Degree Of Blood Pressure Elevation Research Articles

SAT-LB301 Hyperaldosteronism From Adrenal Adenoma in a Young Patient

Introduction Primary aldosteronism (PA) is the most common cause of secondary hypertension (HTN) that is often underdiagnosed. Patients with PA have higher cardiovascular morbidity and mortality than age- and sex- matched patients with essential HTN and the same degree of blood pressure elevation. We present a case of a 17-year old male with primary hyperaldosteronism. Case Report 17-year-old male with no past medical history presented to the emergency department referring bitemporal cephalea, pain in left arm, dyspnea, heart palpitations, a blood pressure (BP) of 220/110 mmHg and a serum potassium of 1.5mmol/L (n. 3.5-5). The patient was admitted to the hospital for better handling of his BP, potassium repositions, monitoring and further management. During hospitalization he referred leg cramps, asthenia, adynamia, nausea, cephalea, and blurred vision. Physical examination demonstrated decreased muscle strength, jugular regurgitation II and hyperreflexia on lower extremities. Thyroid and pulmonary examinations were normal. BP continued elevated despite the concurrent use of 3 antihypertensive drug classes (ARA2, BB, CCB), referred to endocrinologist after being diagnosed with resistant hypertension suspecting of a primary hyperaldosteronism. Lab tests were run obtaining a plasma aldosterone concentration 44ng/dl (n. 4-31), plasma active renin (PRA) 0.05ng/ml/hr (n. 0.2-1.6), aldosterone/PAR ratio 880 (<25 normal). Suprarenal CT scan revealed right suprarenal lesion 2.2 x 2.1 cm, round appearance, hypodense (14 HU) compatible with an adenoma. He underwent unilateral adrenalectomy. Histopathological report from excised adrenal tumor was compatible with a benign adenoma. Patient was discharged with a regularized blood pressure without antihypertensives and normokalemic. No clinical symptoms were reported in follow-up. ConclusionPrimary aldosteronism (PA) is the most common form of secondary hypertension (HTN) with an estimated prevalence of 4% of hypertensive patients in primary care and around 10% of referred patients. PA is characterized by hypertension, hypokalemia, suppressed plasma renin and increased aldosterone excretion. Aldosterone producing adenomas (APAS) account for around 40% and idiopathic hyperaldosteronism for around 60% of PA cases. The most sensitive screening test for PA is the aldosterone-to-renin ratio. After case confirmation, all patients with PA should undergo adrenal CT as the initial study. Unilateral laparoscopic adrenalectomy is the preferential treatment for patients with APAs, and bilateral hyperplasia should be treated with mineralocorticoid antagonist.

Influence of dietary inorganic nitrate on blood pressure and vascular function in hypertension: prospective implications for adjunctive treatment.

