Assessment of cognitive function in patients with essential hypertension treated with lercanidipine.

OBJECTIVES: The aim of this longitudinal, open-label, comparative, multicenter study was to assess cognitive function in hypertensive patients receiving mid-term treatment with lercanidipine. METHODS: Hypertensive patients aged 40 years or older were treated with lercanidipine (10 mg daily) after 7-10 days washout period. The duration of the study was 6 months. Blood pressure (BP) was measured every 4 weeks (JNC 6th report). In patients with inadequate BP control, doxazosin was added and up-titrated. At baseline and after 6 months of treatment, cognitive function was evaluated using the Spanish validated version of the Mini-Mental State Examination (MMSE) and the Trail Making Test (TMT). RESULTS: In the study population of 467 patients, BP decreased from 154.4/95.3 mmHg at baseline to 134.8/80.7 mmHg at 6 months. At the end of the study, 98% of patients were receiving lercanidipine, 20% an angiotensin-converting enzyme inhibitor, and 6% doxazosin. Adequate BP control was obtained in 68% of patients. The mean (standard deviation) MMSE scores improved from 32.35 (2.59) to 33.25 (2.36) (p < 0.0001). Patients with good BP control scored significantly better than those with inadequate BP control (p < 0.05), which was already observed at the first month. CONCLUSIONS: The third-generation calcium channel antagonist, lercanidipine, improved cognitive function after 6 months of treatment especially in patients with good BP control, suggesting that improvements in cognitive function may be associated with a decrease in BP.

Función cognitiva y demencia en la hipertensión arterial / Cognitive function and dementia in high blood pressure

Como consecuencia del envejecimiento de la población las alteraciones de la función cognitiva y las demencias están aumentando. El 90 % corresponden a la enfermedad de Alzheimer y a las demencias vasculares. Para la primera, constituyen factores de riesgo la edad, los antecedentes familiares de demencia y el alelo E4 del gen de la apolipoproteína E. Para la demencia vascular lo son la edad, el género masculino, la hipertensión arterial, la enfermedad coronaria, la diabetes, la aterosclerosis generalizada, el tabaquismo, una concentración elevada de lípidos e historia previa de ictus. El diagnóstico de demencia y deterioro cognitivo está basado en criterios clínicos y pruebas que adolecen de una precisión adecuada, en este sentido las modernas técnicas de neuroimagen (tomografía axial computarizada y resonancia magnética) están aportando valiosísima información al relacionar los infartos lacunares y las lesiones de la sustancia blanca no sólo a la hipertensión arterial y otros factores de riesgo cardiovascular, sino también a la aparición de demencia. En base a la información actualmente disponible se ha postulado que una presión arterial sistólica inicial elevada conduciría a múltiples infartos lacunares y a lesiones de la sustancia blanca cerebral que conducirían a un deterioro cognitivo progresivo y a una posterior reducción de la presión arterial. Aunque los beneficios del control de la presión arterial sobre la longevidad están firmemente establecidos, los costes que pueda tener sobre la función cognitiva no están determinados. Los estudios observacionales en general han demostrado una mejoría de la función cognitiva al tratar la hipertensión arterial. En cuanto al tratamiento farmacológico, los resultados se han de interpretar con precaución. En general, los diuréticos y betabloqueantes no empeoran o mejoran la función cognitiva. Los antagonistas de la angiotensina II, los inhibidores de la enzima conversora de la angiotensina y los calcioantagonistas tienen una influencia positiva sobre la función cognitiva. Los grandes ensayos clínicos (grado de evidencia A), con unas muestras poblaciones y un tiempo de duración más apropiados, han mostrado una reducción de la demencia con calcioantagonsitas dihidropiridínicos (nitrendipino) y con la combinación inhibidor de la enzima conversora de la angiotensina y diurético (perindopril más indapamida)

