Blood pressure effects of CPAP in nonresistant and resistant hypertension associated with OSA: A systematic review of randomized clinical trials.

Obstructive sleep apnea (OSA) is a rather common chronic disorder, associated with increased prevalence of hypertension. The pathophysiological mechanisms for hypertension in OSA are at least in part linked to intermittent hypoxia developed during nightly hypopneas and apneas. Hypoxemia stimulates sympathetic overactivity, systemic inflammation, oxidative stress, and endothelial dysfunction. However, it appears that intermittent hypoxemia is not the only factor in the development of hypertension in OSA. Supplemental oxygen therapy that improved oxyhemoglobin saturation to similar levels to those achieved with CPAP treatment did not reduce BP. In this scenario, it could be proposed that hypoxemia acts as a trigger of sympathetic overdrive, which when set is the main factor in the development of hypertension in OSA. This review appraises evidence provided by randomized controlled trials on the BP-lowering effectiveness of continuous positive airway pressure (CPAP) treatment of OSA patients with nonresistant and resistant hypertension. It suggests that CPAP treatment is more effective in treating resistant hypertension than nonresistant hypertension. A possible explanation is that sympathetic overactivity and altered vascular reactivity in OSA could be more severe in resistant hypertension than in nonresistant hypertension. An intricate interaction among compliance, adherence, and their interaction with demographic characteristics, genetic factors, and comorbidities of the population included might explain the differences found between trials on their influence over the antihypertensive effectiveness of CPAP. Further long-term trials are needed in hypertensive OSA patients to assess whether CPAP treatment in OSA patients consistently restores physiological nocturnal BP fall and adjusts resting and circadian heart rate.

Association between nondipper behavior and serum calcium in hypertensive patients with mild-to-moderate chronic renal dysfunction.

A nondipping BP pattern has been shown to be predictive of end-organ damage, cardiovascular events, and mortality. The mechanisms of blunted nocturnal BP fall are multifactorial. We assessed whether total corrected serum calcium and ionic calcium (iCa) are associated with a blunted nocturnal BP fall in both treated and untreated hypertensive patients with stages 1-3 of the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI). Clinical data and 24-hour ambulatory blood pressure monitoring were obtained in a cohort of 231 essential hypertensive patients. Among the entire cohort, 107 were nondippers and 124 were dippers. Only in nondippers, we found significant correlations between iCa and 24-hour systolic blood pressure (SBP; r = 0.21, P < .03), diurnal SBP (r = 0.21, P < .03), and 24-hour pulse pressure (PP; r = 0.23, P < .02). The ambulatory arterial stiffness index (AASI) was significantly related with 24-hour PP in both dippers and nondippers after adjusting for age. Both AASI and 24-hour PP were higher in nondippers than in dippers. In addition, in nondippers, the prevalence of estimated glomerular filtration rate (eGFR) < 60 mL/minute/1.73 m2 was higher than in dippers (50% vs. 33.7%, P < .02). Logistic regression showed that patients with eGFR ≥ 60 mL/minute/1.73 m2 had lower risk of nondipper status than patients with eGFR < 60 mL/minute/1.73 m2 (odds ratio = 2.445; 95% confidence interval = 1.398-4.277, P < .002). In conclusion, serum iCa could participate in the pathogenesis of nondipping pattern. Increased large artery stiffness may be a mechanism of the deleterious influence of nondipping on cardiovascular outcome. Hypertensive subjects with stage 3 of NKF KDOQI had a greater loss of circadian BP rhythm than those in stages 1 and 2.

Effects of blood pressure changes on Alzheimer's disease.

Alzheimer's disease is the most frequent cause of dementia. Whereas other major causes of death have been decreasing, the number of deaths due to Alzheimer's disease is rising. As there is no cure for this type of dementia at present, preventive measures have assumed great importance. By analyzing data from available longitudinal studies, the current review presents evidence supporting a link between Alzheimer's disease and blood pressure changes.