Dietary inorganic nitrate (nitrate) is a promising adjunctive treatment to reduce blood pressure and improve vascular function in hypertension. However, it remains unknown if the efficacy of nitrate is dependent upon an elevated blood pressure or altered by medication in patients with hypertension. Therefore, blood pressure and vascular function, measured by passive leg movement (PLM) and flow-mediated dilation (FMD), were assessed following 3 days of placebo (nitrate-free beetroot juice) and nitrate (nitrate-rich beetroot juice) administration in 13 patients (age: 53 ± 12 yr) with hypertension taking antihypertensive medications (study 1) and in 14 patients (49 ± 13 yr) with hypertension not taking antihypertensive medications (study 2). In study 1, plasma nitrite concentration was greater for nitrate than placebo (341 ± 118 vs. 308 ± 123 nmol/L, P < 0.05), yet blood pressure and vascular function were unaltered. In study 2, plasma nitrite concentration was greater for nitrate than placebo (340 ± 102 vs. 295 ± 93 nmol/L, P < 0.01). Systolic (136 ± 16 vs. 141 ± 19 mmHg), diastolic (84 ± 13 vs. 88 ± 12 mmHg), and mean (101 ± 12 vs. 106 ± 13 mmHg) blood pressures were lower (P < 0.05), whereas the PLM change in leg vascular conductance (6.0 ± 3.0 vs. 5.1 ± 2.6 mL·min-1·mmHg-1) and FMD (6.1 ± 2.4% vs. 4.1 ± 2.7%) were greater (P < 0.05) for nitrate than placebo. The changes in systolic blood pressure (r = -0.60) and FMD (r = -0.48) induced by nitrate were inversely correlated (P < 0.05) to the respective baseline values obtained in the placebo condition. Thus, the efficacy of nitrate to improve blood pressure and vascular function in hypertension appears to be dependent on the degree of blood pressure elevation and vascular dysfunction and not antihypertensive medication status, per se.NEW & NOTEWORTHY Dietary nitrate (nitrate) is a promising intervention to improve blood pressure and vascular function in hypertension. We demonstrate that these beneficial effects of nitrate are inversely related to the baseline value in a continuous manner with no distinction between antihypertensive medication status. Thus, the efficacy of nitrate to improve blood pressure and vascular function in hypertension appears to be dependent on the degree of blood pressure elevation and vascular dysfunction and not antihypertensive mediation status.

Diagnosis and management of primary aldosteronism.

Primary aldosteronism (PA) is the most common form of secondary hypertension (HTN), with an estimated prevalence of 4% of hypertensive patients in primary care and around 10% of referred patients. Patients with PA have higher cardiovascular morbidity and mortality than age- and sex-matched patients with essential HTN and the same degree of blood pressure elevation. PA is characterized by an autonomous aldosterone production causing sodium retention, plasma renin supression, HTN, cardiovascular damage, and increased potassium excretion, leading to variable degrees of hypokalemia. Aldosterone-producing adenomas (APAs) account for around 40% and idiopathic hyperaldosteronism for around 60% of PA cases. The aldosterone-to-renin ratio is the most sensitive screening test for PA. There are several confirmatory tests and the current literature does not identify a "gold standard" confirmatory test for PA. In our institution, we recommend starting case confirmation with the furosemide test. After case confirmation, all patients with PA should undergo adrenal CT as the initial study in subtype testing to exclude adrenocortical carcinoma. Bilateral adrenal vein sampling (AVS) is the gold standard method to define the PA subtype, but it is not indicated in all cases. An experienced radiologist must perform AVS. Unilateral laparoscopic adrenalectomy is the preferential treatment for patients with APAs, and bilateral hyperplasia should be treated with mineralocorticoid antagonist (spironolactone or eplerenone). Cardiovascular morbidity caused by aldosterone excess can be decreased by either unilateral adrenalectomy or mineralocorticoid antagonist. In this review, we address the most relevant issues regarding PA screening, case confirmation, subtype classification, and treatment.

Relationship between sleep architecture and blood pressure dynamic change in patients with sleep apnea syndrome

To investigate sleep architecture and blood pressure dynamic change in patients with Sleep apnea syndrome by electrocardiogram-based cardiopulmonary coupling analysis system. Seventy-nine sleep disorder participants (PSQI≥8) were enrolled. Electrocardiogram-based cardiopulmonary coupling analysis device and ambulatory blood pressure monitoring were synchronously used to evaluate sleep architecture and blood pressure circadian rhythm. The patients were divided into SAS group (47 participants) and non-SAS group (32 participants) according to the Apnea Hypopnea Index (AHI) that calculated by CPC device. The data of sleep architecture and blood pressure variability were compared between two groups. Compared with non-SAS group, SAS group have less proportion of deep sleep, more proportion of light sleep, higher mean blood pressure in 24 hours and daytime, lower nocturnal blood pressure dipping, faster mean heart rate in night time (P<0.05). AHI has moderate inverse correlation with deep sleep time, wake/dream time (-0.6≤r<-0.3), moderate positive correlation with light sleep time (0.3<r≤0.6), high inverse correlation with nocturnal blood pressure dipping (r=-0.785, P=0.000), moderate positive correlation with mean diastolic blood pressure (r=0.425, P=0.019). Our study shows that less proportion of deep sleep, more proportion of light sleep, 24 hours mean blood pressure and nocturnal blood pressure increase in the patients with Sleep Apnea Syndrome. The severity of Sleep Apnea Syndrome has a positive correlation with the severity of abnormal sleep architecture and the degree of blood pressure elevation.

