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This post hoc analysis assessed the efficacy and tolerability of valsartan for the treatment of hypertension in obese vs non-obese children and adolescents. After a 1-week antihypertensive washout period, 142 obese and 119 non-obese hypertensive children and adolescents aged 6 to 16 years were randomized to 2 weeks of once-daily treatment with valsartan 10 to 20 mg, 40 to 80 mg, or 80 to 160 mg, followed by re-randomization to either valsartan or placebo for an additional 2 weeks. Patients could continue to receive valsartan during an optional 52-week, open-label extension. Valsartan resulted in statistically significant (P<.05) and clinically relevant reductions in mean sitting blood pressure (BP), ranging from approximately 7/4 mm Hg (valsartan 10–20 mg) to 13/9 mm Hg (valsartan 80–160 mg) in both obese and non-obese patients. BP control was achieved in 44% of obese and 56% of non-obese patients. Following re-randomization, non-obese patients experienced an increase in BP during placebo treatment, albeit levels remained below baseline, whereas BP reductions were maintained in valsartan recipients (P<.05). The most frequent adverse events during the open-label phase were headache and fever. Valsartan provides similar antihypertensive efficacy in obese and non-obese hypertensive children and adolescents, with good tolerability in both patient populations.
The efficacy and safety of the angiotensin receptor blocker (ARB) valsartan alone or in combination with other antihypertensive agents is well established for the treatment of hypertension in adults.1–3 In addition, valsartan has been shown to provide morbidity and mortality benefits that extend beyond blood pressure (BP)–lowering.4–7 In 2007, valsartan was approved by the US Food and Drug Administration for the treatment of hypertension in children and adolescents aged 6 to 16 years. The prevalence of hypertension in this population, which has historically been reported to be in the range of 1% to 3%,8 has increased steadily over the past 2 decades and is now estimated to be in the range of 4.5%9 to 10%.10,11
In recent years, the number of antihypertensive agents with clinical data supportive of their use in children and adolescents has increased; however, data are lacking for many of the older, commonly used pharmacologic options. Two adequate and well-controlled studies have assessed the efficacy and safety of valsartan for the treatment of hypertension in children and adolescents. The first study, conducted in 90 patients aged 1 to 5 years with untreated hypertension or treated but uncontrolled hypertension, demonstrated that treatment with low, medium, or high doses of valsartan for 2 weeks resulted in reductions from baseline in mean sitting systolic BP (MSSBP) of 8.3 mm Hg to 8.6 mm Hg and mean sitting diastolic BP (MSDBP) of 5.5 mm Hg to 6.4 mm Hg.12 The second study was conducted in 261 hypertensive patients aged 6 to 16 years who were randomized to 2 weeks of treatment with valsartan 10 to 20 mg/d, 40 to 80 mg/d, 80 to 160 mg/d.13 Treatment with valsartan resulted in statistically significant, clinically relevant, dose-dependent reductions in MSSBP/MSDBP of 7.9/4.6 mm Hg, 9.6/5.8 mm Hg, and 11.5/7.4 mm Hg, respectively (all P<.0001 vs baseline). Reductions in MSSBP and MSDBP were similar in the 6- to 11-year-old and 12- to 16-year-old age groups, and were independent of sex, race, and sexual maturity. Overall patients from non-US sites showed greater reductions in MSSBP and MSDBP than patients from US sites. Treatment with valsartan was well tolerated in both studies.
Of interest, 54% of the children and adolescents in the second study13 were considered to be obese or overweight (body mass index [BMI] ≥95th percentile for sex and age or BMI Z score ≥1.54). The association of hypertension and obesity is particularly worrisome, as the prevalence of overweight and obesity in children and adolescents has tripled over the past 2 decades to more than 30%,14,15 and the rate of hypertension is reported to be 2 to 3 times higher in obese children and adolescents than in their non-obese counterparts.9,16,17 The risk for developing the metabolic (or insulin resistance) syndrome is also of major concern in obese children and adolescents. Overall, the prevalence is approximately 4% in children and adolescents, but the prevalence increases to 30% to 50% in the overweight pediatric population,18,19 and it is estimated that approximately 1 million children and adolescents in the United States currently meet the criteria for the metabolic syndrome.20 Control of BP in obese hypertensive children and adolescents is therefore of critical importance, and greater use of pharmacologic intervention to achieve target BP may be required. The objective of the present post hoc analysis was to determine whether valsartan is as effective for controlling BP in obese hypertensive children and adolescents as it is in non-obese hypertensive children and adolescents.
