Search

BACKGROUND Left ventricular hypertrophy (LVH) and vitamin D deficiency have been linked to hypertension (HTN) and cardiovascular disease, particularly in African Americans (AAs). Our objective was to determine if the addition of vitamin D to antihypertensive therapy would lead to greater regression of LV mass index (LVMI) as determined by cardiac magnetic resonance (CMR) after 1 year in vitamin D deficient AA patients with uncontrolled HTN and LVH. METHODS This study was a randomized, double-blind, placebo-controlled, single-center study. AA patients with HTN (systolic blood pressure [BP] >160 mm Hg), increased LVMI, and vitamin D deficiency ( RESULTS At 1 year, there were no statistical differences between the vitamin D and placebo groups in LVMI (−14.1 ± 14.6 vs. −16.9 ± 13.1 g/m2; P = 0.34) or systolic BP (−25.6 ± 32.1 vs. −25.7 ± 25.6 mm Hg; P = 0.99) reduction, respectively. Serum vitamin D levels increased significantly in the vitamin D group compared with placebo (12.7 ± 2.0 vs. 1.8 ± 8.2 ng/ml; P < 0.001). CONCLUSIONS In this high-risk cohort of AAs we did not find an association between vitamin D supplementation and differential regression of LVMI or reduction in systolic BP. However, our study suffered from a small sample size with low statistical power precluding a definitive conclusion on the therapeutic benefit of vitamin D in such patients. CLINICAL TRIALS REGISTRATION Trial Number NCT01360476. Full trial protocol is available from corresponding author.

Background Previous studies have reported that lean hypertensives have worse clinical outcomes than obese hypertensives as obesity confers pharmacological resistance to antihypertensive therapy. We explored whether the higher prescribed doses of antihypertensives in obese hypertensives were adequate for the attainment of similar on-treatment blood pressure (BP) versus leaner hypertensives. Methods A retrospective chart review of predominantly African American females from a deidentified urban referral clinic was conducted (N = 851; median follow-up = 11.3 months). Body mass index (BMI, kg/m2) was categorized as either below or above or equal to 30. Antihypertensive therapeutic intensity score (TIS) was calculated as the total daily antihypertensive dose/maximum United States Food and Drug Administration (USFDA) approved daily dose, summed across all hypertensive drugs. General linear models were used to estimate the significance of continuous variables across BMI categories. Results At baseline, systolic blood pressure (SBP) was similar between groups (P = 0.14), though 2.7 mm Hg higher in the highest BMI group. Antihypertensive TIS was greater in the highest BMI category at both baseline and end of follow-up (both P < 0.001). After covariate adjustment end of follow-up SBP and diastolic blood pressure was higher in the obese group by 3.4 (0.6–6.1) and 1.8 (0.1–3.53) mm Hg, respectively (P = 0.02, P = 0.04). Conclusions Attained on-treatment BP is higher in obese than non-obese hypertensives despite greater prescription of antihypertensive medications. Whether even more prescription of medications or other interventions will equalize BP responses relative to non obese hypertensives merits further study.

Disordered iron and mineral homeostasis are interrelated complications of chronic kidney disease that may influence cardiovascular and kidney outcomes. In a prospective analysis of 3747 participants in the Chronic Renal Insufficiency Cohort Study, we investigated risks of mortality, heart failure, end-stage kidney disease (ESKD), and atherosclerotic cardiovascular disease according to iron status, and tested for mediation by C-terminal fibroblast growth factor 23 (FGF23), hemoglobin and parathyroid hormone. Study participants were agnostically categorized based on quartiles of transferrin saturation and ferritin as: “Iron Replete” (27.1% of participants; referent group for all outcomes analyses), “Iron Deficiency” (11.1%), “Functional Iron Deficiency” (7.6%), “Mixed Iron Deficiency” (iron indices between the Iron Deficiency and Functional Iron Deficiency groups; 6.3%), “High Iron” (9.2%), or “Non-Classified” (the remaining 38.8% of participants). In multivariable-adjusted Cox models, Iron Deficiency independently associated with mortality (hazard ratio 1.28, 95% confidence interval 1.04–1.58) and heart failure (1.34, 1.05–1.72). Mixed Iron Deficiency associated with mortality (1.61, 1.27–2.04) and ESKD (1.33, 1.02–1.73). High Iron associated with mortality (1.54, 1.24–1.91), heart failure (1.58, 1.21–2.05), and ESKD (1.41, 1.13–1.77). Functional Iron Deficiency did not significantly associate with any outcome, and no iron group significantly associated with atherosclerotic cardiovascular disease. Among the candidate facilitators, FGF23 most significantly mediated the risks of mortality and heart failure conferred by Iron Deficiency. Thus, alterations in iron homeostasis associated with adverse cardiovascular and kidney outcomes in patients with chronic kidney disease.

Angiotensin-converting enzyme inhibitors (ACEi) are part of the indicated treatment in hypertensive African Americans. ACEi have blood pressure-independent effects that may make them preferred for certain patients. We aimed to evaluate the impact of ACEi on anti-fibrotic biomarkers in African American hypertensive patients with left ventricular hypertrophy (LVH). We conducted a post hoc analysis of a randomized controlled trial in which hypertensive African American patients with LVH and vitamin D deficiency were randomized to receive intensive antihypertensive therapy plus vitamin D supplementation or placebo. We selected patients who had detectable lisinopril (lisinopril group) in plasma using liquid-chromatography/mass spectrometry analysis and compared them to subjects who did not (comparison group) at the one-year follow-up. The pro-fibrotic marker type 1 procollagen C-terminal propeptide (PICP) and the anti-fibrotic markers matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), telopeptide of collagen type I (CITP), and N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) peptide were measured. Sixty-six patients were included, and the mean age was 46.2 ± 8 years. No difference was observed in the number and intensity of antihypertensive medications prescribed in each group. Patients with detectable lisinopril had lower blood pressure than those in the comparison group. The anti-fibrotic markers Ac-SDKP, MMP-1, and MMP-1/TIMP-1 ratio were higher in patients with detectable ACEi (all p < .05). In a model adjusted for systolic blood pressure, MMP-1/TIMP-1 (p = .02) and Ac-SDKP (p < .001) levels were associated with lisinopril. We conclude that ACEi increase anti-fibrotic biomarkers in hypertensive African Americans with LVH, suggesting that they may offer added benefit over other agents in such patients.