Establishing targets for hypertension control in patients with comorbidities.

Most current guidelines recommend tighter blood pressure (BP) control in hypertensive patients with comorbidities. These recommendations are based on epidemiologic data indicating that cardiovascular risk increases at lower BP levels in hypertensive patients with comorbidities than in those without comorbidities. Hypertension guidelines usually reflect outcomes from previous studies, but current recommendations for patients with comorbidities have preceded the evidence. We review recent studies investigating whether these new targets can be achieved, whether they are well tolerated, and whether they positively affect the outcomes. The results of the few current studies about outcomes in lower BP target groups are either negative or somewhat--but not decidedly--positive. There is a need for new trials designed to evaluate the validity of current recommendations for tighter BP control in hypertensive patients with comorbidities. Additionally, existing data from published trials could be reanalyzed to provide further clarification.

Statins in hypertension: are they a new class of antihypertensive agents?

High blood pressure is a very common disease in hypercholesterolemic and diabetic patients and contributes to the increase in cardiovascular risk. Inhibitors of 3OH-3methyl-glutaryl-coenzyme A reductase are the most effective and widely used cholesterol-lowering drugs. They significantly reduce the risk of cardiovascular events and death in both primary and secondary prevention of cardiovascular disease. Although the long-term benefit by statin treatment is largely attributed to their cholesterol-lowering action, increasing attention focuses on additional actions called "pleitropic effects" that might explain the cardiovascular protection seen shortly after the initiation of therapy. Very few and small studies have investigated the antihypertensive effect of statins in patients with hypertension associated with hypercholesterolemia, and the results of recently published large statin studies (albeit not designed to answer this question) have attracted the interest on this subject. Many other studies, also not specifically aimed at the evaluation of the statins' antihypertensive effect, have provided information concerning changes in blood pressure during treatment with statins, but severe limitations such as inadequate study design, small or very small sample size, too short of a treatment period, and modification of concomitant antihypertensive therapy have prevented finding a definitive effect on blood pressure. From the available results, it appears consistent that statins may be useful in hypertensives with high serum total cholesterol, in those whose hypertension is not well controlled with antihypertensive agents even without high serum total cholesterol, in hypertensive subjects well controlled with antihypertensives without high serum cholesterol when they have high polymerase chain reaction levels, in those who require preventive measures because of other concomitant cardiovascular risk factors, or when they require secondary prevention. Future research could further characterize the impact of statin use alone or in combination with antihypertensive agents to delay the development of Stage 1 hypertension in prehypertension.

Primary care survey of awareness and control of hypertension: a hospital-based study.

The objectives of this cross-sectional study were to determine awareness degree, treatment status, and control of hypertension and its predictors in a consecutive group of attendees at a Buenos Aires University School Hospital primary care setting from April 2003 to May 2006. Results for 1733 hypertensive subjects, all of them white (578 men and 1155 women), were available for analyses. Mean age of hypertensive subjects was 66.61 +/- 12.34 years. Eighty-seven percent of hypertensive patients knew their diagnosis. Prevalence of hypertension was consistently higher in overweight-obese than in normal weight subjects (P < 0.001). Overall prevalence of hypertension treatment was 62%, and blood pressure (BP) control rate was 30%. Among knowledgeable treated hypertensive patients, 80.4% used only one antihypertensive drug, 17.6% used two, and 2% used three (P < 0.001). Only 8% of hypertensive patients carried out consensus-recommended dietarian guidelines. A prevention index performed with periodic general prevention measures during the past 5 years was calculated. Logistic regression model showed that independent variables more likely to be associated with poor BP control were being overweight (odds ratio [OR] 1.53, 95% confidence interval [CI] 1.057-2.208), obesity (OR 2.1, 95% CI 1.307-3.286), and previous stroke (OR 2.9, 95% CI 1.099-7.652). Conversely, the higher the prevention index, the less odds of uncontrolled BP (OR 0.841, 95% CI 0.725-0.975). These results highlight the consistency of general primary care prevention measures with achieving BP control. The poor control rates of BP found in patients who already suffered from stroke suggest that, after hospital discharge for that event, antihypertensive therapy was inadequate and document the challenge that these situations impose on primary care physicians.