Adrenal histopathology in primary aldosteronism: is it time for a change?

Primary aldosteronism (PA) entails a group of disorders characterized by excess aldosterone production, relatively independent from the renin–angiotensin system.1 Because PA is the most common form of secondary hypertension and patients with PA have higher cardiovascular morbidity and mortality than age- and sex-matched patients with essential hypertension and the same degree of blood pressure elevation,2–5 early recognition of PA is of utmost importance to cure the high blood pressure and prevent deleterious cardiovascular effects. The 2 major PA subgroups are the unilateral forms, mainly aldosterone-producing adenoma (APA), and bilateral forms, mostly adrenal zona glomerulosa (ZG) hyperplasia, which require surgical or medical treatment, respectively. Adrenal vein sampling (AVS) is the best available method to distinguish between unilateral and bilateral aldosterone hypersecretion.6–8 In medical centers where AVS is available and strict cutoff values for the lateralization index are used,9 almost two thirds of PA cases are attributed to an APA, whereas one third remain classified as bilateral idiopathic forms. The opposite is seen when AVS is unavailable.10 Hence, the availability of AVS greatly affects the recognition of unilateral forms of PA that can be successfully treated with adrenalectomy. After surgery, demonstration of an adenoma at pathology is needed to reach a conclusive diagnosis of the only PA subtype that can be unequivocally diagnosed, eg, APA. After the introduction of the 4 corner criteria,10 an APA can be diagnosed when (1) there is evidence of PA at the screening tests, with an inappropriately high aldosterone/renin ratio and confirmation as needed; (2) aldosterone secretion is lateralized at AVS; (3) an adenoma is detected at pathology; and crucially important, (4) PA is corrected by adrenalectomy. However, at pathology, the identification of an APA may be challenging …

Role of the morphogenetic proteins FGF-23 and Klotho and the glycoprotein sclerostin in the assessment of the risk of cardiovascular diseases and the prognosis of chronic kidney disease

AIM. To analyze changes in the serum concentrations of the morphogenetic proteins fibroblast growth factor 23 (FGF-23) and Klotho, as well as sclerostin, an osteocyte-secreted glycoprotein, in relation to the degree of hypertension, left ventricular (LV) hypertrophy, and arterial stiffness in patients with chronic kidney disease (CKD) at its different stages. Sixty-five patients (33 men and 32 women) aged 20-65 years, including 25 with chronic glomerulonephritis, 15 with tubulointerstitial nephritis, and 25 with hypertensive nephrosclerosis, were examined. A control group consisted of 15 healthy volunteers matched to the study group patients for age and gender. Serum FGF-23 concentrations and blood pressure (BP) were measured in the all subjects. Patients with BPs > 140/80 mm Hg underwent echocardiography, followed by determination of LV mass (LVM) and calculation of LVM index. Vascular circulation, pulse wave velocity, cardiac and vascular calcifications, and vascular functional properties were estimated. There was a strong direct Correlation between the serum concentration of FGF-23 and the stage of CKD and an inverse correlation between the levels of Klotho and sclerostin and the stage of CKD. As the glomerular filtration rate became lower, the concentration of FGF-23 increased and that of Klotho and sclerostin decreased just in Stage III CKD while hyperphosphatemia and elevated parathyroid hormone levels were noted in Stages IV-V CKD. As CKD progressed, the serum concentrations of Klotho and sclerostin were inversely correlated with the levels of phosphorus and parathyroid hormone. The degree of blood pressure elevation correlated positively with serum FGF-23 concentrations and inversely with Klotho levels. There was no significant correlation of the level of sclerostin with the degree of BP increase. The direct correlation between higher FGF-23 level and higher VLM is most pronounced in hypertensive patients. There was a strong direct relationship between FGF-23 and Klotho levels and a strong inverse relationship between sclerostin levels and pulse wave velocity. Lower Klotho concentrations were associated with the detection rate of calcifications in the heart valves and large arteries (the abdominal aorta). The reduced serum levels of Klotho and sclerostin were also correlated with concentric LV remodeling. It was demonstrated that there was a clear link between increased serum FGF-23 and decreased Klotho concentration as CKD progressed, and that between arterial stiffness and calcification and myocardial remodelling regardless of traditional risk factors. More experimental and clinical studies are required to clarify the role of sclerostin in CKD.

