nocturnal dips were more frequent in the group with progression of the visual field compared to those in the group with non-progression of the visual field in NTG. CONCLUSIONS: Dipper caused a progression of glaucomatous visual field defects in NTG and was influenced by hypertension treatment in NTG and POAG. Performing 24hr ABPM should be helpful for glaucoma patients with progression of a glaucomatous visual field defect even when the IOP is less than the target pressure. In addition, hypertension treatment should be considered an important factor in the treatment of glaucoma.