Mechanical circulatory support with durable continuous-flow ventricular assist devices has become an important therapeutic management strategy for patients with advanced heart failure. As more patients have received these devices and the duration of support per patient has increased, the postimplantation complications have become more apparent, and the need for approaches to manage these complications has become more compelling. Continuous-flow ventricular assist devices, including axial-flow and centrifugal-flow pumps, are the most commonly used mechanical circulatory support devices. Continuous-flow ventricular assist devices and the native heart have a constant physiological interplay dependent on pump speed that affects pressure-flow relationships and patient hemodynamics. A major postimplantation complication is cerebrovascular vascular accidents. The causes of cerebrovascular vascular accidents in ventricular assist device recipients may be related to hypertension, thromboembolic events, bleeding from anticoagulation, or some combination of these. The most readily identifiable and preventable cause is hypertension. Hypertension management in these patients has been hampered by the fact that it is difficult to accurately measure blood pressure because these ventricular assist devices have continuous flow and are often not pulsatile. Mean arterial pressures have to be identified by Doppler or oscillometric cuff and treated. Although guidelines for hypertension management after ventricular assist device implantation are based largely on expert consensus and conventional wisdom, the mainstay of treatment for hypertension includes guideline-directed medical therapy for heart failure with reduced ejection fraction because this may reduce adverse effects associated with hypertension and increase the likelihood of favorable ventricular remodeling. The use of systemic anticoagulation in ventricular assist device recipients may at a given blood pressure increase the risk of stroke.

Heart disease is a leading cause of death for African Americans. A community-academic partnership cross-trained community health workers to engage African American adults in a 6-month heart health education and risk reduction intervention. We conducted a one-group feasibility study using a one group (pre-posttest) design. A total of 100 adults were recruited from 27 zip codes in an African American majority city through community-based organizations (46%), churches (36%), and home visits (12%). Ninety-six percent were African American; 55% were female, 39% were male, and 6% were transgender. Their mean age was 44.6 years (SD = 15.9). Ninety-two percent had health insurance. Seventy-six percent of participants averaged blood pressure (BP) readings > 130/80 mmHg. Eleven percent of participants had a 30% or higher probability of developing cardiovascular disease in the next 10 years. Six-month follow-up was completed with 96% of participants. There were statistically significant increases in knowledge and in perception of personal risk for heart disease. However, slightly more participants (n = 77, 80.2%) had BP > 130/80 mmHg. The Community Advisory Group recommended expanding the intervention to 12 months and incorporating telehealth with home BP monitoring. Limited intervention duration did not meet longer term objectives such as better control of high BP and sharing risk reduction planning with primary care providers.

BACKGROUND Intensively treated participants in the SPRINT study experienced fewer primary cardiovascular composite study endpoints (CVD events) and lower mortality, although 38% of participants experienced a serious adverse event (SAE). The relationship of SAEs with CVD events is unknown. METHODS CVD events were defined as either myocardial infarction, acute coronary syndrome, decompensated heart failure, stroke, or death from cardiovascular causes. Cox models were utilized to understand the occurrence of SAEs with CVD events according to baseline atherosclerotic cardiovascular disease (ASCVD) risk. RESULTS SAEs occurred in 96% of those experiencing a CVD event but only in 34% (P < 0.001) of those not experiencing a CVD event. Occurrence of SAEs monotonically increased across the range of baseline ASCVD risk being approximately twice as great in the highest compared with the lowest risk category. SAE occurrence was strongly associated with ASCVD risk but was similar within risk groups across treatment arms. In adjusted Cox models, experiencing a CVD event was the strongest predictor of SAEs in all risk groups. By the end of year 1, the hazard ratios for the low, middle, and high ASCVD risk tertiles, and baseline clinical CVD group were 2.56 (95% CI = 1.39–4.71); 2.52 (1.63–3.89); 3.61 (2.79–4.68); 1.86 (1.37–2.54), respectively—a trend observed in subsequent years until study end. Intensive treatment independently predicted SAEs only in the second ASVCD risk tertile. CONCLUSIONS The occurrence of SAEs is multifactorial and mostly related to prerandomization patient characteristics, most prominently ASCVD risk, which, in turn, relates to in-study CVD events.

Contains fulltext : 286841.pdf (Publisher’s version ) (Closed access) BACKGROUND: Resistant hypertension is associated with increased cardiovascular risk. The endothelin pathway has been implicated in the pathogenesis of hypertension, but it is currently not targeted therapeutically, thereby leaving this relevant pathophysiological pathway unopposed with currently available drugs. The aim of the study was to assess the blood pressure lowering efficacy of the dual endothelin antagonist aprocitentan in patients with resistant hypertension. METHODS: PRECISION was a multicentre, blinded, randomised, parallel-group, phase 3 study, which was done in hospitals or research centres in Europe, North America, Asia, and Australia. Patients were eligible for randomisation if their sitting systolic blood pressure was 140 mm Hg or higher despite taking standardised background therapy consisting of three antihypertensive drugs, including a diuretic. The study consisted of three sequential parts: part 1 was the 4-week double-blind, randomised, and placebo-controlled part, in which patients received aprocitentan 12·5 mg, aprocitentan 25 mg, or placebo in a 1:1:1 ratio; part 2 was a 32-week single (patient)-blind part, in which all patients received aprocitentan 25 mg; and part 3 was a 12-week double-blind, randomised, and placebo-controlled withdrawal part, in which patients were re-randomised to aprocitentan 25 mg or placebo in a 1:1 ratio. The primary and key secondary endpoints were changes in unattended office systolic blood pressure from baseline to week 4 and from withdrawal baseline to week 40, respectively. Secondary endpoints included 24-h ambulatory blood pressure changes. The study is registered on ClinicalTrials.gov, NCT03541174. FINDINGS: The PRECISION study was done from June 18, 2018, to April 25, 2022. 1965 individuals were screened and 730 were randomly assigned. Of these 730 patients, 704 (96%) completed part 1 of the study; of these, 613 (87%) completed part 2 and, of these, 577 (94%) completed part 3 of the study. The least square mean (SE) change in office systolic blood pressure at 4 weeks was -15·3 (SE 0·9) mm Hg for aprocitentan 12·5 mg, -15·2 (0·9) mm Hg for aprocitentan 25 mg, and -11·5 (0·9) mm Hg for placebo, for a difference versus placebo of -3·8 (1·3) mm Hg (97·5% CI -6·8 to -0·8, p=0·0042) and -3·7 (1·3) mm Hg (-6·7 to -0·8; p=0·0046), respectively. The respective difference for 24 h ambulatory systolic blood pressure was -4·2 mm Hg (95% CI -6·2 to -2·1) and -5·9 mm Hg (-7·9 to -3·8). After 4 weeks of withdrawal, office systolic blood pressure significantly increased with placebo versus aprocitentan (5·8 mm Hg, 95% CI 3·7 to 7·9, p