Relationship among 25-hydroxyvitamin D concentrations, insulin action, and cardiovascular disease risk in patients with essential hypertension.

Although low plasma 25-hydroxyvitamin D (25(OH)D) concentrations have been shown to predict risk of hypertension and associated cardiovascular disease (CVD), vitamin D repletion has not consistently lowered blood pressure or decreased CVD. One possibility for this discrepancy is the presence of considerable metabolic heterogeneity in patients with hypertension. To evaluate this possibility, we quantified relationships among insulin resistance, 25(OH)D concentration, and CVD risk factor profile in patients with essential hypertension. Measurements were made of 25(OH)D concentrations, multiple CVD risk factors, and insulin resistance by the steady-state plasma glucose concentration during the insulin suppression test in 140 otherwise healthy patients with essential hypertension. As a group, the patients were overweight/obese and insulin resistant and had low 25(OH)D concentrations. The more insulin resistant the patients were, the worse the CVD risk profile was. In addition, the most insulin-resistant quartile had significantly lower 25(OH)D concentrations than the most insulin-sensitive quartile (20.3±1.4 vs. 25.8±1.4ng/ml; P = 0.005). In the entire group, 25(OH)D concentration significantly correlated with magnitude of insulin resistance (steady-state plasma glucose concentration; r = -0.20; P = 0.02). There was considerable metabolic heterogeneity and substantial difference in magnitude of conventional CVD risk factors in patients with similar degrees of blood pressure elevation. The most insulin-resistant quartile of subjects had the lowest 25(OH)D concentration and the most adverse CVD risk profile, and they may be the subset of patients with essential hypertension most likely to benefit from vitamin D repletion.