As a consequence of aging of the population, cognitive function disorders and dementias are increasing. A total of 90 % correspond to Alzheimer's disease and vascular dementias. For the former, the risk factors are age, family background of dementia and E4 allele of the apolipoprotein E gene. For the vascular dementia one, they are age, male gender, HBP, coronary disease, diabetes, generalized atherosclerosis, smoking, elevated lipid concentration and previous history of stroke. Diagnosis of dementia and cognitive deterioration is based on clinical criteria and tests that lack adequate accuracy. In this sense, modern neuroimaging techniques (CT scan and MRI) are supplying very valuable information, as it relates lacunar infarction and white substance lesions not only to HBP and other cardiovascular risk factors but also to the appearance of dementia. Based on the presently available information, it has been hypothesized that an initially elevated systolic BP would lead to multiple lacunar infarctions and to lesions of the brain white substance that would lead to progressive cognitive deterioration and to a later reduction of BP. Although the benefits of controlling BP on longevity are firmly established, the costs that it may have on cognitive function have not been determined. Observational studies in general have demonstrated improvement of cognitive function when HPB is treated. Regarding drug treatment, the results must be interpreted with care. In general, diuretics and beta blockers do not worsen or improve cognitive function. The antagonists of angiotensin II, ACE inhibitors and calcium antagonist have a positive affect on cognitive function. The large clinical trials (evidence A grade), with more appropriate population samples and duration time have shown a reduction of dementia with dihydropyridine calcium antagonists (nitrendipine) and with the ACE inhibitor and diuretic combination (perindopril plus indapamide)As a consequence of aging of the population, cognitive function disorders and dementias are increasing. A total of 90 % correspond to Alzheimer's disease and vascular dementias. For the former, the risk factors are age, family background of dementia and E4 allele of the apolipoprotein E gene. For the vascular dementia one, they are age, male gender, HBP, coronary disease, diabetes, generalized atherosclerosis, smoking, elevated lipid concentration and previous history of stroke. Diagnosis of dementia and cognitive deterioration is based on clinical criteria and tests that lack adequate accuracy. In this sense, modern neuroimaging techniques (CT scan and MRI) are supplying very valuable information, as it relates lacunar infarction and white substance lesions not only to HBP and other cardiovascular risk factors but also to the appearance of dementia. Based on the presently available information, it has been hypothesized that an initially elevated systolic BP would lead to multiple lacunar infarctions and to lesions of the brain white substance that would lead to progressive cognitive deterioration and to a later reduction of BP. Although the benefits of controlling BP on longevity are firmly established, the costs that it may have on cognitive function have not been determined. Observational studies in general have demonstrated improvement of cognitive function when HPB is treated. Regarding drug treatment, the results must be interpreted with care. In general, diuretics and beta blockers do not worsen or improve cognitive function. The antagonists of angiotensin II, ACE inhibitors and calcium antagonist have a positive affect on cognitive function. The large clinical trials (evidence A grade), with more appropriate population samples and duration time have shown a reduction of dementia with dihydropyridine calcium antagonists (nitrendipine) and with the ACE inhibitor and diuretic combination (perindopril plus indapamide)As a consequence of aging of the population, cognitive function disorders and dementias are increasing. A total of 90 % correspond to Alzheimer's disease and vascular dementias. For the former, the risk factors are age, family background of dementia and E4 allele of the apolipoprotein E gene. For the vascular dementia one, they are age, male gender, HBP, coronary disease, diabetes, generalized atherosclerosis, smoking, elevated lipid concentration and previous history of stroke. Diagnosis of dementia and cognitive deterioration is based on clinical criteria and tests that lack adequate accuracy. In this sense, modern neuroimaging techniques (CT scan and MRI) are supplying very valuable information, as it relates lacunar infarction and white substance lesions not only to HBP and other cardiovascular risk factors but also to the appearance of dementia. Based on the presently available information, it has been hypothesized that an initially elevated systolic BP would lead to multiple lacunar infarctions and to lesions of the brain white substance that would lead to progressive cognitive deterioration and to a later reduction of BP. Although the benefits of controlling BP on longevity are firmly established, the costs that it may have on cognitive function have not been determined. Observational studies in general have demonstrated improvement of cognitive function when HPB is treated. Regarding drug treatment, the results must be interpreted with care. In general, diuretics and beta blockers do not worsen or improve cognitive function. The antagonists of angiotensin II, ACE inhibitors and calcium antagonist have a positive affect on cognitive function. The large clinical trials (evidence A grade), with more appropriate population samples and duration time have shown a reduction of dementia with dihydropyridine calcium antagonists (nitrendipine) and with the ACE inhibitor and diuretic combination (perindopril plus indapamide)