Long-term effects of parathyroidectomy on hypertension prevalence and circadian blood pressure profile in primary hyperparathyroidism.

Our aims were to evaluate the prevalence and outcome of hypertension in patients with primary hyperparathyroidism (PHPT), previously and after follow-up of parathyroidectomy. A group of 46 consecutive patients with sporadic PHPT due to adenoma undergoing surgery were followed an average of 3.5 years (range 36 to 53 months). In 16 nonselected, consecutive parathyroidectomized patients, with normalized biochemical measurements, circadian rhythm of blood pressure was evaluated with ambulatory blood pressure monitoring (ABPM). Prevalence of hypertension in PHPT was 54.35%, and there was no significant association of PTH, total and ionic calcium levels with SBP and DBP. During follow-up, none of the patients with presurgical hypertension became normotensive and five of the normotensive patients developed clinical hypertension. In ABPM, 6/11 hypertensive and 3/5 normotensive subjects showed nondipper behavior. Serum total calcium was significantly related to night-time systolic blood pressure (SBP) (r = 0.620, P < 0.02), and night-time diastolic blood pressure (DBP) (r = 0.758, P < 0.002). In dippers, creatinine clearance was significantly higher (91.3 +/- 18.5 vs. 64.3 +/- 11.5 ml/min, P < 0.01), while serum total calcium was lower (2.42 +/- 0.13 vs. 2.23 +/- 0.17 mmol/L, P < 0.04) than in nondippers. In conclusion, our results suggest that parathyroidectomy has little effect on hypertension prevalence. Renal impairment, a condition that did not improve after parathyroidectomy, may be a causal factor of hypertension in PHPT. Also, the high prevalence of nondipper behavior in hypertensive and normotensive subjects after parathyroidectomy, suggests that target organ risk persists. We hypothesized that slight elevations of serum total calcium even in the normal range could be involved in the alteration of the circadian rhythm of blood pressure.

Role of endothelin in the pathogenesis of hypertension.

In 1985, investigators characterized a potent vasoconstrictor of endothelial origin called endothelin (ET). Subsequently, 3 peptides were recognized that had a comparable molecular structure but different receptors that mediate potent vasoconstrictive and mild vasodilative effects. The renal effects are characterized by natriuresis despite renal vasoconstriction. This effect, along with the stimulation of ET by high sodium intake, suggests that ET may be responsible for maintaining sodium balance when the renin-angiotensin system is depressed. Endothelin is activated in desoxycorticosterone acetate salt hypertension models and salt-sensitive hypertension. However, ET involvement with spontaneous hypertension models and renovascular hypertension in rats appears minimal. In humans, the role of ET appears similar to that in experimental animals; in both, ET regulates salt metabolism. Salt-sensitive patients exhibit a blunted renal ET-1 response during sodium load. The role of ET in humans has been investigated using nonspecific ET receptor blockers that inhibit the vasoconstrictive and vasodilative components of ET. However, the effects of ET blockade should be investigated with ET subtype A receptor blockers that mediate vasoconstriction alone. Effects of ET blockade also should be evaluated with respect to stimulation of oxidative stress and tissue damage, important mechanisms responsible for tissue fibrosis. This review offers the clinician a balanced view on the hypertensive mechanisms involved with activation of ET and associated clinical implications.

[Treatment of hypertension in type 2 diabetes: importance of therapeutic selection]. / Tratamiento de la hipertension arterial en la diabetes tipo 2: importancia de la selección terapeutica.