Clinical Implications

HomeHypertensionVol. 62, No. 1Clinical Implications Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBClinical Implications Originally published1 Jul 2013https://doi.org/10.1161/HYP.0b013e31829d4408Hypertension. 2013;62:2Angiotensinogen Expression in Human Adipose Tissue (page 41)Blood pressure is a heritable trait; the genetic causes of essential hypertension remain unclear. Despite being the first gene linked to hypertension, the importance of polymorphisms in angiotensinogen, the precursor to angiotensin-II, remains controversial. The renin–angiotensin system has both endocrine and intracrine functions controlling arterial pressure. The mechanisms regulating angiotensinogen expression is complicated. Because sequence variants in the promoter may differentially affect transcription factor binding, the mechanisms regulating angiotensinogen may differ depending on the polymorphism(s) carried. The current issue of Hypertension reports an effective strategy to examine whether variation in the angiotensinogen promoter effects its expression through differential binding of transcription factors in adipose tissue. The investigators report increased expression of angiotensinogen mRNA and binding of the transcription factor USF2 in chromatin specifically from the −20C allele in subcutaneous adipose tissue from subjects heterozygous for the −20A/C alleles of angiotensinogen. Thus, subjects carrying high-expressing alleles may have increased levels of angiotensinogen and angiotensin-II in some fat depots. This may be clinically important because circulating angiotensinogen derived from adipose tissue is increased in obesity and evidence implicates a role for angiotensin-II derived from adipose angiotensinogen in the regulation of metabolism and blood pressure. Consequently, further studies will need to assess whether this and other polymorphisms control the level of angiotensin-II in hypertensive and obese subjects.Download figureDownload PowerPointCD8+ T Cells and Chemokines in Human Hypertension (page 126)The pathogenic role of T cells in the development of hypertension has been well documented in animal studies. However, the existence of T-cell–driven inflammation in human hypertension has not been demonstrated. In this issue of Hypertension, Youn et al reported an increased fraction of immunosenescent, proinflammatory, cytotoxic CD8+ T cell, and increased circulating levels of T cell chemokines (MIG, IP-10, and I-TAC) in patients with hypertension. In patients with hypertensive nephrosclerosis, I-TAC was expressed more abundantly in the proximal and distal tubules. This evidence, along with an increased level of serum granzyme B, supports the increased activity of cytotoxic T cells in human hypertension. The authors provide evidence for the first time in favor of the existence of T-cell–driven inflammation in human hypertension.Download figureDownload PowerPointCardiac Effects of Hyperaldosteronism (page 62)Affecting >11% of the patients referred to specialized hypertension centers, primary aldosteronism (PA) is the most common endocrine cause of high blood pressure. Furthermore, it induces cardiovascular damage in excess of that expected based on the degree of blood pressure elevation. PA is potentially curable with a targeted treatment, but whether normalization of the blood pressure and regression of associated cardiovascular damage could be achieved in the long term remained uncertain. Rossi et al prospectively assigned 180 PA patients to either adrenalectomy (n=110) or medical therapy (n=70), based on whether there was lateralization of aldosterone excess at adrenal vein sampling. Long-term follow-up study with serial echocardiography evaluations showed for the first time in a prospective study that atrial fibrillation was ≈6-fold higher in PA than in essential hypertensive patients. After treatment blood pressure fell comparably in adrenalectomized and medically treated PA, as it did in optimally treated essential hypertensives. Left ventricular (LV) mass index and the rate of LV hypertrophy also fell mainly through LV inward remodeling in PA patients. Notwithstanding this, the rate of LV mass that was disproportionally elevated for cardiac workload and sex in PA subjects unexpectedly increased. While highlighting the cardiovascular consequences of PA patients, these findings underscore the importance of a timely identification of PA to enable reversal of the LV abnormalities and lowering cardiovascular risk.Download figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetails July 2013Vol 62, Issue 1 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/HYP.0b013e31829d4408 Originally publishedJuly 1, 2013 PDF download Advertisement

Fixed combination of lercanidipine and enalapril in the management of hypertension: focus on patient preference and adherence

Hypertension is one of the most important and widespread risk factors for the development of cardiovascular disease. Once, combination therapy was traditionally reserved as a third-line or fourth-line approach in the management of hypertension. However, several major intervention trials in high-risk patient populations have shown that an average of 2–4 antihypertensive agents are required to achieve effective blood pressure control. Combination treatment should be considered as a first choice in patients at high cardiovascular risk and in individuals for whom blood pressure is markedly above the hypertension threshold (eg, more than 20 mmHg systolic or 10 mmHg diastolic), or when milder degrees of blood pressure elevation are associated with multiple risk factors, subclinical organ damage, diabetes, renal failure, or associated cardiovascular disease. A number of clinical trials have demonstrated that a fixed combination of lercanidipine and enalapril has better efficacy and tolerability than monotherapy with either agents. The fixed-dose formulation of lercanidipine–enalapril was well tolerated in all clinical trials, with an adverse event rate similar to that of the component drugs as monotherapy. The advantages of combination therapy include improved adherence to therapy and minimization of blood pressure variability. In addition, combining two antihypertensive agents with different mechanisms of action may provide greater protection against major cardiovascular events and the development of end-organ damage.