BACKGROUND Vascular calcification contributes to cardiovascular disease (CVD) and mortality in individuals with chronic kidney disease (CKD). Vitamin K-dependent proteins function as calcification inhibitors in vascular tissue. OBJECTIVE We sought to determine the association of vitamin K status with mortality and CVD events in adults with CKD. DESIGN Plasma dephospho-uncarboxylated matrix gla protein ((dp)ucMGP), which increases when vitamin K status is low, and plasma phylloquinone (vitamin K1), which decreases when vitamin K status is low, were measured in 3066 Chronic Renal Insufficiency Cohort participants (median age = 61 years, 45% female, 41% non-Hispanic Black, median eGFR = 41 mL/min/1.73m2). The association of vitamin K status biomarkers with all-cause mortality and atherosclerotic-related CVD was determined using multivariable Cox proportional hazards regression. RESULTS There were 1122 deaths and 599 atherosclerotic CVD events over the median 12.8 follow-up years. All-cause mortality risk was 21-29% lower among participants with plasma (dp)ucMGP

Background: The landmark Systolic Blood Pressure Intervention Trial (SPRINT) showed that more intensive systolic blood pressure treatment (SBP < 120 mm Hg) was associated with lower risk for cardiovascular events and mortality but higher risk for serious adverse events (SAEs). However, it is unclear if the magnitude and/or the direction of the BP change determines SAE risk. In this study, we aim to determine how the magnitude and direction of BP change impacts SAE risk. Methods: This is a secondary analysis of 7922 participants in SPRINT. Time-varying Cox proportional hazards models were used to explore the relationship between visit-to-visit BP change and SAE risk. BP change was categorized using five intervals: 1) decreases ≥30 mm Hg, 2) decreases 10-29 mm Hg, 3) increases or decreases Results: The hazard ratio (HR) for SAEs compared to the minimal BP change category was greatest for BP increases above 30 mm Hg (HR = 1.62, 95% confidence interval [1.30, 2.01]). However, the HR was similar for sharp BP decreases over 30 mm Hg (HR = 1.52 [1.23, 1.87]). Milder BP increases and decreases were associated with lower SAE risk (HR = 1.18 [1.06, 1.32] and HR = 1.10 [0.98, 1.22] for BP changes 10 to 30 mm Hg and -30 to -10 mm Hg, respectively). There were no significant interactions between BP change, intensive treatment, and baseline ASCVD risk. Conclusions: SAE risk was similar for similarly sized increases and decreases in BP between visits, with higher magnitude changes associated with higher SAE risk. When accounting for the magnitude of BP change, no significant effect of intensive treatment or baseline ASCVD risk was found.

A quantitative survey was completed by 103 primary care physicians (PCPs) and 59 cardiologists who regularly prescribed β-blockers to assess knowledge and use of this heterogeneous drug class for hypertension. More cardiologists than PCPs chose β-blockers as initial antihypertensive therapy (30% vs 17%, P < 0.01). Metoprolol and carvedilol were the most commonly prescribed β-blockers. Cardiologists rated "impact on energy" and "arterial vasodilation" as more important than PCPs (P < 0.05/

Background: Refractory hypertension can be defined as uncontrolled blood pressure (BP at or above 140/90 mmHg) when taking five or more classes of antihypertensive medication, including a diuretic for patients with chronic kidney disease. The prognosis for patients with refractory hypertension is not understood. Methods: Refractory hypertension was assessed in the Chronic Renal Insufficiency Cohort (CRIC). A total of 3314 treated hypertensive patients were included, and patients were assigned a hypertensive phenotype (i.e., refractory hypertension, apparent treatment resistant hypertension [aTRH], hypertension) based on their baseline visit. Cox proportional hazards models were used to analyze differences in outcome risk across hypertensive phenotypes after controlling for age, race, diabetes, smoking, BMI, urine protein, eGFR, systolic blood pressure, education, and study site. Results: Refractory hypertension was found in 4.5% (149/3314) of treated hypertensive patients. When compared with those with aTRH, patients with refractory hypertension were significantly more likely to experience renal events - composite of end-stage renal disease and/or 50% drop in eGFR (hazard ratio [95% confidence interval], 1.64 [1.29, 2.09]); and cardiovascular events - composite of myocardial infarction, stroke, peripheral arterial disease, and congestive heart failure (1.34 [1.04, 1.73]); but showed no significant difference in all-cause mortality risk (1.06 [0.80, 1.41]). Conclusions: Refractory hypertension increases the risk for renal and cardiovascular disease over that previously observed for aTRH in patients with chronic kidney disease.

Background: SPRINT was the first large-scale trial to investigate the benefits of intensive versus standard blood pressure treatment (goal of Methods: SAEs were predicted using multivariable cox models. The variables were CVD composite (the original SPRINT primary outcome, included in this analyses to capture the effect of having a study event), treatment (intensive or standard), albumin (normal, micro, macro), BMI ( Results: In all groups, including the in-study CVD composite primary endpoint improved the harrell’s C-index of model fit. In the multivariable models, CVD composite was a predictor of SAEs in ASCVD tertiles (T1, T2, T3) and the clinical CVD group (Hazard Ratio [HR] 5.01 CI 3.86-6.51; HR 5.10 CI 4.23-6.28; HR 4.40 CI 3.79-5.10; and HR 3.67 CI 3.18-4.23, respectively). Kidney function as measured by eGFR Conclusions: These analyses demonstrated that experiencing the primary composite CVD endpoint was the strongest predictor of SAEs in all groups and that intensive treatment was a modest, infrequent predictor of SAEs.

Objectives Refractory hypertension has been defined as uncontrolled blood pressure (at or above 140/90 mmHg) when on five or more classes of antihypertensive medication, inclusive of a diuretic. Because unbiased estimates of the prevalence of refractory hypertension in the United States are lacking, we aim to provide such estimates using data from the National Health and Nutrition Examination Surveys (NHANES). Methods Refractory hypertension was assessed across multiple NHANES cycles using the aforementioned definition. Eight cycles of NHANES surveys (1999-2014) representing 41 552 patients are the subject of this study. Prevalence of refractory hypertension across these surveys was estimated in the drug-treated hypertensive population after adjusting for the complex survey design and standardizing for age. Results Across all surveys, refractory hypertension prevalence was 0.6% [95% confidence interval (CI) (0.5, 0.7)] amongst drug-treated hypertensive adults; 6.2% [95% CI (5.1, 7.6)] of individuals with treatment-resistant hypertension actually had refractory hypertension. Although the prevalence of refractory hypertension ranged from 0.3% [95% CI (0.1, 1.0)] to 0.9% [95% CI (0.6, 1.2)] over the eight cycles considered, there was no significant trend in prevalence over time. Refractory hypertension prevalence amongst those prescribed five or more drugs was 34.5% [95% CI (27.9, 41.9)]. Refractory hypertension was associated with advancing age, lower household income, black race, and also chronic kidney disease, albuminuria, diabetes, prior stroke, and coronary heart disease. Conclusions We provided the first nationally representative estimate of refractory hypertension prevalence in US adults.