BACKGROUND: Type 2 diabetes and essential hypertension are the most common causes of end-stage renal disease in Argentina. Over 887 organ transplantations performed in the year 2004, 577 were kidney transplants. In urban and rural populations hypertension was more prevalent in type 2 diabetics, in particular systolic hypertension. Outcome studies are used to measure clinically meaningful primary end points, such as mortality and cardiovascular morbidity. Our current knowledge of the effects of antihypertensive agents on cardiovascular risk in hypertensive patients with type 2 diabetes has been achieved from subgroups included in large-scale studies. SCOPE: The present study, based on a search of MEDLINE literature in the period 1990-2005, revised major randomised studies with the purpose of finding out which are the most advisable therapeutic strategies against this morbid association. The majority of patients require 2 to 4 antihypertensive medications to achive BP levels that correlate with diminished progression of target organ damages. Despite the advantages of renin-angiotensin system inhibitors the initial choice of medications should be based on the evidences of target organ damages. In those patients without any evidence of complications, the primary goal seems to be achieving their BP to < 130/80 mm Hg beyond the differences among antihypertensive drugs classes, while in those with target organ damage evidences maintain BP < 120/75 mm Hg.

Early treatment of hypertension in acute ischemic and intracerebral hemorrhagic stroke: progress achieved, challenges, and perspectives.

Hypertension is the leading risk factor for ischemic and intracerebral hemorrhagic subtypes of stroke. Additionally, high blood pressure (BP) in the acute cerebrovascular event is associated with poor outcome, and a high percentage of stroke survivors have inadequate control of hypertension. The present is a systematic review of prospective, randomized, and controlled trials carried out on safety and efficacy of antihypertensive treatment of both subtypes of acute stroke. Six trials involving 7512 patients were included, which revealed controversies on the speed and the goals of treatment. These controversies could be due at least in part, from the fact that some studies analyzed the results of antihypertensive treatment in ischemic and intracerebral hemorrhagic subtypes of acute stroke together, and from a different prevalence of past-stroke in the randomized groups. Further research is necessary to establish whether standard antihypertensive treatment provides greater benefit than simple observation in patients with ischemic acute stroke and Stage 2 hypertension of JNC 7, albeit they were not candidates for acute reperfusion. In that case, the target reduction in BP could be 10% to 15% within 24 hours. The recently published INTERACT 2 has provided evidence that patients with hemorrhagic stroke may receive intensive antihypertensive treatment safely with the goal of reducing systolic BP to levels no lower than 130 mm Hg. It is important to take into account that marked BP lowering in acute stroke increases the risk of poor outcome by worsening cerebral ischemia from deterioration of cerebral blood flow autoregulation.

Lowering blood pressure to prevent stroke recurrence: a systematic review of long-term randomized trials.

Albeit hypertension is a leading risk factor for an initial stroke, the role of blood pressure (BP) lowering to prevent a subsequent stroke is controversial. The present systematic review searched randomized trials published from January 1990 to January 2014 with the aim to assess antihypertensive treatment effects on recurrent stroke prevention. Seven randomized placebo-controlled trials enrolling 49,518 patients, two randomized trials not placebo controlled comparing antihypertensive drugs, and one randomized trial that compared the effects of intensive systolic BP lowering with a more conservative systolic BP management, were identified. The placebo-controlled trials had substantial methodological differences, explaining the difficulties to compare their results. An important obstacle arises from the large dispersion in the window's time between the qualifying stroke and randomization. Another barrier is the variation among studies in the recruited patient's stroke subtypes. Differences between trials could not be attributed to disparity in lowering BP or to different degrees of no adherence. The American Heart Association/American Stroke Association stated that although an absolute target of BP level has not been clearly defined, a reduction in recurrent stroke has been associated with an average lowering of 10/5 mm Hg. It should be taken into account that it is not advisable to reduce BP levels to <120/80 mm Hg. It should carry out an individualized selection, based on demographic characteristics and comorbidities (cardiovascular disease, diabetes mellitus, and chronic disease) among diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, or calcium channel blockers.