Wall-to-lumen ratio of retinal arterioles

Wall-to-lumen ratio of retinal arterioles

Hypertensive crisis

Hypertensive crisis

Factores de riesgo en los pacientes con hipertensión arterial sin eventos cardiovasculares previos

Background and objective Guidelines recommend management of patients based not only on the degree of blood pressure elevation, but in total cardiovascular risk. The aim of the present study was to evaluate the distribution of cardiovascular risk categories in hypertensive patients without evidence of previous cardiovascular events, as well as the relative contribution of each factor responsible for this distribution. Patients and methods Cross-sectional, observational, and multicentre study in a cohort of 6,762 treated hypertensive patients, without evidence of previous cardiovascular events. Data responsible for cardiovascular risk stratification (additional cardiovascular risk factors and target organ damage) were collected. The presence of such factors, as well as changes in risk stratification due to individual removal were evaluated. Results Most patients fulfilled criteria of high or very-high cardiovascular risk. Most frequently present factors were lipid alterations (73.6%) followed by advanced age (sex-adjusted) in 50.8% and abdominal obesity (31.7%). Regarding target organ damage, abnormalities in renal function (24.1%), left ventricular hypertrophy (16.4%) and microalbuminuria (10.7%) were the most frequently observed. A 29% of patients would reduce their cardiovascular risk categorization if lipid abnormalities were absent. In comparison, when other risk factors were removed from risk categorization, it affected less than 10% of patients. Conclusion Most of the hypertensive subjects fall in high or very-high cardiovascular risk categories. Lipid abnormalities are the most frequent risk modificator and has the most important quantitative impact in risk categorization.

Central and Peripheral Mechanisms of T-Lymphocyte Activation and Vascular Inflammation Produced by Angiotensin II–Induced Hypertension

We have previously found that T lymphocytes are essential for development of angiotensin II-induced hypertension; however, the mechanisms responsible for T-cell activation in hypertension remain undefined. We sought to study the roles of the CNS and pressure elevation in T-cell activation and vascular inflammation caused by angiotensin II. To prevent the central actions of angiotensin II, we created anteroventral third cerebral ventricle (AV3V) lesions in mice. The elevation in blood pressure in response to angiotensin II was virtually eliminated by AV3V lesions, as was activation of circulating T cells and the vascular infiltration of leukocytes. In contrast, AV3V lesioning did not prevent the hypertension and T-cell activation caused by the peripheral acting agonist norepinephrine. To determine whether T-cell activation and vascular inflammation are attributable to central influences or are mediated by blood pressure elevation, we administered hydralazine (250 mg/L) in the drinking water. Hydralazine prevented the hypertension and abrogated the increase in circulating activated T cells and vascular infiltration of leukocytes caused by angiotensin II. We conclude that the central and pressor effects of angiotensin II are critical for T-cell activation and development of vascular inflammation. These findings also support a feed-forward mechanism in which modest degrees of blood pressure elevation lead to T-cell activation, which in turn promotes inflammation and further raises blood pressure, leading to severe hypertension.

Association of Capillary Density and Function Measures With Blood Pressure, Fasting Plasma Glucose, and Insulin Sensitivity

The pathophysiology underlying the association between hypertension and insulin resistance remains unclear. The study purpose was to determine whether reduced capillary density and/or function underlie, and may therefore explain, this association. The study was conducted on 115 black and non-black participants aged 18 to 55 years: 91 with normal blood pressure (systolic blood pressure [SBP] <130 mm Hg) and 24 with mild blood pressure elevation (SBP 130-159 mm Hg). Capillary density and function were quantified using direct capillaroscopy measures. Insulin sensitivity (IS) was estimated using the Quantitative Insulin Sensitivity Check Index (QUICKI). Endothelial function (EF) was measured using strain-gauge plethysmography. Data were analyzed by linear regression adjusted for age, sex, race, and body mass index (BMI). After adjustment for BMI, capillary density and function measures were significant predictors of SBP ( P<.01), fasting plasma glucose (P=.012, P=.03, and P=.004, respectively), and EF (P=.033, P=.001, and P=.009, respectively). However, none of the capillary measures were significant predictors of fasting insulin or IS. These capillaroscopy data demonstrated an association with SBP but not insulin resistance, suggesting that capillary measures are unlikely to explain the association between hypertension and insulin resistance, at least with modest degrees of blood pressure elevation.