Función cognitiva y demencia en la hipertensión arterial / Cognitive function and dementia in high blood pressure

Como consecuencia del envejecimiento de la población las alteraciones de la función cognitiva y las demencias están aumentando. El 90 % corresponden a la enfermedad de Alzheimer y a las demencias vasculares. Para la primera, constituyen factores de riesgo la edad, los antecedentes familiares de demencia y el alelo E4 del gen de la apolipoproteína E. Para la demencia vascular lo son la edad, el género masculino, la hipertensión arterial, la enfermedad coronaria, la diabetes, la aterosclerosis generalizada, el tabaquismo, una concentración elevada de lípidos e historia previa de ictus. El diagnóstico de demencia y deterioro cognitivo está basado en criterios clínicos y pruebas que adolecen de una precisión adecuada, en este sentido las modernas técnicas de neuroimagen (tomografía axial computarizada y resonancia magnética) están aportando valiosísima información al relacionar los infartos lacunares y las lesiones de la sustancia blanca no sólo a la hipertensión arterial y otros factores de riesgo cardiovascular, sino también a la aparición de demencia. En base a la información actualmente disponible se ha postulado que una presión arterial sistólica inicial elevada conduciría a múltiples infartos lacunares y a lesiones de la sustancia blanca cerebral que conducirían a un deterioro cognitivo progresivo y a una posterior reducción de la presión arterial. Aunque los beneficios del control de la presión arterial sobre la longevidad están firmemente establecidos, los costes que pueda tener sobre la función cognitiva no están determinados. Los estudios observacionales en general han demostrado una mejoría de la función cognitiva al tratar la hipertensión arterial. En cuanto al tratamiento farmacológico, los resultados se han de interpretar con precaución. En general, los diuréticos y betabloqueantes no empeoran o mejoran la función cognitiva. Los antagonistas de la angiotensina II, los inhibidores de la enzima conversora de la angiotensina y los calcioantagonistas tienen una influencia positiva sobre la función cognitiva. Los grandes ensayos clínicos (grado de evidencia A), con unas muestras poblaciones y un tiempo de duración más apropiados, han mostrado una reducción de la demencia con calcioantagonsitas dihidropiridínicos (nitrendipino) y con la combinación inhibidor de la enzima conversora de la angiotensina y diurético (perindopril más indapamida)

As a consequence of aging of the population, cognitive function disorders and dementias are increasing. A total of 90 % correspond to Alzheimer's disease and vascular dementias. For the former, the risk factors are age, family background of dementia and E4 allele of the apolipoprotein E gene. For the vascular dementia one, they are age, male gender, HBP, coronary disease, diabetes, generalized atherosclerosis, smoking, elevated lipid concentration and previous history of stroke. Diagnosis of dementia and cognitive deterioration is based on clinical criteria and tests that lack adequate accuracy. In this sense, modern neuroimaging techniques (CT scan and MRI) are supplying very valuable information, as it relates lacunar infarction and white substance lesions not only to HBP and other cardiovascular risk factors but also to the appearance of dementia. Based on the presently available information, it has been hypothesized that an initially elevated systolic BP would lead to multiple lacunar infarctions and to lesions of the brain white substance that would lead to progressive cognitive deterioration and to a later reduction of BP. Although the benefits of controlling BP on longevity are firmly established, the costs that it may have on cognitive function have not been determined. Observational studies in general have demonstrated improvement of cognitive function when HPB is treated. Regarding drug treatment, the results must be interpreted with care. In general, diuretics and beta blockers do not worsen or improve cognitive function. The antagonists of angiotensin II, ACE inhibitors and calcium antagonist have a positive affect on cognitive function. The large clinical trials (evidence A grade), with more appropriate population samples and duration time have shown a reduction of dementia with dihydropyridine calcium antagonists (nitrendipine) and with the ACE inhibitor and diuretic combination (perindopril plus indapamide)

Efecto del tratamiento antihipertensivo con candesartán sobre la presión de pulso / Effect of antihypertensive treatment with candesartan on pulse pressure

