Nieves Martell-Claros

Efficacy of a home blood pressure monitoring programme on therapeutic compliance in hypertension: the EAPACUM- HTA study

Objective To evaluate the efficacy of a programme of home blood pressure measurement (HBPM) on therapeutic compliance in mild-to-moderate hypertension. Design A prospective controlled multicentre clinical trial. Setting Forty primary care centres in Spain, with a duration of 6 months. Patients A total of 250 patients with newly diagnosed or uncontrolled hypertension were included. Interventions The patients were randomly selected and distributed in two groups: (1) the control group (CG) who received standard health intervention; (2) the intervention group (IG): the patients in this group received an OMRON in their homes for a programme of HBPM. Main outcome measure Four visits were scheduled, for the measurement of blood pressure (BP). They were provided with an electronic monitor for measuring compliance (monitoring events medication system; MEMS). Therapeutic compliance was defined as a drug consumption of 80–110%. A number of variables were calculated using the MEMS. The mean BP were calculated and the percentage of controlled patients. Results A total of 200 patients completed the study (100 in each group). Compliance was observed in 74 and 92%, respectively, in the CG and IG [95% confidence interval (CI) 63.9–84.1 and 86.7–97.3; P = 0.0001], the mean percentage compliances were 87.6 and 93.5% (95% CI 81.2–94 and 80.7–98.3; P = 0.0001), the percentages of correct days were 83.6 and 89.4%, the percentages of subjects who took the medication at the prescribed time were 79.89 and 88.06%, and the levels of therapeutic cover were 86.7 and 93.1%. The number needed to treat to avoid one case of non-compliance was 5.6 patients. The differences in the mean decreases in BP were significant for diastolic BP, with a greater decrease observed in the IG. Conclusions An HBPM programme using electronic monitors is effective in improving compliance in arterial hypertension, measured using the MEMS.

Management of resistant arterial hypertension: role of spironolactone versus double blockade of the renin-angiotensin-aldosterone system

Background Currently there is no consensus regarding which add-on therapy to use in resistant hypertension. This study was designed to compare two treatment options, spironolactone (SPR) versus dual blockade of the renin–angiotensin–aldosterone system (RAAS). Methods Forty-two patients with true resistant hypertension were included in the study. An open-label prospective crossover design was used to add a second RAAS blocker to previous treatment and then SPR following 1 month of wash-out. BP was measured in the office and by ambulatory blood pressure monitoring (ABPM). Changes in laboratory tests were also studied for both treatments. The predictive values of aldosterone–renin ratio (ARR) and serum potassium of determining the antihypertensive response were analyzed for both arms. Results Following the first stage of dual blockade, SBP dropped significantly both in office (reduction of 12.9 ± 19.2 mmHg)) and by ABPM (reduction of 7.1 ± 13.4 mmHg). Office DBP was unchanged but was significantly reduced as measured by ABPM (3.4 ± 6.2 mmHg). On SPR treatment, office BP was reduced 32.2 ± 20.6/10.9 ± 11.6 mmHg. By ABPM the reduction was 20.8 ± 14.6/8.8 ± 7.3 mmHg (P < 0.001). The BP control was achieved by 25.6% of patients in dual blockade and 53.8% in SPR with office blood pressure. By ABPM, 20.5% were controlled on dual blockade and up to 56.4% with SPR. Serum potassium was a weak inverse predictor of the blood pressure-lowering effect of SPR. Conclusion SPR has a greater antihypertensive effect than dual blockade of the RAAS in resistant hypertension. SPR at daily doses of 25–50 mg shows a potent antihypertensive effect when added to prior regimes of single RAAS axis blockade in patients with resistant arterial hypertension.

Blood pressure and low-density lipoprotein-cholesterol lowering for prevention of strokes and cognitive decline: a review of available trial evidence.