Nocturia in arterial hypertension: a prevalent, underreported, and sometimes underestimated association.

Nocturia is a risk factor for morbidity and mortality but is frequently overlooked and underreported by patients and unrecognized by physicians. Epidemiologic studies reported that nocturnal voiding is associated not only with aging and benign prostatic hyperplasia, but also with many other clinical conditions. The majority of epidemiologic studies reported a significant relationship between nocturia and hypertension. However, the cause-and-effect relationship between them has not been established. Some physiopathological changes in hypertension are conducive to result in nocturia. These include the effects of hypertension on glomerular filtration and tubular transport, resetting of the kidney pressure-natriuresis relationship, atrial stretch and release of atrial natriuretic peptide when congestive heart failure complicates hypertension, and peripheral edema. Another link between hypertension and nocturia is obstructive sleep apnea. Furthermore, some evidence supports the relationship between nondipping behavior of blood pressure and an increased prevalence of nocturia. The use of some classes of antihypertensive agents may result in nocturia. The present review aims to provide a comprehensive evaluation of the epidemiologic evidence and physiopathological links that correlate hypertension and nocturia. Emphasis is placed on the need to take a pro-active attitude to detect and treat this hazardous condition.

Association between chronic blood pressure changes and development of Alzheimer's disease.

Epidemiological studies suggest an association between chronic blood pressure (BP) changes and Alzheimer's disease (AD). In particular, there is growing evidence that hypertensive people that do not have their BP adequately treated and controlled in midlife are more likely to develop AD in late-life. It has been hypothesized that cerebrovascular disease is a common pathway which connects hypertension and AD in individuals with apolipoprotein E genotype through brain hypoperfusion and hypoxia. This could accelerate amyloid-ß aggregation that disrupts cell-to-cell connectivity and leads to eventual brain neuron loss. Also, high BP contributes to worsen AD by raising oxidative stress and inflammatory response. Aging-related structural and functional disturbances appear to exacerbate the deleterious effect of chronic hypertension on cerebral blood flow autoregulation. There is evidence suggesting that some antihypertensive drug classes reduce the risk and progression of AD more than others. Further prospective randomized studies comparing different classes of antihypertensive drugs are needed to provide more evidence regarding their effects on AD risk. Hypotension could be a consequence of the incident dementia and conversely deteriorate the outcome of AD by worsening brain hypoperfusion. Frequent home BP monitoring should be carried out in AD patients to detect harmful orthostatic hypotension.

Orthostatic hypotension: a common, serious and underrecognized problem in hospitalized patients.

Orthostatic hypotension (OH) is strongly age-dependent, with a prevalence ranging from 5% to 11% in middle age to 30% or higher in the elderly. It is also closely associated with other common chronic diseases, including hypertension, congestive heart failure, diabetes mellitus, and Parkinson's disease. Most studies of OH have been performed in population cohorts or elderly residents of extended care facilities, but in this review, we draw attention to a problem little studied to date: OH in hospitalized patients. The prevalence of OH in all hospitalized patients is not known because most studies have included only older individuals with multiple comorbid diseases, but in some settings as many as 60% of hospitalized adults have postural hypotension. Hospitalized patients are particularly vulnerable to the consequences of OH, particularly falls, because postural blood pressure (BP) regulation may be disturbed by many common acute illnesses as well as by bed rest and drug treatment. The temporal course of OH in hospitalized patients is uncertain, both because the reproducibility of OH is poor and because conditions affecting postural BP regulation may vary during hospitalization. Finally, OH during hospitalization often persists after discharge, where, in addition to creating an ongoing risk of falls and syncope, it is strongly associated with risk of incident cardiovascular complications, including myocardial infarction, heart failure, stroke, and all-cause mortality. Because OH is a common, easily diagnosable, remediable condition with important clinical implications, we encourage caregivers to monitor postural BP change in patients throughout hospitalization.