Objetivos. Candesartán es un fármaco antihipertensivo, antagonista de los receptores AT1 de la angiotensina II (ARA) que ha demostrado una alta eficacia y seguridad en ensayos clínicos. El presente estudio pretende evaluar la efectividad y tolerabilidad de candesartán en condiciones de práctica clínica real y el efecto sobre la presión arterial (PA) y la presión de pulso (PP) en pacientes con hipertensión arterial (HTA) esencial leve-moderada no controlada. Material y métodos. Estudio prospectivo observacional realizado en una cohorte de 9.013 pacientes afectos de HTA esencial (54 por ciento mujeres), con una edad media de 60,7 ñ 11,5 años, en tratamiento con candesartán y un seguimiento de 12 semanas. Todos los pacientes fueron tratados en régimen ambulatorio y recibieron candesartán durante 12 semanas. Las variables de eficacia analizadas fueron el descenso absoluto de la PA y PP y el porcentaje de pacientes que alcanzaron cifras inferiores a 140/90 mmHg. La variable de seguridad fue la tasa de reacciones adversas aparecidas durante el tratamiento con candesartán. Resultados. Después de 12 semanas de tratamiento candesartán produjo un descenso significativo (p < 0,001) de la PAS (23,9 mmHg), de la PAD (14,3 mmHg) y de la PP (9,7 mmHg). Este último parámetro descendió de forma significativa más marcada en las mujeres respecto a los varones (10,4 mmHg frente a 9,3 mmHg; p < 0,05), en los pacientes diabéticos respecto a los no diabéticos (10,7 mmHg frente a 9,5 mmHg; p<0,05) y en aquellos con factores asociados de riesgo cardiovascular respecto a los que no tenían (10,1 mmHg frente a 9,4 mmHg; p<0,05). La tasa de control estricto (cifras inferiores a 140/90 mmHg) con candesartán fue del 30,4 por ciento. En los pacientes con HTA sistólica aislada los descensos de PA observados después del tratamiento con candesartán fueron de 20,5 mmHg para la PAS, de 3 mmHg para la PAD y de 17,5 mmHg para la PP. La tasa de reacciones adversas al fármaco fue del 2,1 por ciento. Conclusiones. Candesartán es un fármaco efectivo y bien tolerado capaz de reducir la PP, especialmente en los pacientes diabéticos, con factores asociados de riesgo vascular o con HTA sistólica aislada. En estos últimos además la modificación de la PAD es insignificante, lo que otorgaría al fármaco un mejor perfil de seguridad (AU)

Tratamiento del paciente hipertenso con hiperplasia benigna de próstata / Treatment of hypertensive patients with benign prostate hyperplasia

La hiperplasia benigna de próstata (HBP) es el tumor benigno más frecuente en el varón por encima de los 50 años y al igual que la hipertensión arterial (HTA) aumenta con la edad. Existe un nexo común entre la HTA y la HBP a través del sistema nervioso simpático. El tejido prostático responde al estímulo de los receptores 1 adrenérgicos y éstos son fundamentales en el control de la presión arterial. Esto explica que los alfabloqueantes mejoren los síntomas de la HBP, y en la actualidad ya constituyen el 50 por ciento de los fármacos prescritos para esta patología. La alfuzosina y la tamsulosina están desprovistos de efecto cardiovascular significativo. Sólo la doxazosina y la terazosina tienen la doble indicación, como antihipertensivos y para aliviar los síntomas de la HBP. En pacientes hipertensos con HBP que precisan un solo fármaco los alfabloqueantes pueden constituir un grupo de elección, teniendo cierta precaución en sujetos con insuficiencia cardíaca. Cuando se precisa un tratamiento combinado se ha de considerar la asociación a un diurético (AU)

Validación de equipos automáticos de medición de la presión arterial / Validation of automated blood pressure measuring devices

No disponible

Riesgo cardiovascular en el paciente trasplantado renal. Introducción / No disponible

No disponible

Clinical characteristics of ischaemic renal disease.