This multicenter, randomized, double-blind trial was conducted in accordance with Good Clinical Practice guidelines. The study protocol and informed consent forms were reviewed and approved by institutional review boards or ethics committees at each site. Prior to enrollment in the study, a signed informed consent form was obtained from the parent or legal guardian of each child or adolescent participating in the study, along with a pediatric assent form signed by the patient, if applicable. The inclusion and exclusion criteria, study design, and methods for this clinical trial have been reported in detail by Wells and colleagues13 and are briefly summarized below.
Males and females aged 6 to 16 years were eligible for the study if they weighed ≥20 kg and the mean of 3 consecutive MSSBP measurements at screening was ≥95th percentile for age, sex, and height, but <5% above the 99th percentile. Exclusion criteria included a creatinine clearance <40 mL/min per 1.73 m2, hyperkalemia, cardiac arrhythmias, significant coarctation of the aorta (gradient ≥30 mm Hg), previous solid organ transplant (except renal transplant ≥1 year before enrollment), bilateral renal artery stenosis (unilateral for patients with a single kidney), pregnancy or lactation, human immunodeficiency virus or hepatitis, gastrointestinal disease that might affect absorption of the study medication, and known sensitivity to ARBs. In addition, patients were ineligible to participate in the study if they were receiving antipsychotics, tricyclic antidepressants, monoamine oxidase inhibitors, lithium, anticonvulsants, or other drugs known to have a significant effect on BP.
This international study was conducted at 55 centers. After a 1-week, single-blind, antihypertensive washout period, patients were randomized in a 2:1:2 ratio to receive 2 weeks of double-blind treatment with low-, medium-, or high-dose valsartan, depending on body weight (phase 1). Patients who weighed <35 kg received valsartan 10 mg, 40 mg, or 80 mg once daily. Those who weighed ≥35 kg received 20 mg, 80 mg, or 160 mg once daily. Patients who completed phase 1 were re-randomized in a 1:1 ratio to receive 2 additional weeks of double-blind treatment with valsartan at their phase 1 dose or matching placebo (phase 2). This was followed by an optional 52-week, open-label extension (OLE) phase. Patients participating in the OLE phase initially received valsartan 40 mg once daily. The dose of valsartan could be increased to 80 mg once daily and then to 160 mg once daily if trough MSSBP measurements, assessed at 2-week intervals, were above the target BP goal (<95th percentile for age, sex, and height). Patients receiving valsartan 160 mg who did not achieve the target BP received add-on treatment with hydrochlorothiazide (HCTZ) 12.5 mg once daily.
Clinic visits occurred on day-7 (screening), day 0 (baseline), day 7, and day 14 during phase 1 of the study, days 21 and 28 during phase 2, and at various time points during the OLE phase. Efficacy assessments included determination of MSSBP and MSDBP from 3 consecutive BP readings. BP measurements were obtained in the morning at drug trough level at each study visit according to accepted standards21 using a calibrated mercury sphygmomanometer or a calibrated aneroid sphygmomanometer and appropriate cuff size. Adverse events (AEs) were monitored and recorded throughout the study.
Results for obese or overweight (BMI ≥95th percentile for sex and age or BMI Z score ≥1.54) and non-obese patients were evaluated separately in this post hoc analysis. Efficacy was assessed using last-observation-carried-forward (LOCF) data obtained from the intent-to-treat (ITT) population (ie, all randomized patients who received ≥1 dose of study medication and had ≥1 postbaseline efficacy evaluation). Within-treatment comparisons with P values and 95% confidence intervals (CIs) of the mean change in MSSBP and MSDBP from baseline to the end of phase 1 and from the end of phase 1 to the end of phase 2 were conducted using paired t tests. P values and 95% CIs for between-treatment comparisons in phase 2 were derived using an analysis of covariance (ANCOVA) model with treatment, region, race, and weight as factors, and MSSBP at visit 4 (ie, the end of phase 1) as the covariate. All statistical tests were conducted using a 2-sided alternative hypothesis at a significance level of .05. The safety population comprised all patients in the ITT population.
Patient Disposition and Baseline Characteristics
A total of 261 patients (142 obese, 119 non-obese) were randomized in phase 1, and 245 patients (93.9%) were re-randomized in phase 2 (Figure 1). A total of 235 patients (90.0%) entered the OLE phase of the study, and 177 (67.8%) completed 52 weeks of treatment. The ITT efficacy and safety populations were composed of 259 patients in phase 1 and 245 patients in phase 2. The ITT safety population for the OLE phase of the study included 235 patients.
Patient demographic and baseline characteristics are presented in Table I. The overall mean age of patients was approximately 11 years. About half of the patients were aged 6 to 11 years and half were aged 12 to 16 years. The majority of patients (61%) were male, and nearly half were black. At baseline, the mean BMI was 33.9 kg/m2 among obese patients and 18.7 kg/m2 among non-obese patients. Prior to randomization, the most frequently used antihypertensive therapies included angiotensin-converting enzyme inhibitors (ACEIs; 32% obese, 49% non-obese), dihydropyridine calcium channel blockers (CCBs; 11%, 34%), and HCTZ (12%, 3%).