The complex interaction between overweight, hypertension, and sympathetic overactivity.

There is ample evidence in the epidemiological and clinical literature that hypertension and overweight are closely and causally interrelated. Sympathetic nervous system (SNS) overactivity has been well documented in both hypertension and overweight, but it is not clear whether this is a coincidental finding or whether the association reflects a mechanistic role of SNS in these two interrelated clinical conditions. Whereas in this review we focus on the evidence for a primary role of SNS in the development of hypertension and overweight, it is clear that the process can be initiated from other starting points such as primary overeating or sleep apnea. After overweight evolves, hormones secreted by fat cells further accelerate SNS overactivity, weight gain, and blood pressure increase. The main thesis of this article is that regardless of where the process started, the same clinical picture of hypertension, overweight, and SNS overactivity will emerge. There is good evidence that in genetically prone individuals, prolonged SNS stimulation elicits a down regulation of beta-adrenergic receptors. This in turn decreases the ability to dissipate calories and diminishes the beta-adrenoceptor-mediated vasodilatation. We hypothesize that beta-adrenoceptor downregulation is the linchpin in the association of SNS with overweight and hypertension.

Statins as antihypertensives.

The beneficial effects of statins in hypertension stem from their effects on endothelial function, their interactions with the renin-angiotensin system, and their influence on large artery compliance. Substantial evidence has recently accumulated showing that statins exert pleiotropic effects in vascular function. These include an increase in the synthesis of NO, inhibition of vascular smooth muscle cell proliferation and migration, anti-inflammatory actions, downregulation of angiotensin II type 1 receptor expression, and anti-oxidative effects. These effects occur before reduction of cholesterolemia. Available data support only a modest BP-lowering effect of statins which is most prominent in those patients with poorly controlled hypertension. Even though they only cause a minor reduction in BP, they may play a role in the prevention of cardiovascular disease. Statins may be useful therapeutic agents in hypertensives with high serum total cholesterol, in patients with poorly controlled hypertension even without hypercholesterolemia, in normocholesterolemic well-controlled hypertensive subjects with high C reactive protein levels, and in those subjects who need secondary prevention. Future research is needed to further characterize the impact of statins alone or in combination with antihypertensive agents to prevent or delay the development of stage 1 hypertension. This review article also includes relevant patents.

[Resistant hypertension]. / Hipertensión arterial resistente.

Resistant hypertension, defined as a persistent blood pressure over 140/90 mmHg despite the use of three antihypertensive drugs including a diuretic, is unusual. The diagnosis requires ruling out initially pseudoresistance and a lack of compliance with treatment. Ambulatory blood pressure recording allow the recognition of white coat hypertension. When there is a clinical or laboratory suspicion, secondary causes of hypertension should be discarded. Excessive salt intake, the presence of concomitant diseases such as diabetes mellitus, chronic renal disease, obesity, and psychiatric conditions such as panic attacks, anxiety and depression, should also be sought. The presence of target organ damage requires a more aggressive treatment of hypertension. Recent clinical studies indicate that the administration of aldosterone antagonists as a fourth therapeutic line provides significant additional blood pressure reduction, when added to previous antihypertensive regimens in subjects with resistant hypertension. The possible blood pressure lowering effects of prolonged electrical activation of carotid baroreceptors is under investigation.

Management of hypertensive crises.