BACKGROUND: Longer life expectancy has favoured the ever more frequent development of ischaemic nephropathy characterized by the presence of atherosclerotic stenosis in both renal arteries. METHODS: This is an observational and multicentre study carried out during a 14-month follow-up period in 20 hospitals in SPAIN: Inclusion criteria were the presence of bilateral renal artery stenosis > 50% and a creatinine level of > or = 1.5 mg/dl. The diagnosis should be made by arterial digital angiography in every case. RESULTS: A total of 156 patients were included. Their mean age was 68.7+/-9 years, and 78.5% were male. The mean creatinine value of the group was 2.9+/-1.7 mg/dl. Arterial hypertension (BP) with a duration of 12+/-9 years was present in 97.4% of the cases, smoking habits in 69.8%, hypercholesterolaemia (> or = 240 mg/dl) in 62.9% and diabetes in 32.1%. Only 8% of the patients had a body mass index > or = 30 kg/m(2). Associated cardiovascular disease was very frequent: peripheral arteriopathy in 67.5% of the cases, ischaemic cardiopathy in 44.8%, cardiac insufficiency in 32.6% and stroke in 27.3%. In 94.4% of the patients, the lesion affected both renal arteries, with complete obstruction in 23% of the cases. CONCLUSIONS: Diagnostic suspicion of ischaemic nephropathy can be established in non-obese elderly males with chronic renal insufficiency, long-term BP evolution and cardiovascular disease at other levels, above all, peripheral arteriopathy.

Effect of angiotensin II receptor blockade on renal disease progression in patients with non-diabetic chronic renal failure.

BACKGROUND: The aim of the present study was to investigate the effect of losartan on the progression of renal function in non-diabetic patients with chronic renal failure in an open, prospective, follow-up study of 1 year. METHODS: Twenty-nine hypertensive patients (14 females and 15 males; mean age 63 years.) with non-diabetic chronic renal failure of several causes received losartan 50 mg/day (plus other antihypertensive agents if needed) and were followed-up prospectively during 13+/-1 months. Eighteen patients received angiotensin-converting enzyme inhibitors plus other antihypertensive drugs at baseline. Patients had been followed-up for 44+/-4 months prior to the treatment with losartan. The rate of progression of renal insufficiency was evaluated as the slope of the reciprocal of serum creatinine vs time in months. RESULTS: Blood pressure, creatinine clearance and urinary protein excretion at baseline and after 1 year of treatment with losartan were: 149+/-3/90+/-1 vs 142+/-2/84+/-1 mmHg (P<0.01/P<0.05), 29+/-3 vs 29+/-3 ml/min (P=NS), and 1.7+/-0.4 vs 1.2+/-0.2 g/24 h (P=0.11, NS). Serum creatinine at baseline, and after 6 months and 1 year of treatment with losartan was: 3.18+/-0.24, 3.24+/-0.27 (P=NS vs baseline) and 3.49+/-0.32 mg ml (P<0.05 vs baseline). The rate of progression of renal disease before and after 1 year of treatment with losartan was -0.0039+/-0.0058 vs -0.0012+/-0.0073 mg/month (P<0.01). Changes in proteinuria after 1 year of treatment with losartan correlated with the change in renal disease progression (r=-0.519, P<0.01). CONCLUSIONS: The rate of progression of renal function in patients with non-diabetic chronic renal failure is slowed down after 1 year of treatment with losartan. The results of this preliminary study suggest that AT1 receptor blockade treatment offers renoprotection in this subset of patients, although these results need to be confirmed in appropriate controlled trials.

Adrenomedulina: un nuevo péptido vasoactivo / Adrenomedullin: a new vasoactive peptide

No disponible

[Study of the clinically useful interval in ambulatory monitoring of blood pressure]. / Estudio del intervalo clínicamente útil para monitorizar la presión arterial ambulatoria.