Background and objectives: It is well established by a large number of randomized controlled trials that lowering blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C) by drugs are powerful means to reduce stroke incidence, but the optimal BP and LDL-C levels to be achieved are largely uncertain. Concerning BP targets, two hypotheses are being confronted: first, the lower the BP, the better the treatment outcome, and second, the hypothesis that too low BP values are accompanied by a lower benefit and even higher risk. It is also unknown whether BP lowering and LDL-C lowering have additive beneficial effects for the primary and secondary prevention of stroke, and whether these treatments can prevent cognitive decline after stroke. Results: A review of existing data from randomized controlled trials confirms that solid evidence on optimal BP and LDL-C targets is missing, possible interactions between BP and LDL-C lowering treatments have never been directly investigated, and evidence in favour of a beneficial effect of BP or LDL-C lowering on cognitive decline is, at best, very weak. Conclusion: A new, large randomized controlled trial is needed to determine the optimal level of BP and LDL-C for the prevention of recurrent stroke and cognitive decline.

Continuation of the ESH-CHL-SHOT trial after publication of the SPRINT: rationale for further study on blood pressure targets of antihypertensive treatment after stroke.

Alberto Zanchetti, Lisheng Liu, Giuseppe Mancia, Gianfranco Parati, Guido Grassi, Marco Stramba-Badiale, Vincenzo Silani, Grzegorz Bilo, Giovanni Corrao, Antonella Zambon, Lorenza Scotti, Xinhua Zhang, Ting Rui Guan, Yuqing Zhang, Xuezhong Zhang, Eivind Berge, Josep Redon, Krzysztof Narkiewicz, Anna Dominiczak, Peter Nilsson, Margus Viigimaa, Stéphane Laurent, Enrico Agabiti-Rosei, Zhaosu Wu, Dingliang Zhu, José Luis Rodicio, Luis Miguel Ruilope, Nieves Martell-Claros, Fernando Pinto Roland E. Schmieder, Michel Burnier, Maciej Banach, Renata Cifkova, Csaba Farsang, Alexandra Konradi, Irina Lazareva, Yuriy Sirenko, Maria Dorobantu, Arman Postadzhiyan, Rok Accetto, Bojan Jelakovic, Dragan Lovic, Athanasios J. Manolis, Philippos Stylianou, Dror Dicker, Gangzhi Wei, Chengbin Xu, Hengge Xie, Antonio Coca, John O’Brien, Gary Ford, on behalf of the ESH-CHL-SHOT trial investigators

Hipertensión por hiperaldosteronismo: más lesión cardiaca, mayor riesgo cardiovascular

INTRODUCTION AND OBJECTIVES Primary hyperaldosteronism is the most common cause of secondary hypertension. Elevated aldosterone levels cause heart damage and increase cardiovascular morbidity and mortality. Early diagnosis could change the course of this entity. The objective of this report was to study the clinical characteristics, cardiac damage and cardiovascular risk associated with primary hyperaldosteronism. METHODS We studied 157 patients with this diagnosis. We analyzed the reason for etiological investigation, and the routinely performed tests, including echocardiography. We used a cohort of 720 essential hypertensive patients followed in our unit for comparison. RESULTS Compared with essential hypertensive patients, those with hyperaldosteronism were younger (56.9 [11.7] years vs 60 [14.4] years; P<.001), had higher blood pressure prior to the etiological diagnosis (136 [20.6] mmHg vs 156 [23.2] mmHg), more frequently had a family history of early cardiovascular disease (25.5% vs 2.2%; P<.001), and had a higher prevalence of concentric left ventricular hypertrophy (69% vs 25.7%) and higher cardiovascular risk. Specific treatment resulted in optimal control of systolic and diastolic blood pressures (from 150.7 [23.0] mmHg and 86.15 [14.07] mmHg to 12.69 [15.3] mmHg and 76.34 [9.7] mmHg, respectively). We suspected the presence of hyperaldosteronism because of resistant hypertension (33.1%), hypokalemia (38.2%), and hypertensive crises (12.7%). Only 4.6% of these patients had been referred from primary care with a suspected diagnosis of hyperaldosteronism. CONCLUSIONS Hyperaldosteronism should be suspected in cases of resistant hypertension, hypokalemia and hypertensive crises. The diagnosis of hyperaldosteronism allows better blood pressure control. The most prevalent target organ damage is left ventricular hypertrophy.