The 2009 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 1 – blood pressure measurement, diagnosis and assessment of risk

To provide updated, evidence-based recommendations for the diagnosis and assessment of adults with hypertension. The diagnosis of hypertension is dependent on appropriate blood pressure measurement, the timely assessment of serially elevated readings, the degree of blood pressure elevation, the method of measurement (office, ambulatory, home) and associated comorbidities. The presence of cardiovascular risk factors and target organ damage should be ascertained to assess global cardiovascular risk and determine the urgency, intensity and type of treatment required. MEDLINE searches were conducted from November 2007 to October 2008 with the aid of a medical librarian. Reference lists were scanned, experts were contacted, and the personal files of authors and subgroup members were used to identify additional studies. Content and methodological experts assessed studies using prespecified, standardized evidence-based algorithms. Recommendations were based on evidence from peer-reviewed full-text articles only. Recommendations for blood pressure measurement, criteria for hypertension diagnosis and follow-up, assessment of global cardiovascular risk, diagnostic testing, diagnosis of renovascular and endocrine causes of hypertension, home and ambulatory monitoring, and the use of echocardiography in hypertensive individuals are outlined. Key messages include continued emphasis on the expedited, accurate diagnosis of hypertension, the importance of global risk assessment and the need for ongoing monitoring of hypertensive patients to identify incident type 2 diabetes. All recommendations were graded according to strength of the evidence and voted on by the 57 members of the Canadian Hypertension Education Program Evidence-Based Recommendations Task Force. All recommendations were required to be supported by at least 70% of task force members. These guidelines will continue to be updated annually.

The Diagnosis and Treatment of Hypertensive Crises

Hypertension (HTN) is one of the most common chronic medical conditions, affecting nearly 72 million people in the United States. A systolic blood pressure (BP) > 180 mm Hg or a diastolic BP > 120 mm Hg is considered a “hypertensive crisis.” Hypertensive crises are categorized as either hypertensive emergencies or urgencies depending on the degree of BP elevation and presence of end-organ damage. The primary goal of intervention in a hypertensive crisis is to safely reduce BP. Immediate reduction in BP is required only in patients with acute end-organ damage (ie, hypertensive emergency). This requires treatment with a titratable short-acting intravenous (IV) antihypertensive agent, while severe HTN with no acute end-organ damage (ie, hypertensive urgency) is usually treated with oral antihypertensive agents.Patients with hypertensive emergencies are best treated in an intensive care unit (ICU) with titratable IV hypotensive agents. Rapid-acting IV antihypertensive agents are available, including clevidipine, labetalol, esmolol, fenoldopam, nicardipine, and sodium nitroprusside. Newer agents such as clevidipine have considerable advantages compared with other available agents in the management of hypertensive crises. Sodium nitroprusside is an extremely toxic drug, and its use in the treatment of hypertensive emergencies should be avoided. Likewise, nifedipine, nitroglycerin, and hydralazine should not to be considered first-line therapies in the management of hypertensive crises because these agents are associated with significant toxicities and/or side effects.

All Thiazide‐Like Diuretics Are Not Chlorthalidone: Putting the ACCOMPLISH Study Into Perspective

All Thiazide‐Like Diuretics Are Not Chlorthalidone: Putting the ACCOMPLISH Study Into Perspective