The ACC/AHA hypertension guidelines cover virtually all aspects of the diagnosis, evaluation, monitoring, secondary causes as well as drug and non-drug treatment of hypertension. Substantial and appropriate emphasis has been given to the strategies necessary for accurate measurement of blood pressure in any setting where valid blood pressure measurements are desired. Most "errors" made during blood pressure measurement bias readings upwards resulting in over-diagnosis of hypertension and, amongst those already on drug therapy, underestimating the true magnitude of blood pressure lowering resulting in over-treatment. Hypertension is diagnosed when blood pressure is consistently ≥130 and/or ≥80 mm Hg. However, the majority of patients with hypertension between 130-139/80-89 mm Hg (stage 1 hypertension) do not qualify for immediate drug therapy. The guideline breaks new ground with some of its recommendations. Absolute cardiovascular risk is utilized, for the first time, to determine high-risk status when BP 130-139/80-89 mm Hg (Stage 1 hypertension) and high-risk patient characteristics/co-morbidities are absent including age 65 and older, diabetes, chronic kidney disease, known cardiovascular disease; high-risk individuals initiate drug therapy when BP ≥ 130/80 mm Hg. The exception amongst high-risk individuals is for secondary stroke prevention in drug naïve individuals as drug therapy is initiated when blood pressure ≥140/90 mm Hg. Non-high risk individuals will initiate drug therapy when BP is ≥140/90 mm Hg. Irrespective of blood pressure threshold for initiation of drug therapy, the target BP is minimally130/80 mm Hg in most. However, target BP is130 systolic amongst those 65 and older as the committee made no recommendation for a DBP target. Treatment should be initiated with two drugs having complementary mechanisms of action when blood pressure is20/10 mm Hg above goal.

The “totality” of hypertension clinical trial endpoint data has shown that the absolute benefit of pharmacological blood pressure (BP) lowering is directly related to the BP level and baseline cardiovascular risk, albeit with attenuation of the relative risk reduction per unit of BP lowering in patients with diabetes and chronic kidney disease. Absolute risk reductions with pharmacological treatment are greater with advancing age. Cardiovascular risk and mortality reductions attributable to pharmacological BP lowering have been demonstrated for progressively lower BP levels extending well below the conventional BP threshold (140/90mm Hg) for hypertension. Hypertension endpoint trials have shifted from determining the relative clinical benefits of various antihypertensive drugs to exploring whether lower than conventional BP targets in persons with BP levels spanning the prehypertensive to much higher BP strata confer clinical benefit. The more recent of these trials were “relatively” agnostic to the drugs used for BP lowering although several trials provided, but did not mandate the use of, specific agents. Pharmacological treatment benefit has been demonstrated at pretreatment BP levels even lower than the intensive SPRINT BP target (

The National, Heart, Lung, and Blood Institute convened a Think Tank meeting to obtain insight and recommendations regarding the objectives and design of the next generation of research aimed at reducing health inequities in the United States. The panel recommended several specific actions, including: 1) embrace broad and inclusive research themes; 2) develop research platforms that optimize the ability to conduct informative and innovative research, and promote systems science approaches; 3) develop networks of collaborators and stakeholders, and launch transformative studies that can serve as benchmarks; 4) optimize the use of new data sources, platforms, and natural experiments; and 5) develop unique transdisciplinary training programs to build research capacity. Confronting health inequities will require engaging multiple disciplines and sectors (including communities), using systems science, and intervening through combinations of individual, family, provider, health system, and community-targeted approaches. Details of the panel's remarks and recommendations are provided in this report.

Pulmonary hypertension (PH) is associated with poor outcomes in the dialysis and general populations, but its effect in CKD is unclear. We evaluated the prevalence and predictors of PH measures and their associations with long–term clinical outcomes in patients with nondialysis-dependent CKD. Chronic Renal Insufficiency Cohort (CRIC) Study participants who had Doppler echocardiography performed were considered for inclusion. PH was defined as the presence of estimated pulmonary artery systolic pressure (PASP) >35 mmHg and/or tricuspid regurgitant velocity (TRV) >2.5 m/s. Associations between PH, PASP, and TRV and cardiovascular events, renal events, and all-cause mortality were examined using Cox proportional hazards models. Of 2959 eligible participants, 21% (n=625) had PH, with higher rates among those with lower levels of kidney function. In the multivariate model, older age, anemia, lower left ventricular ejection fraction, and presence of left ventricular hypertrophy were associated with greater odds of having PH. After adjusting for relevant confounding variables, PH was independently associated with higher risk for death (hazard ratio, 1.38; 95% confidence interval, 1.10 to 1.72) and cardiovascular events (hazard ratio, 1.23; 95% confidence interval, 1.00 to 1.52) but not renal events. Similarly, TRV and PASP were associated with death and cardiovascular events but not renal events. In this study of patients with CKD and preserved left ventricular systolic function, we report a high prevalence of PH. PH and higher TRV and PASP (echocardiographic measures of PH) are associated with adverse outcomes in CKD. Future studies may explain the mechanisms that underlie these findings.

The association between apparent treatment resistant hypertension (ATRH) and clinical outcomes is not well studied in chronic kidney disease. We analyzed data on 3367 hypertensive participants in the Chronic Renal Insufficiency Cohort (CRIC) to determine prevalence, associations, and clinical outcomes of ATRH in nondialysis chronic kidney disease patients. ATRH was defined as blood pressure ≥140/90 mm Hg on ≥3 antihypertensives, or use of ≥4 antihypertensives with blood pressure at goal at baseline visit. Prevalence of ATRH was 40.4%. Older age, male sex, black race, diabetes mellitus, and higher body mass index were independently associated with higher odds of having ATRH. Participants with ATRH had a higher risk of clinical events than participants without ATRH—composite of myocardial infarction, stroke, peripheral arterial disease, congestive heart failure (CHF), and all-cause mortality (hazard ratio [95% confidence interval], 1.38 [1.22–1.56]); renal events (1.28 [1.11–1.46]); CHF (1.66 [1.38–2.00]); and all-cause mortality (1.24 [1.06–1.45]). The subset of participants with ATRH and blood pressure at goal on ≥4 medications also had higher risk for composite of myocardial infarction, stroke, peripheral arterial disease, CHF, and all-cause mortality (hazard ratio [95% confidence interval], (1.30 [1.12–1.51]) and CHF (1.59 [1.28–1.99]) than those without ATRH. ATRH was associated with significantly higher risk for CHF and renal events only among those with estimated glomerular filtration rate ≥30 mL/min per 1.73 m 2 . Our findings show that ATRH is common and associated with high risk of adverse outcomes in a cohort of patients with chronic kidney disease. This underscores the need for early identification and management of patients with ATRH and chronic kidney disease.