Early predictors of gestational hypertension in a low-risk cohort. Results of a pilot study.

Objective: To determine if the clinical or biochemical markers used in pregnancy can be applied as early predictors of gestational hypertension. Design: Prospective cohort study. Population: 315 pregnant women referred from the Prenatal Diagnosis Unit between weeks 10–13 of pregnancy and followed up to the childbirth. Methods: Biomarkers were measured in serum specimens in the first and second trimester of pregnancy. Blood pressure (BP) was measured in the first, second and third trimester. Results: The cumulative incidence of gestational hypertension was 6.01%. In the first trimester gestational hypertension predictors were uric acid greater than 3.15 mg/dl (P = 0.01), BMI greater than 24 kg/m2 (P = 0.003) SBP at least 120 mmHg (P = 0.02) and DBP at least 71 mmHg (P = 0.007). After applied multivariate analysis just uric acid and SBP were statistically significant. Conclusion: In our cohort of healthy pregnant women uric acid above 3.15 mg/dl and SBP at least 120 mmHg are consistent predictors of gestational hypertension in the first trimester. The most important implication of our study is the possibility to identify in the first trimester women at risk to develop gestational hypertension using available markers.

Primary aldosteronism and its various clinical scenarios

Background: : Primary aldosteronism is the most frequent endocrine cause of secondary hypertension. Aldosterone excess damages the cardiovascular system. Objectives: We compared biochemical; morphological, and cardiovascular risk differences among hypokalemic and normokalemic primary aldosteronism. We evaluated either both presentations correspond to two different entities or a unique disease in different evolutive stage. Material and methods: This is a retrospective study including 157 patients with primary aldosteronism divided into two groups: typical presentation (serum potassium < 3.5 mmol/l, n = 87) and atypical presentation (serum potassium > 3.5 mmol/l, n = 70). Results: The typical presentation group showed higher family background of ischemic heart disease (P = 0.028), plasmatic aldosterone levels (P = 0.001), and cardiovascular added risk (P = 0.013). Although kalemia was corrected in the hypokalemic group after specific treatment, typical presentation maintained lower levels. Predictors of typical presentation were the highest tertile of aldosterone level, baseline DBP, and a longer evolution of hypertension. Aldosterone serum levels increased along time in primary aldosteronism and it can be considered as the most discriminative factor for the type of presentation. Conclusion: Primary aldosteronism presentation along with normokalemia or hypokalemia could be the same disease at different evolution stages. Adequate detection of normokalemic primary aldosteronism deserves an early and intentional diagnostic attitude.

Análisis del proceso de derivación del paciente hipertenso en España : Estudio DERIVA

Resumen Introducción La buena comunicación entre niveles asistenciales es clave para el control de la hipertensión arterial. Objetivos Valorar la adecuación de la derivación del hipertenso desde atención primaria a atención especializada. Como objetivos secundarios, valoramos el contenido del informe de derivación y la concordancia entre el motivo de derivación y el diagnóstico final. Diseño Estudio observacional descriptivo. Emplazamiento Estudio realizado a nivel nacional. Participantes Médicos de atención especializada que reciben pacientes hipertensos derivados de atención primaria. Mediciones principales En una visita basal, el médico de atención especializada evaluó la calidad del informe de derivación y al paciente, y en visita final se establecen diagnóstico y tratamiento definitivos. Resultados Se incluyeron 1.769 sujetos, edad media de 62,4 (13,6) años, 45% mujeres. El tiempo medio de diagnóstico de hipertensión fue de 8,0 (7,7) años. Algo más de la mitad de los informes de derivación contienen información muy buena (5,4%; IC 4,3-6,5) o suficiente (50,7%; IC 48,4-53,0). Un 7,1% (IC 5,9-8,3) no indican causa de derivación. Fueron correctas el 74,7% de las derivaciones, y el 30% de estas fueron tardías. La concordancia entre las causas de derivación y los diagnósticos finales fueron bajas (índice Kappa 0,208). Conclusiones Una cuarta parte de los pacientes se derivan innecesariamente, y del 75% de los bien derivados, un 30% lo fueron tardíamente. Se debería mejorar la coordinación operativa entre los 2 niveles de atención en el área de hipertensión y del riesgo cardiovascular.