Table I. Demographic and Baseline Characteristics
Obese Patients (n=142)
Non-Obese Patients (n=119)
Abbreviations: BMI, body mass index; MSDBP, mean sitting diastolic blood pressure; MSSBP, mean sitting systolic blood pressure; SD, standard deviation; US, United States.
Age, mean (SD), y
6–11 y, No. (%)
12–16 y, No. (%)
Sex, No. (%)
Race, No. (%)
Region, No. (%)
Weight, kg, mean (SD)
BMI, kg/m2, mean (SD)
Tanner stage, No. (%)
MSSBP (SD), mm Hg
MSDBP (SD), mm Hg
Weight-adjusted valsartan dose, mg/kg
The MSSBP at baseline was similar between obese patients (132.6–133.9 mm Hg across dose groups) and non-obese patients (129.9–132.8 mm Hg), whereas the MSDBP at baseline was approximately 5 mm Hg lower in obese patients (74.2–76.1 mm Hg) than non-obese patients (79.3–80.7 mm Hg). There was a relatively strong association between obesity and race: the majority of obese patients were black (54%), whereas the majority of non-obese patients were non-black (58%). Obese patients were predominantly from US centers (70%), whereas non-obese patients were predominantly from non-US centers (75%). The mean weight-adjusted dose of valsartan was lower in obese patients (1.2 mg/kg) than in non-obese patients (1.9 mg/kg) despite the fact that in each of the 3 arms of the study (low, medium, and high), patients weighing ≥35 kg received valsartan at doses that were twice as high as the doses received by patients weighing <35 kg.
Phase 1. Treatment with low, medium, or high doses of valsartan resulted in statistically significant and clinically relevant reductions in MSSBP (P<.0001 for all comparisons) and MSDBP (P≤.043 for all comparisons) from baseline to the end of phase 1 in both obese and non-obese patients (Figure 2). Mean reductions in MSSBP ranged from 7.1 mm Hg to 10.4 mm Hg in obese patients and from 8.6 mm Hg to 12.7 mm Hg in non-obese patients, and mean reductions in MSDBP ranged from 4.3 mm Hg to 7.0 mm Hg in obese patients and from 4.2 mm Hg to 9.2 mm Hg in non-obese patients. At the end of phase 1, the proportion of patients who achieved the target MSSBP (<95th percentile for age, sex, and height) was slightly higher among non-obese patients (56%) than among obese patients (44%).
In an attempt to find a clinically useful dosing range, the relationship between weight-adjusted dose and BP response was evaluated (Table II). Non-obese patients received higher mean weight-adjusted doses than did obese patients within each valsartan dose group. Among obese patients, the most pronounced mean reductions in BP (10.4/7.0 mm Hg) occurred in the medium-dose group, at a mean weight-adjusted dose of 1.1 mg/kg. There was no further mean reduction in BP with a higher dose (10.3/5.6 mm Hg at 2.1 mg/kg). Among non-obese patients, the most pronounced mean reductions in BP were observed in the high-dose group (12.7/9.2 mm Hg at 3.2 mg/kg).
Table II. Summary of Weight-Adjusted Dose at Baseline and Blood Pressure Response in Phase 1
Low Dose (n=57)
Medium Dose (n=30)
High Dose (n=53)
Low Dose (n=45)
Medium Dose (n=22)
High Dose (n=52)
Values are expressed as means (standard deviation). Abbreviations: MSDBP, mean sitting diastolic blood pressure; MSSBP, mean sitting systolic blood pressure.
Baseline weight, kg
Baseline weight-adjusted dose, mg/kg
Change in MSSBP, mm Hg
Change in MSDBP, mm Hg
Phase 2. At the end of phase 1, MSSBP and MSDBP values were numerically similar between groups that were re-randomized to double-blind valsartan (124.6/71.0 mm Hg in obese and 120.6/73.7 mm Hg in non-obese patients) or placebo (123.4/68.3 mm Hg in obese and 119.6/72.6 mm Hg in non-obese patients). Reductions in BP were maintained in non-obese patients receiving valsartan (mean change from end of phase 1 to end of phase 2 was 0.4/−1.4 mm Hg; Figure 3). Conversely, non-obese patients receiving placebo experienced significant mean increases in BP during the 2-week treatment period (5.5/5.3 mm Hg; both P<.0001). Differences between valsartan and placebo in non-obese patients were significant (P=.0153 for MSSBP and P=.0003 for MSDBP).