Background Obstructive sleep apnea (OSA) is associated with activation of the sympathetic nervous system, and patients with this condition often experience elevated blood pressure (BP), increased BP variability, and nocturnal BP surges. Methods and results The SYMPLICITY HTN-3 trial was a large prospective, randomized, blinded, sham-controlled trial of renal denervation for treatment of uncontrolled, apparently treatment-resistant hypertension. In a post hoc analysis, we examined the effect of renal denervation vs. sham control on office and ambulatory (including nocturnal) systolic BP in patients with and without OSA. 26% (94/364) of renal denervation subjects and 32% (54/171) of sham control subjects had OSA. Baseline office and nighttime systolic BP values were similar in both arms, including in subjects with and without OSA. Compared with sham control, renal denervation reduced the 6-month office systolic BP in subjects with (-17.0±22.4 vs. -6.3±26.1 mmHg, P=0.01) but not in subjects without OSA (-14.7±24.5 vs. -13.4±26.4 mmHg, P=0.64), P=0.07 for the interaction between treatment arm and OSA status. In those with sleep apnea, renal denervation was also associated with a reduction in maximum (-4.8±21.8 vs. 4.5±24.6 mmHg, P=0.03) and average peak (-5.6±20.4 vs. 3.2±22.4 mmHg, P=0.02) nighttime systolic BP. Conclusions OSA subjects appeared to be responsive to renal denervation therapy. However, this hypothesis requires prospective testing. (Circ J 2016; 80: 1404-1412).

ACEi are first line treatment in hypertension; however, there is controversy regarding the benefit over other antihypertensive drugs. ACEi have pressure independent effects that may make them preferable for certain patients. We aimed to evaluate the impact of ACEi on antifibrotic biomarkers in hypertensive patients with left ventricular hypertrophy (LVH). We conducted a post hoc analysis of a randomized controlled trial where hypertensive African American patients with LVH and vitamin D (VTD) deficiency were randomized to receive standard antihypertensive therapy plus VTD supplementation or placebo. We selected patients who had detectable lisinopril in plasma at one year follow-up and compared them to subjects who did not. The profibrotic marker propeptide of procollagen type I (CPIP) and the antifibrotic markers: matrix metalloproteinase-1 (MMP-1), tissue inhibitor of MMP1 (TIMP-1), the MMP-1/TIMP-1 ratio, telopeptide of collagen type I (CITP) and Ac-SDKP peptide were measured. Sixty six patients were included. Table 1 shows patients characteristics. Patients with lisinopril had lower blood pressure at one-year but no differences were observed in left ventricular mass index (LVMI). The antifibrotic markers Ac-SDKP (3.9±2.6 vs 6.3±2.8; p

Background: Refractory hypertension is defined as uncontrolled blood pressure (BP) when taking five or more classes of antihypertensive medication, including a thiazide or thiazide-like diuretic and a mineralocorticoid receptor antagonist. Refractory hypertension represents a potential extreme along the spectrum of hypertension phenotypes. However, due to the rarity and recent definition of refractory hypertension, relatively little is known about quantifying risk of this phenotype. Methods: Refractory hypertension was retrospectively assessed in patients seen at an urban referral hypertension clinic using a BP goal of 140/90 mmHg. Patients with advanced chronic kidney disease (eGFR < 30) were excluded, and the 1179 included patients had at least one follow-up visit in a window 28 to 240 days after their index visit. Patients were mostly African-American (86%; 1018/1179) and female (65%; 766/1179). Risk for refractory hypertension was estimated using logistic regression with patient characteristics at index visit as predictors (i.e., age, BMI, eGFR, number of adequately dosed antihypertensive medication classes taken at the index visit, BP above goal, diabetes, gender, race, and smoking status). Performance of this risk score at discriminating refractory hypertension over follow-up was assessed using AUC and was internally validated using bootstrapping. Results: Only 25/1179 (2.1%) developed refractory hypertension. Old age, higher BMI, more antihypertensive medication classes taken at index visit, higher BP, and diabetes were all associated with increased refractory hypertension risk. The risk score discriminated well (AUC = 0.88, bootstrapped 95% CI [0.82, 0.92]). In our patient population, 683/1179 (57.9%) had estimated risks for development of refractory hypertension < 1%. Of these low-risk patients, 682/683 (99.9%) failed to develop refractory hypertension (negative predictive value, 0.997 [0.99, 1.00]). Conclusions: We created a novel clinical score that discriminates well between those who will and will not develop refractory hypertension and that is particularly useful at identifying patients with little to no risk of refractory hypertension.

Background: Refractory hypertension has been defined as uncontrolled blood pressure (BP at or above 140/90 mmHg) when taking five or more classes of antihypertensive medication. Unbiased estimates of the prevalence of refractory hypertension in the United States are lacking. Methods: Refractory hypertension was assessed in the National Health and Nutrition Examination Survey. Eight cycles of NHANES surveys (1999-2014) representing 41,552 patients were included. Patients younger than 18 and who were pregnant were excluded. Prevalence of refractory hypertension was estimated in the hypertensive population (systolic BP ≥140 or diastolic BP ≥90 or taking an antihypertensive medication) after adjusting for the complex survey design and standardizing for age. Logistic regression was used to test for temporal trends and to compare prevalence across age classes (18-39, 40-59, 60+), genders, races, and chronic kidney disease status. Results: Refractory hypertension was found in 0.30% of all hypertensive individuals. Although prevalence of refractory hypertension peaked at 0.54% of hypertensive individuals in the 2005-2006 cycle, there was no significant trend in prevalence through time (p = 0.29). No individuals under 40 years old were observed with refractory hypertension, and refractory hypertension was more common in individuals 60 and older than in individuals 40-60 years old (odds ratio = 4.55, p = 0.004). There was no difference in the prevalence of refractory hypertension between males and females (p = 0.24), but white and black individuals were more likely to have refractory hypertension than individuals of Hispanic or other descent (OR = 4.63, p = 0.002). Finally, individuals with chronic kidney disease were significantly more likely to have refractory hypertension (OR = 9.88, p < 0.001). Conclusions: We provided the first nationally representative estimate of the prevalence of refractory hypertension in the U.S. Recently lowered BP targets, an aging population, and increased incidence of co-morbidities like chronic kidney disease all create the potential for increases in this hypertensive phenotype in the future.