BACKGROUND: Ambulatory blood pressure monitoring (ABPM) throughout 24 hours has been introduced for clinical practice, improving the diagnosis and treatment of hypertension. However, there is not an agreement concerning how often the blood pressure have to be measured. SUBJECTS AND METHODS: An ABPM was performed in 29 normotensive and hypertensive subjects (16-73 years) throughout 24 hours recording the blood pressure every 15 minutes. The average of systolic and diastolic blood pressure of the diurnal and nocturnal periods of the interval of 15 minutes, were compared with the two intervals of 30 minutes and the four of 60 minutes, according to Bland and Altman method. RESULTS: Between 90% and 100% of the differences of the interval 15 minutes versus 30 minutes, and 15 minutes versus 60 minutes, were within +2 and -2 standard deviation of the mean. However, only between 95% and 100% of the difference of the intervals 15 minutes versus 30 minutes were within the limits of agreement for systolic and diastolic blood pressure in the nocturnal period. CONCLUSIONS: A clinical satisfactory information using ABPM can be obtained monitoring the blood pressure every 15 minutes during the day and 30 minutes at night.

[Relationship of the renin-angiotensin-aldosterone system with auricular natriuretic factor in its response to the action of thiazide diuretics and to nifedipine, a sustained-release calcium antagonist]. / Relaciones del sistema renina-angiotensina-aldosterona con el factor natriurético auricular en su respuesta a la acción de diuréticos-tiacídicos y al antagonista del calcio nifedipino de liberación sostenida.

BACKGROUND: Blood pressure (BP) response to diuretics may be considered as an index of salt-sensitivity. Salt-sensitive patients may have an enhanced response to calcium channel blockers. In this study we correlate the basal values of two of the hormonal systems involved in the control of Na balance comparing them with the antihypertensive effects of a calcium channel blocker and a diuretic, to assess if BP response depends of a particular hormonal pattern by which we could define salt-sensitive patients. METHODS: We studied 21 essential hypertensive patients in a lineal sequence in an open protocol, first treated with slow release nifedipine (Nif-30), 30 mg daily, as a single dose, for 30 days, followed by amiloride+hydrochlorothiazide (HCT+Am), 50 mg and 5 mg, daily, for another month. Plasma renin activity (PRA), plasma aldosterone (PAld) and 24 hours urinary aldosterone (UAld) and atrial natriuretic factor (ANF), were measured at the start and end of the study. The hormonal values on each group were compared and correlated with changes observed in BP at the end of each period of treatment. RESULTS: HCT+Am decreased median arterial pressure (MAP) from 121.4 +/- 11 to 110.4 +/- 8 mmHg and Nif-30 to 108.7 +/- 12.4 mmHg, both p < 0.0004. There were 76% controlling MAP with Nif-30 whereas 48% did so with HCT+Am, p < 0.01, HCT+Am also increased PRA, PAld and decreased ANF, Ca urinary excretion and plasma PTH. Nif-30 did not alter the renin-angiotensin-aldosterone system, nor ANF. PTH remained unchanged. The MAP decrement caused by HCT+Am depended on baseline BP, r = -0.69, p < 0.0005, whereas Nif-30 decreased MAP independent from its baseline values, r = -0.02, NS. PAld showed a reverse correlation with ANF after treatment, r = -0.43, p < 0.05. The decrease of MAP holds a reverse relationship with ANF, both with HCT+Am, r = -0.47, p < 0.02, and with Nif-30, r = -0.45, p < 0.04. CONCLUSIONS: Treatment with Nif-30 was superior to HCT+Am in number of patients controlled, but the decrease in MAP is similar. Since the antihypertensive response to diuretic therapy and to calcium channel-blockers is related to low levels of ANF this fact could indicate some sort of defect of ANF secretion.

[The evaluation of a noninvasive monitor to record ambulatory arterial pressure: the DIASYS 200 Novacor]. / Validación de un monitor no invasivo de registro de presión arterial ambulatoria: el DIASYS 200 Novacor.