Management of pediatric hypertension

Hypertension is one of the major contributors to cardiovascular, renal and CNS morbidity and mortality. Although it is more prevalent in adults, hypertension and its sequelae are being seen with increasing frequency in pediatrics recently. The majority of children have hypertension secondary to renovascular and renal parenchymal disease, and it appears that the increased incidence is primarily related to the epidemic of obesity, which is a known risk factor for the development of the condition. After the diagnosis of hypertension is established, a thorough evaluation for secondary causes should be conducted according to existing guidelines. Nonpharmacologic interventions should be discussed in any child, even though the diagnosis of hypertension may not be confi rmed, but if risk factors are identifi ed. Those interventions should be even more encouraged if the diagnosis of hypertension or prehypertension is confi rmed. Nonpharmacologic intervention focuses on salt restriction, diet modifi cation, exercise and physical activity, as well as improved sleep habits. Initiation of medical therapy is guided by the degree of blood pressure elevation, presence of symptoms and existing risk factors. A wide variety of oral medications and intravenous therapies are available for use in children with mild, moderate or severe blood pressure elevations. This article reviews the diagnosis and evaluation of hypertension in children, and provides an update on the pharmacologic and nonpharmacologic treatment options for hypertension, including hypertensive urgency and emergency.

Combined knockout of collecting duct endothelin A and B receptors causes hypertension and sodium retention

The collecting duct (CD) endothelin (ET) system regulates blood pressure (BP) and Na excretion. CD-specific knockout (KO) of ET-1 causes hypertension, CD-specific KO of the ETA receptor does not alter BP, while CD-specific KO of the ETB receptor increases BP to a lesser extent than CD ET-1 KO. These findings suggest a paracrine role for CD-derived ET-1; however, they do not exclude compensation for the loss of one ET receptor by the other. To examine this, mice with CD-specific KO of both ETA and ETB receptors were generated (CD ETA/B KO). CD ETA/B KO mice excreted less urinary Na than controls during acute or chronic Na loading. Urinary aldosterone excretion and plasma renin concentration were similar during Na intake and both fell comparably during Na loading. On a normal sodium diet, CD ETA/B KO mice had increased BP, which increased further with high salt intake. The degree of BP elevation during normal Na intake was similar to CD ET-1 KO mice and higher than CD ETB KO animals. During 1 wk of Na loading, CD ETA/B KO mice had higher BPs than CD ETB KO, while BP was less than CD ET-1 KOs until the latter days of Na loading. These studies suggest that 1) CD ETA/B deficiency causes salt-sensitive hypertension, 2) CD ETA/B KO-associated Na retention is associated with failure to suppress the renin-angiotensin-aldosterone system, and 3) CD ETA and ETB receptors exerts a combined hypotensive effect that exceeds that of either receptor alone.

The 2008 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 1 – blood pressure measurement, diagnosis and assessment of risk

To provide updated, evidence-based recommendations for the diagnosis and assessment of adults with hypertension. The diagnosis of hypertension is dependent on appropriate blood pressure measurement, the timely assessment of serially elevated readings, degree of blood pressure elevation, method of measurement (office, ambulatory, home) and associated comorbidities. The presence of cardiovascular risk factors and target organ damage should be ascertained to assess global cardiovascular risk and determine the urgency, intensity and type of treatment required. MEDLINE searches were conducted from November 2006 to October 2007 with the aid of a medical librarian. Reference lists were scanned, experts were contacted, and the personal files of authors and subgroup members were used to identify additional studies. Content and methodological experts assessed studies using prespecified, standardized evidence-based algorithms. Recommendations were based on evidence from peer-reviewed, full-text articles only. Recommendations for blood pressure measurement, criteria for hypertension diagnosis and follow-up, assessment of global cardiovascular risk, diagnostic testing, diagnosis of renovascular and endocrine causes of hypertension, home and ambulatory monitoring, and the use of echocardiography in hypertensive individuals are outlined. Key messages in 2008 include continued emphasis on the expedited, accurate diagnosis of hypertension, the importance of global risk assessment and the need for ongoing monitoring of hypertensive patients to identify incident type 2 diabetes. All recommendations were graded according to strength of the evidence and voted on by the 57 members of the Canadian Hypertension Education Program Evidence-Based Recommendations Task Force. All recommendations reported here received at least 70% consensus. These guidelines will continue to be updated annually.