Apparent treatment-resistant hypertension (aTRH) is associated with higher prevalence of secondary hypertension, greater risk for adverse pressure-related clinical outcomes, and influences diagnostic and therapeutic decision-making. We previously showed that cross-sectional prevalence estimates of aTRH are lower than its true prevalence as patients with uncontrolled hypertension undergoing intensification/optimization of therapy will, over time, increasingly satisfy diagnostic criteria for aTRH. aTRH was assessed in an urban referral hypertension clinic using a 140/90 mm Hg goal blood pressure target in 745 patients with uncontrolled blood pressure, who were predominately African-American (86%) and female (65%). Analyses were stratified according to existing prescription of diuretic at initial visit. Risk for aTRH was estimated using logistic regression with patient characteristics at index visit as predictors. Among those prescribed diuretics, 84/363 developed aTRH; the risk score discriminated well (area under the receiver operating curve = 0.77, bootstrapped 95% CI [0.71, 0.81]). In patients not prescribed a diuretic, 44/382 developed aTRH, and the risk score showed a significantly better discriminative ability (area under the receiver operating curve = 0.82 [0.76, 0.87]; P .001). In the diuretic and nondiuretic cohorts, 145/363 and 290/382 of patients had estimated risks for development of aTRH15%. Of these low-risk patients, 139/145 and 278/290 did not develop aTRH (negative predictive value, diuretics - 0.94 [0.91, 0.98], no diuretics - 0.95 [0.93, 0.97]). We created a novel clinical score that discriminates well between those who will and will not develop aTRH, especially among those without existing diuretic prescriptions. Irrespective of baseline diuretic treatment status, a low-risk score had very high negative predictive value.

Objectives: This study was conducted to examine perceptions, knowledge, and rationale for prescribing β-blockers among physicians who treat patients with hypertension. Methods: In August/September 2016, 103 primary care physicians (PCPs) and 59 cardiologists participated in a 20-minute quantitative, online survey regarding their use and perceptions of β-blockers. Significant between-group differences were examined via t-tests and z-tests. Results: Significantly more cardiologists chose β-blockers as first-line therapy than PCPs (30% vs 17%, P P P P 1 -selectivity; efficacy in patients aged >60 years; efficacy in African-American patients; and arterial vasodilation. Metoprolol was closely associated with heart rate reduction, and atenolol was associated with heart rate reduction, fatigue, erectile dysfunction, and impact on mood. Physicians had a positive response to using drugs other than metoprolol or atenolol that could lower the risk of new onset diabetes for pre-diabetic or obese patients. Clinical practice guidelines influenced prescribing behaviors more than formulary or performance metrics; continuing medical education and publications were commonly accessed materials for hypertension education. Conclusions: This survey highlights several educational gaps, including differences between PCPs and cardiologists, on the perceptions of β-blockers for hypertension treatment. Future efforts should include physician education on relevant evidence-based differences between β-blockers, given their heterogeneity.

SYMPLICITY HTN-3, the first trial of renal denervation (RDN) versus sham, enrolled 26% African Americans, a prospectively stratified cohort. Although the 6-month systolic blood pressure (SBP) reduction in African Americans (AAs) was similar in the RDN group (-15.5 ± 25.4 mm Hg, n = 85 vs. -17.8 ± 29.2, n = 49, P = .641), the sham SBP response was 9.2 mm Hg greater (P = .057) in AAs than non-AAs. In multivariate analyses, sham SBP response was predicted by an interaction between AA and a complex antihypertensive regimen (at least one antihypertensive medication prescribed ≥3 times daily), while in the RDN group, SBP response was predicted by an interaction between AA race and baseline BP ≥ 180 mm Hg. AA race did not independently predict SBP response in either sham or RDN. There appears to be effect modification by race with individual-level patient characteristics in both treatment arms that affect the observed pattern of SBP responses.

Objectives The objective is of the study to evaluate the effect of antihypertensive therapy in emergency department (ED) patients with markedly elevated blood pressure (BP) but no signs/symptoms of acute target organ damage (TOD). Methods This is a retrospective cohort study of ED patients age 18 years and older with an initial BP greater than or equal to 180/100 mm Hg and no acute TOD, who were discharged with a primary diagnosis of hypertension. Patients were divided based on receipt of antihypertensive therapy and outcomes (ED revisits and mortality) and were compared. Results Of 1016 patients, 435 (42.8%) received antihypertensive therapy, primarily (88.5%) oral clonidine. Average age was 49.2 years, and 94.5% were African American. Treated patients more often had a history of hypertension (93.1% vs 84.3%; difference = − 8.8; 95% confidence interval [CI], − 12.5 to − 4.9) and had higher mean initial systolic (202 vs 185 mm Hg; difference = 16.9; 95% CI, − 19.7 to − 14.1) and diastolic (115 vs 106 mm Hg; difference = − 8.6; 95% CI, − 10.3 to − 6.9) BP. Emergency department revisits at 24 hours (4.4% vs 2.4%; difference = − 2.0; 95% CI, − 4.5 to 0.3) and 30 days (18.9% vs 15.2%; difference = − 3.7; 95% CI, − 8.5 to 0.9) and mortality at 30 days (0.2% vs 0.2%; difference = 0; 95% CI, − 1.1 to 0.8) and 1 year (2.1% vs 1.6%; difference = − 0.5; 95% CI, − 2.5 to 1.2) were similar. Conclusions Revisits and mortality were similar for ED patients with markedly elevated BP but no acute TOD, whether they were treated with antihypertensive therapy, suggesting relative safety with either approach.

Background Results of the SYMPLICITY HTN-3 (Renal Denervation in Patients With Uncontrolled Hypertension) trial confirmed the safety but not the efficacy of renal denervation for treatment-resistant hypertension at 6 months post procedure. Objectives This study sought to analyze the 12-month SYMPLICITY HTN-3 results for the original denervation group, the sham subjects who underwent denervation after the 6-month endpoint (crossover group), and the sham subjects who did not undergo denervation after 6 months (non-crossover group). Methods Eligible subjects were randomized 2:1 to denervation or sham procedure. Subjects were unblinded to their treatment group after the 6-month primary endpoint was ascertained; subjects in the sham group meeting eligibility requirements could undergo denervation. Change in blood pressure (BP) at 12 months post randomization (6 months for crossover subjects) was analyzed. Results The 12-month follow-up was available for 319 of 361 denervation subjects and 48 of 101 non-crossover subjects; 6-month denervation follow-up was available for 93 of 101 crossover subjects. In denervation subjects, the 12-month office systolic BP (SBP) change was greater than that observed at 6 months (−15.5 ± 24.1 mm Hg vs. −18.9 ± 25.4 mm Hg, respectively; p = 0.025), but the 24-h SBP change was not significantly different at 12 months (p = 0.229). The non-crossover group office SBP decreased by −32.9 ± 28.1 mm Hg at 6 months, but this response regressed to −21.4 ± 19.9 mm Hg (p = 0.01) at 12 months, increasing to 11.5 ± 29.8 mm Hg. Conclusions These data support no further reduction in office or ambulatory BP after 1-year follow-up. Loss of BP reduction in the non-crossover group may reflect decreased medication adherence or other related factors. (Renal Denervation in Patients With Uncontrolled Hypertension [SYMPLICITY HTN-3]; NCT01418261 )