Modification over time of pulse wave velocity parallel to changes in aortic BP, as well as in 24-h ambulatory brachial BP

Arterial stiffness as assessed by carotid–femoral pulse wave velocity (cfPWV) is a marker of preclinical organ damage and a predictor of cardiovascular outcomes, independently of blood pressure (BP). However, limited evidence exists on the association between long-term variation (Δ) on aortic BP (aoBP) and ΔcfPWV. We aimed to evaluate the relationship of ΔBP with ΔcfPWV over time, as assessed by office and 24-h ambulatory peripheral BP, and aoBP. AoBP and cfPWV were evaluated in 209 hypertensive patients with either diabetes or metabolic syndrome by applanation tonometry (Sphygmocor) at baseline(b) and at 12 months of follow-up(fu). Peripheral BP was also determined by using validated oscillometric devices (office(o)-BP) and on an outpatient basis by using a validated (Spacelabs-90207) device (24-h ambulatory BP). ΔcfPWV over time was calculated as follows: ΔcfPWV=[(cfPWVfu–cfPWVb)/cfPWVb] × 100. ΔBP over time resulted from the same formula applied to BP values obtained with the three different measurement techniques. Correlations (Spearman ‘Rho’) between ΔBP and ΔcfPWV were calculated. Mean age was 62 years, 39% were female and 80% had type 2 diabetes. Baseline office brachial BP (mm Hg) was 143±20/82±12. Follow-up (12 months later) office brachial BP (mm Hg) was 136±20/79±12. ΔcfPWV correlated with ΔoSBP (Rho=0.212; P=0.002), Δ24-h SBP (Rho=0.254; P<0.001), Δdaytime SBP (Rho=0.232; P=0.001), Δnighttime SBP (Rho=0.320; P<0.001) and ΔaoSBP (Rho=0.320; P<0.001). A multiple linear regression analysis included the following independent variables: ΔoSBP, Δ24-h SBP, Δdaytime SBP, Δnighttime SBP and ΔaoSBP. ΔcfPWV was independently associated with Δ24-h SBP (β-coefficient=0.195; P=0.012) and ΔaoSBP (β-coefficient= 0.185; P=0.018). We conclude that changes in both 24-h SBP and aoSBP more accurately reflect changes in arterial stiffness than do office BP measurements.

Night-time heart rate cut-off point definition by resting office tachycardia in untreated hypertensive patients: data of the Spanish ABPM registry.

Objective: Epidemiological studies have shown that an elevated resting heart rate (HR) is a risk factor for both total and cardiovascular mortality. Our aim was to estimate the night-time HR cut-off point that best predicts cardiovascular risk office tachycardia in hypertensive patients. Design and method: Untreated hypertensive patients without concomitant cardiovascular diseases were included. Office and ambulatory HRs were measured. Cardiovascular risk office tachycardia was defined by office HR at least 85 beats per minute (bpm). Different night-time HR cut-offs were estimated by receiver operating characteristic curve analyses to predict cardiovascular risk office tachycardia. The best cut-off was selected on the basis of its combined sensitivity and specificity. Results: A total of 32 569 hypertensive patients were included: 46.5% women, mean age (SD) 52 (14) years, office blood pressure 146 (16)/89 (11) mmHg, diabetes 10.3%, smoking 19.2%, BMI 29 (6.8) kg/m2, office HR 77 (11.2) bpm, and night-time HR 64.9 (9.3) bpm. A total of 7070 (21.7%) patients were found to have cardiovascular risk office tachycardia. The night-time HR value that better predicted cardiovascular risk office tachycardia was more than 66 bpm. In comparison with patients with night HR below this value, those with night-time tachycardia were predominantly women, younger, with higher ambulatory blood pressure, greater BMI, and higher prevalence of diabetes and smoking. All comparisons were statistically significant (P less than 0.001). Conclusion: A mean night-time HR more than 66 bpm is a good predictor of cardiovascular risk office tachycardia in untreated hypertensive patients and could be considered a variable associated with an increased cardiovascular risk.