BACKGROUND: The aim of this study was to validate the measurement precision of the portable automatic non invasive monitor of blood pressure-Novacor DIASYS 200. METHODS: A mercury sphygmomanometer was used as the reference measurer. To validate the DIASYS 87 persons (45 males, 42 females--age range 17-76 years) with a systolic blood pressure between 90-225 mmHg and diastolic blood pressure of between 64-149 mmHg were selected. RESULTS: The differences between the two apparatus were: systolic blood pressure 6.1 +/- 12.2 mmHg (r = 0.909); diastolic blood pressure -1.9 +/- 6.8 mmHg (r = 0.929) and cardiac frequency -2.0 +/- 6.3 ppm (r = 0.942). In healthy subjects of under 31 years of age (n = 20) the differences for systolic and diastolic blood pressure and cardiac frequency were 0.2 +/- 8.0 mmHg; -1.3 +/- 5.8 mmHg and -0.1 +/- 8.0 ppm, respectively. For subjects over the age of 59 years (n = 29) the measurements were 9.2 +/- 12.0 mmHg, 2.5 +/- 6.0 mmHg, -1.5 +/- 4.4 ppm, respectively. With the sample subdivided according to blood pressure the differences found in the normotensive subgroup (n = 23) were: -1.7 +/- 7.8 mmHg, -2. +/- 4.9 mmHg, and -2.4 +/- 7.9 ppm, respectively; in the subgroup with slightly high blood pressure (n = 40) 6.4 +/- 14.0 mmHg, -2.8 +/- 6.0 mmHg and -2.3 +/- 5.1 ppm, and in the subgroup with moderate-severe high blood pressure (n = 24) 10.4 +/- 10.9 mmHg, 0.2 +/- 9.1 mmHg and -0.9 +/- 6.5 ppm, respectively. CONCLUSIONS: The DIASYS fulfills the criteria of validation and precision for the measurement of diastolic blood pressure and cardiac frequency in all the cases. However criteria for systolic blood pressure are only fulfilled in normotensive and young subjects (less than 31 years of age).

[A clinical study of the verapamil and captopril combination in hypertensive patients uncontrolled by monotherapy. An evaluation by recording the 24-hour ambulatory blood pressure]. / Estudio clínico de la asociación verapamilo y captopril en pacientes hipertensos no controlados con monoterapia. Valoración mediante el registro de presión arterial ambulatoria durante 24 horas.

BACKGROUND: By measuring ambulatory blood pressure monitoring (ABPM), the pharmacologic association of verapamil plus captopril in essential hypertensive patients not responding to isolated monotherapy of these drugs was studied since a synergism has been described between these two drugs. METHODS: A lineal clinical trial with a previous period of selection (PeSe) in which verapamil and captopril were administered in two consecutive phases was carried out in 57 essential hypertensive patients of 52 +/- 19 years of age with those controlling their blood pressure (BP) being excluded. Following a lavage phase the remaining subjects were included in the experimental period (ExPe) in wash out the association of verapamil 120 mg+captopril 25 mg was administered and if the BP was not controlled this was increased to 240 mg + 50 mg, respectively. ABPM was performed prior to and at the end of the ExPe. RESULTS: Of the 57 patients 21 were excluded in the SePe due to control or adverse effects. Of the 26 individuals who passed into the ExPe 20 presented mild-moderate HTA (M-HTA) and 6 severe HTA (S-HTA). In the M-HTA group, the reduction of BP (in mmHg) was 157 +/- 15/106 +/- 5 to 147 +/- 12/97 +/- 7 (p < 0.05/p < 0.001), five controlled BP, in the remaining subjects the reduction in the following phase was 150 +/- 11/100 +/- 6 at 136 +/- 11/93 +/- 6 (p < 0.01/p < 0.01). In the S-HTA group the BP descended in the ExPe from 184 +/- 15/121 +/- 6 to 167 +/- 24/107 +/- 10 (p < 0.05/p < 0.05). The 24 hour measurement of BP in the ExPe decreased from 140 +/- 13/96 +/- 8 to 124 +/- 10/86 +/- 7 (p < 0.001/p < 0.001). BP descended significantly in all the hours with the exception of the hours 24, 1, 6, 7, and 5. CONCLUSIONS: The association of verapamil-captopril demonstrates efficacy and synergism in hypertensive patients previously uncontrolled by monotherapy of these drugs.

[Day-night differences of arterial pressure in "white coat" arterial hypertension]. / Diferencias día-noche de presión arterial en la hipertensión arterial de "bata blanca".