Background Considerable uncertainty exists as to whether lowering low-density lipoprotein cholesterol (LDL-C) by inhibiting the Niemann-Pick C1-Like 1 (NPC1L1) receptor with ezetimibe, either alone or in combination with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) inhibitor (statin), will reduce the risk of coronary heart disease (CHD). Objectives This study evaluated the effect of naturally random allocation to lower LDL-C mediated by polymorphisms in the NPC1L1 gene (target of ezetimibe), the HMGCR gene (target of statins), or both (target of combination therapy) on the risk of CHD. Methods We constructed NPC1L1 and HMGCR genetic LDL-C scores to naturally randomize participants into 4 groups: reference, lower LDL-C mediated by NPC1L1 polymorphisms, lower LDL-C mediated by HMGCR polymorphisms, or lower LDL-C mediated by polymorphisms in both NPC1L1 and HMGCR . We compared the risk of CHD (fatal or nonfatal myocardial infarction) among each group using a 2 × 2 factorial mendelian randomization study design. Results A total of 108,376 persons (10,464 CHD events) from 14 studies were included. There were no significant differences in baseline characteristics among the 4 groups, thus confirming that allocation was random. Compared to the reference group, the NPC1L1 group had 2.4 mg/dl lower LDL-C and 4.8% lower risk of CHD (odds ratio [OR]: 0.952, 95% confidence interval [CI]: 0.920 to 0.985); whereas the HMGCR group had 2.9 mg/dl lower LDL-C and a similar 5.3% lower risk of CHD (OR: 0.947, 95% CI: 0.909 to 0.986). The group with lower LDL-C mediated by both NPC1L1 and HMGCR polymorphisms had 5.8 mg/dl additively lower LDL-C and a 10.8% log-linearly additive lower risk of CHD (OR: 0.892, 95% CI: 0.854 to 0.932). Conclusions The effect of lower LDL-C on the risk of CHD mediated by polymorphisms in NPC1L1 , HMGCR, or both is approximately the same per unit lower LDL-C and log-linearly proportional to the absolute exposure to lower LDL-C.

Aims The SYMPLICITY HTN-3 randomized, blinded, sham-controlled trial confirmed the safety of renal denervation (RDN), but did not meet its primary efficacy endpoint. Prior RDN studies have demonstrated significant and durable reductions in blood pressure. This analysis investigated factors that may help explain these disparate results. Methods and results Patients with resistant hypertension were randomized 2 : 1 to RDN ( n = 364) or sham ( n = 171). The primary endpoint was the difference in office systolic blood pressure (SBP) change at 6 months. A multivariable analysis identified predictors of SBP change. Additional analyses examined the influence of medication changes, results in selected subgroups and procedural factors. Between randomization and the 6-month endpoint, 39% of patients underwent medication changes. Predictors of office SBP reduction at 6 months were baseline office SBP ≥180 mmHg, aldosterone antagonist use, and non-use of vasodilators; number of ablations was a predictor in the RDN group. Non-African-American patients receiving RDN had a significantly greater change in office SBP than those receiving sham; –15.2 ± 23.5 vs. –8.6 ± 24.8 mmHg, respectively ( P = 0.012). Greater reductions in office and ambulatory SBP, and heart rate were observed with a higher number of ablations and energy delivery in a four-quadrant pattern. Conclusions Post hoc analyses, although derived from limited patient cohorts, reveal several potential confounding factors that may partially explain the unexpected blood pressure responses in both the sham control and RDN groups. These hypothesis-generating data further inform the design of subsequent research to evaluate the potential role of RDN in the treatment of resistant hypertension. ClinicalTrials.gov identifier NCT01418261.

SPRINT was a well designed and executed randomized clinical trial funded by the National Institutes of Health (NIH) in which 9,361 hypertensive patients at high risk of cardiovascular disease with blood pressure (BP) above 130 mm H g and below 180 mm H g, were randomly assigned to be treated to a goal systolic BP (SBP) of less than 140 vs. less than 120 mm Hg. The trial recruited hypertensive individuals in the United States who were older than 50 years of age and had never had a stroke and were not diabetic, but were either older than 75 years of age (28% of subjects), had chronic kidney disease with estimated glomerular filtration rate (eGFR) 20 m l/min/1.73 m 2 of body surface (28% of subjects), or had clinical or subclinical cardiovascular disease or a Framingham score indicating 10-year risk of >15% of cardiovascular disease. By 1-year post-randomization, the trial achieved SBPs of 121.4 mm H g in the intensive treatment group and 136.2 mm H g in the standard treatment group, a difference that was maintained throughout the trial. SPRINT was stopped early after a median follow-up of 3.26 years because of a 25% relative risk reduction in the intensive treatment group of the primary endpoint (myocardial infarction or other coronary syndromes, stroke, heart failure, or death from cardiovascular causes) and 27% in all-cause mortality. In order to achieve these results, patients in the intensive therapy group took a mean of approximately 3 vs. 2 antihypertensive drugs in the standard therapy group. About 3,000 patients in each group completed 3 years of the trial, a little more than 1,000 completed 4 and slightly less than 300 in each group completed 5 years of the trial. The beneficial results were found across all prespecified groups. However, it is noteworthy that individuals older than 75 years of age appeared to benefit more than younger subjects. Is it possible that these older individuals were “survivors,” who although at high cardiovascular risk, were able to benefit more than the more “mixed” younger group? As well, those subjects who entered the trial with SBP of

Background: Apparent treatment resistant hypertension (aTRH) is associated with increased prevalence of secondary hypertension and adverse pressure-related clinical outcomes. We previously showed that cross-sectional prevalence estimates of aTRH are lower than its true prevalence as patients with uncontrolled hypertension undergoing intensification/optimization of therapy will, over time, increasingly satisfy diagnostic criteria for aTRH. Methods: aTRH (SBP and/or DBP at or above a clinically defined goal BP [140/90, 130/85, 130/80, or 125/75 mmHg] over two consecutive office visits when on ≥ 3 antihypertensive drug classes, including a diuretic; or SBP and DBP below goal when on ≥ 4 drug classes, including a diuretic) was assessed in an urban referral hypertension clinic in 924 patients ≥ 30 years old (57.7 ± 12.6) with at least two follow-up visits over 240 days. Patients were mostly African-American (86%; 795/924) and female (65%; 601/924). A minority (28.7%; 265/924) were taking diuretics at their index visit, and analyses were stratified according to this use. Risk for aTRH was estimated using logistic regression with patient characteristics at index visit as predictors. Performance of this risk score at discriminating aTRH status over follow-up was assessed using AUC and was internally validated using bootstrapping. Results: Amongst those on diuretics, 80/265 (30.2%) developed aTRH; the risk score discriminated well (AUC = 0.79, bootstrapped 95% CI [0.73, 0.84]). In patients not on a diuretic, 151/659 (22.9%) developed aTRH, and the risk score showed moderate, but significantly lower, discriminative ability (AUC = 0.71 [0.66, 0.74]; p < 0.001). In the diuretic and non-diuretic cohorts, 43/265 (16.2%) and 101/265 (38.1%) of patients, respectively, had estimated risks for development of aTRH < 10%. Of these low-risk patients, 42/43 (97.7%) and 97/101 (96.0%) did not develop aTRH (negative predictive value, diuretics – 0.95 [0.93, 1.00], no diuretics – 0.96 [0.91, 1.00]). Conclusions: We created a novel clinical score that discriminates well between those who will and will not develop aTRH, especially amongst those taking diuretics initially. Irrespective of diuretic treatment status, a low risk score had very high negative predictive value.