Hypertensive emergencies are life-threatening conditions because their course is complicated with acute target organ damage. They can present with neurological, renal, cardiovascular, microangiopathic hemolytic anemia, and obstetric complications. After diagnosis, they require the immediate reduction of blood pressure (in <1 hour) with intravenous drugs such as sodium nitroprusside, administered in an intensive care unit. These patients present with a mean arterial pressure >140 mm Hg and grade III to IV retinopathy. Only occasionally do they have hypertensive encephalopathy, reflecting cerebral hyperperfusion, loss of autoregulation, and disruption of the blood-brain barrier. In hypertensive emergencies, blood pressure should be reduced about 10% during the first hour and another 15% gradually over the next 2 to 3 hours to prevent cerebral hypoperfusion. The exception to this management strategy is aortic dissection, for which the target is systolic blood pressure <120 mm Hg after 20 minutes. Oral antihypertensive therapy can usually be instituted after 6 to 12 hours of parenteral therapy. Hypertensive urgencies are severe elevations of blood pressure without evidence of acute and progressive dysfunction of target organs. They demand adequate control of blood pressure within 24 hours to several days with use of orally administered agents. The purpose of this review is to provide a rational approach to hypertensive crisis management.

Role of endothelins in hypertension.

There are three peptides of endothelial origin, called endothelins (ETs), having different receptors that mediate a potent vasoconstrictor effect and also a mild vasodilation. Their renal effects are characterized by natriuresis in spite of the renal vasoconstriction. This effect, along with the stimulation of ETs by high sodium intake, suggests that ETs may be responsible for maintaining sodium balance when the renin angiotensin system is depressed. ET is activated in deoxycorticosterone acetate (DOCA) salt hypertension models and salt-sensitive hypertension. In humans, the role of ET seems to be similar to that shown in experimental animals; in both, ET participates in the regulation of salt metabolism. Salt-sensitive patients exhibit a blunted renal ET-1 response during sodium load. The role of ETs in humans has been investigated with use of nonspecific ET receptor blockers that inhibit the vasoconstriction and vasodilator components of ET. However, the effects of ET blockade should be investigated with ETA receptor blockers that mediate vasoconstriction alone. Effects of ET blockade should also be evaluated with respect to stimulation of oxidative stress and tissue damage, important mechanisms responsible for tissue fibrosis.

A comparison of body mass index and waist-to-hip ratio as indicators of hypertension risk in an urban Argentine population: a hospital-based study.

BACKGROUND AND AIM: To examine the relationship between 24-h ambulatory blood pressure monitoring (ABPM) and three commonest anthropometric measurements for obesity [body mass index (BMI), waist circumference (WC) and waist-hip ratio (WHR)] in patients with essential hypertension never treated or after a 3 week placebo period, living in Buenos Aires. METHODS AND RESULTS: Cross-sectional survey among outpatients at the Hypertension Program of Buenos Aires University Hospital de Clinicas. Three-hundred seventy-seven essential hypertensives, aged 18-86 years, of either sex, were consecutively recruited. All subjects underwent 24 h ABPM performed with a blood pressure (BP) device. The prevalence of overweight-obesity was 56.76% in women and 75.86% in men. High WHR prevalence in non-obese women was 4.5% and 4.1% in non-obese men while high values of WC were observed in 3.0% of non-obese women and in 0% of non-obese men. The two-way ANCOVA showed that in women with high values of WHR, 24 h DBP was higher in those with BMI<25 than in those with BMI> or =25. Those females with a BMI> or =25 had a higher prevalence of top tertile values of PP (> or =68 mmHg) (P<0.05) than non-obese females. Only in women was mean pulse pressure (PP) significantly correlated with age (r=0.38; P<0.0001), WC (r=0.22; P<0.005), WHR (r=0.21, P<0.008), and BMI (r=0.20; P<0.01) while in men there was no significant correlation between variables. Logistic regression showed that the odds of morning blood pressure surge (MBPS) increased with age, central obesity (represented by high WHR and dipper status), while the odds of higher mean PP increased with age and high WHR. CONCLUSION: These results indicated a high prevalence of overweight-obesity (more than 56% of women and 75% of men) in our hospital-based sample of essential hypertension and that the WHR offers additional information beyond BMI and WC to predict the hypertension risk according to the ABPM.