Prevalence and day-night differences of blood pressure (BP) are studied in "White Coat" Hypertension (AHT). An outpatient register of BP was performed during 24 hours in 95 patients with mild AHT. "White Coat" Hypertension was defined when diastolic BP during the day was below 90 mmHg (WCH group) and with no "White Coat" Hypertension (non-WCH) when it was over said figure. BP values for WCH group (n = 36) in comparison with non-WCH (n = 59) were: Day period 130 +/- 13/85 +/- 4 versus 143 +/- 14/99 +/- 7 mmHg (p < 0.001; p < 0.001). Night period 119 +/- 18/74 +/- 8 versus 127 +/- 15/84 +/- 8 mmHg (p < 0.05/p < 0.001). Day-night differences in BP were lower in WCH in comparison with non-WCH group: 11 +/- 9/11 +/- 8 versus 17 +/- 10/15 +/- 7 mmHg (p < 0.01; p < 0.01). A positive correlation was observed between BP variability in 24 hours and day-night difference in non-WCH group (Systolic BP: r = 0.512, p < 0.001; Diastolic BP: r = 0.676, p < 0.001). This correlation was not found in the WCH group. "White Coat" Hypertension is present in 38% of the subjects with mild AHT and could constitute an independent aspect of the alert reaction.

Atrial natriuretic factor in patients on continuous ambulatory peritoneal dialysis.

The aim of this study was to compare the levels of the atrial natriuretic factor (ANF) and the renin system in patients on continuous ambulatory peritoneal dialysis (CAPD) with patients on chronic hemodialysis (HD). We studied three groups. The CAPD group comprised 10 patients (25-66 years); the HD group: 10 patients (35-69 years), before (pre-HD) and after (post-HD) a HD session. The control group comprised 10 subjects with normal renal function (29-65 years), matched for age, height, weight, and diastolic pressure with the CAPD group. Blood pressure (BP) and blood samples for plasma renin activity (PRA), plasma aldosterone (PA), and ANF were taken. The BP and levels of ANF, PRA and PA were: in the control group, 121 +/- 15/75 +/- 4 mmHg, 7.3 +/- 5.6 pmol/L, 1.1 +/- 0.8 ng/mL/hour, 0.4 +/- 0.3 nmol/L. In the CAPD group, 132 +/- 26/76 +/- 12 mmHg (NS), 8.3 +/- 3.5 pmol/L (NS), 5.6 +/- 4.4 ng/mL/hour (p < 0.001), 4.9 +/- 4.0 nmol/L (p < 0.001). In the pre-HD, 159 +/- 25/95 +/- 12 mmHg (p < 0.001), 16.0 +/- 8.5 pmol/L (p < 0.005), 11.99 +/- 9.0 ng/mL/hour (p < 0.001), 2.6 +/- 2.3 nmol/L (p < 0.001). In the post-HD, 145 +/- 29/84 +/- 15 mmHg (p < 0.05 vs CG), 13.4 +/- 6.9 pmol/L (p < 0.05 vs control), 14.9 +/- 10.3 ng/mL/hour (p < 0.001 vs control), 3.8 +/- 2.9 nmol/L (p < 0.001 vs control).(ABSTRACT TRUNCATED AT 250 WORDS)

White coat hypertension and related phenomena. A clinical approach.

In this paper, several clinical problems associated with the diagnosis of hypertension are discussed. Blood pressure variability and reactivity are factors underlying the difficulties in the diagnosis of hypertension. These phenomena are interrelated and mixed. White coat hypertension (WCH), referring to the phenomenon of a high diastolic pressure at the doctor's office and a normal diurnal diastolic pressure when it is measured by ambulatory monitoring, is the most important clinical problem of diagnosis. Blood pressure variability is described, since it is essential to understand changes in pressure throughout the day, and its phasic and tonic components. Blood pressure differences between activity and rest, usually seen as daytime/night-time differences, allow for blood pressure control in most patients with moderate hypertension. Prevalence of WCH depends on the cut-off point used by the investigators for normal diurnal blood pressure; thus, between 53% and 12% of patients may have WCH. In our studies, a prevalence of 35% has been found. The alert reaction, labile and borderline hypertension and WCH result from a mix of both variability and reactivity, and patients with these conditions are at a higher cardiovascular risk than normotensive controls. Ambulatory blood pressure monitoring, which enables true hypertensives to be distinguished from false hypertensives, is the most useful technique available to date for the diagnosis of hypertension.