Background Prior studies of catheter-based renal artery denervation have not systematically performed ambulatory blood pressure monitoring (ABPM) to assess the efficacy of the procedure. Objectives SYMPLICITY HTN-3 (Renal Denervation in Patients With Uncontrolled Hypertension) was a prospective, blinded, randomized, sham-controlled trial. The current analysis details the effect of renal denervation or a sham procedure on ABPM measurements 6 months post-randomization. Methods Patients with resistant hypertension were randomized 2:1 to renal denervation or sham control. Patients were on a stable antihypertensive regimen including maximally tolerated doses of at least 3 drugs including a diuretic before randomization. The powered secondary efficacy endpoint was a change in mean 24-h ambulatory systolic blood pressure (SBP). Nondipper to dipper (nighttime blood pressure [BP] 10% to 20% lower than daytime BP) conversion was calculated at 6 months. Results The 24-h ambulatory SBP changed −6.8 ± 15.1 mm Hg in the denervation group and −4.8 ± 17.3 mm Hg in the sham group: difference of −2.0 mm Hg (95% confidence interval [CI]: −5.0 to 1.1; p = 0.98 with a 2 mm Hg superiority margin). The daytime ambulatory SBP change difference between groups was −1.1 (95% CI: −4.3 to 2.2; p = 0.52). The nocturnal ambulatory SBP change difference between groups was −3.3 (95 CI: −6.7 to 0.1; p = 0.06). The percent of nondippers converted to dippers was 21.2% in the denervation group and 15.0% in the sham group (95% CI: −3.8% to 16.2%; p = 0.30). Change in 24-h heart rate was −1.4 ± 7.4 in the denervation group and −1.3 ± 7.3 in the sham group; (95% CI: −1.5 to 1.4; p = 0.94). Conclusions This trial did not demonstrate a benefit of renal artery denervation on reduction in ambulatory BP in either the 24-h or day and night periods compared with sham (Renal Denervation in Patients With Uncontrolled Hypertension [SYMPLICITY HTN-3]; NCT01418261 )

The role of antihypertensive therapy in reducing the risk of cardiovascular complications such as heart failure is well established, but the effects of different blood pressure goals on patient-perceived health status has not been well defined. We sought to determine if adverse effects on perceived health status will occur with lower blood pressure goals or more intensive antihypertensive therapy. Data were prospectively collected as a part of a single center, randomized controlled trial designed to evaluate standard (Seventh Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure-compliant) versus intense (

A total of 535 patients underwent randomization. The mean (±SD) change in systolic blood pressure at 6 months was −14.13±23.93 mm Hg in the denervation group as compared with −11.74±25.94 mm Hg in the sham-procedure group (P

STATEMENTOF PURPOSE: These guidelines have been written to provide a straightforward approach to managing hypertension in the community. We have intended that this brief curriculum and set of recommendations be useful not only for primary care physicians and medical students, but for all professionals who work as hands-on practitioners. We are aware that there is a great variability in access to medical care among communities. Even in so-called wealthy countries, there are sizable communities in which economic, logistic, and geographic issues put constraints on medical care. And, at the same time, we are been reminded that even in countries with highly limited resources, medical leaders have assigned the highest priority to supporting their colleagues in confronting the growing toll of devastating strokes, cardiovascular events, and kidney failure caused by hypertension. Our goal has been to give sufficient information to enable healthcare practitioners, wherever they are located, to provide professional care for people with hypertension. All the same, we recognize that it will often not be possible to carry out all of our suggestions for clinical evaluation, tests, and therapies. Indeed, there are situations in which the most simple and empirical care for hypertension-simply distributing whatever antihypertensive drugs might be available to people with high blood pressure-is better than doing nothing at all. We hope that we have allowed sufficient flexibility in this statement to enable responsible clinicians to devise workable plans for providing the best possible care of hypertension in their communities. We have divided this brief document into the following sections: 1. General introduction, 2. Epidemiology, 3. Special issues with black patients (African ancestry), 4. How is hypertension defined?, 5. How is hypertension classified?, 6. Causes of hypertension, 7. Making the diagnosis of hypertension, 8. Evaluating the patient, 9. Physical examination, 10. Tests, 11. Goals of treating hypertension, 12. Nonpharmacologic treatment of hypertension, 13. Drug treatment of hypertension, 14. Brief comments on drug classes, 15. Treatment-resistant hypertension. Fil: Weber, Michael A.. State University of New York; Estados Unidos Fil: Schiffrin, Ernesto L.. McGill University; Canadá Fil: White, William B.. University of Connecticut; Estados Unidos Fil: Mann, Samuel. Weil Cornell College of Medicine; Estados Unidos Fil: Lindholm, Lars H.. Universidad de Umea; Suecia Fil: Kenerson, John G.. Cardiovascular Associates; Estados Unidos Fil: Flack, John M.. Wayne State University; Estados Unidos Fil: Carter, Barry L.. University of Iowa; Estados Unidos Fil: Materson, Barry J.. University of Miami; Estados Unidos Fil: Ram, C. Venkata S.. MediCiti Institutions; India Fil: Cohen, Debbie L.. University of Pennsylvania; Estados Unidos Fil: Cadet, Jean Claude. State University School of Medicine; Estados Unidos Fil: Jean Charles, Roger R.. Hypertension Center of Haiti; Haití Fil: Taler, Sandra. Mayo Clinic. Department of Medicine; Estados Unidos Fil: Kountz, David. Jersey Shore University Medical Center; Estados Unidos Fil: Townsend, Raymond. University of Pennsylvania; Estados Unidos Fil: Chalmers, John. University of Sydney; Australia Fil: Ramírez, Agustín José. Fundación Favaloro; Argentina. Universidad Favaloro; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Bakris, George L.. University of Chicago; Estados Unidos Fil: Wang, Jiguang. Shanghai Jiaotong University; China Fil: Schutte, Aletta E.. North West University; Sudáfrica Fil: Bisognano, John D.. University of Rochester; Estados Unidos Fil: Touyz, Rhian M.. University of Glasgow; Reino Unido Fil: Sica, Dominic. Virginia Commonwealth University; Estados Unidos Fil: Harrap, Stephen B.. University of Melbourne; Australia