Among obese patients, BP increased from the end of phase 1 to the end of phase 2 to a similar extent in both treatment groups: mean of 2.4/1.9 mm Hg with valsartan and 1.8/2.0 mm Hg with placebo (Figure 3). The increases in MSSBP with valsartan and MSDBP with placebo were significant (both P<.05).
During the OLE phase of the study, most patients received valsartan alone (80% obese, 86% non-obese) and the remaining patients were treated with valsartan in combination with HCTZ. Study medication was well tolerated in both obese and non-obese patients. The most frequent AEs during the OLE phase, regardless of relationship to study medication, were headache (34% obese, 33% non-obese), fever (14%, 26%), nasopharyngitis (18%, 19%), and cough (14%, 23%) (Table III). Throughout the study, few AEs were reported as possibly or probably related to study medication (Table IV). Serious AEs occurred in 9 obese patients and 9 non-obese patients during the OLE phase. The only serious AEs to be reported by more than 1 patient were diarrhea, gastroenteritis, and fever, each of which occurred in 2 patients in the non-obese group.
Table III. Adverse Events Reported by ≥5% of Patients in Either Obese or Non-Obese Patients During the Open-Label Extension Phase
Adverse Event, No. (%)
Obese Patients (n=125)
Non-Obese Patients (n=110)
Upper respiratory tract infection
Pain in extremity
Upper abdominal pain
Table IV. Adverse Events Suspected to Be Related to Study Medication Reported by at Least 2 Patients in Any Study Phase
Adverse Event, No. (%)
Phase 1 (n=140)
Phase 2 (n=132)
Phase 1 (n=119)
Phase 2 (n=113)
Abbreviation: ECG, electrocardiographic.
ECG QT/QTc prolonged
Increased blood creatinine
Current hypertension guidelines recommend initiation of therapeutic lifestyle changes as the initial approach to managing prehypertension and mild to moderate hypertension in children and adolescents with no evidence of hypertension-related target-organ disease.21,22 Lifestyle changes should include diet modification (eg, lower salt, sugar, and fat intake; greater consumption of fruits, vegetables, and whole grains), increased and regular physical activity, and cessation of the use of tobacco and alcohol. In overweight and obese individuals, loss of weight is particularly important, as it results in beneficial effects on BP and other cardiovascular risk factors, such as dyslipidemia and insulin resistance. However, the success rate with lifestyle modifications is disappointingly small, and pharmacologic intervention is indicated when these measures fail to reduce BP to target levels (<95th percentile in patients without relevant concurrent conditions; <90th percentile in patients with relevant concurrent conditions). Pharmacologic intervention is also indicated when initiating treatment in children and adolescents with stage 2 hypertension, symptomatic hypertension, secondary hypertension, diabetes, and/or evidence of organ damage.21 The recommendations for drug selection are generally the same as for adults.22 Preferential consideration should be given to ARBs and ACEIs in children and adolescents with type 1 or 2 diabetes; those with microalbuminuria, macroalbuminuria, glomerulonephritis, and other forms of renal disease; and those with high levels of plasma renin.12,21 In obese patients, ARBs may also offer therapeutic advantages over other classes of antihypertensive agents, as they do not increase norepinephrine levels and they have a favorable effect on insulin sensitivity. In addition, most ARBs do not increase leptin.23–27
This is the first clinical trial to prospectively study the efficacy and safety of short-term treatment with valsartan for reducing BP in a large population of obese children and adolescents with hypertension. The obese and non-obese groups were well-matched with respect to age (mean, 11.4 and 11.3 years in the obese and non-obese groups, respectively, with approximately half of each group aged 6–11 years and half aged 12–16 years). Fifty-four percent of obese patients and 42% of non-obese patients were black. Baseline BP was comparable in obese and non-obese patients (133.2/75.2 mm Hg and 131.5/80.4 mm Hg, respectively). Prior to randomization, non-obese patients were more likely than obese patients to have previously used ACEIs (49% vs 32%) or CCBs (34% vs 11%), but were less likely to have previously used HCTZ (3% vs 12%, respectively). Data from this post hoc analysis demonstrate that once-daily treatment with valsartan 10 mg to 160 mg results in statistically significant and clinically relevant mean reductions in MSSBP/MSDBP within 2 weeks that range from approximately 7/4 mm Hg with valsartan 10 mg to 20 mg to 13/9 mm Hg with valsartan 80 mg to 160 mg. Forty-four percent of obese patients achieved the target BP goal (MSSBP <95th percentile for age, sex, and height) compared with 56% of non-obese patients. The reductions in BP achieved with valsartan in obese children and adolescents with hypertension in this study are consistent with the reductions in BP observed in several clinical trials that enrolled hypertensive adults who were overweight or obese. In a meta-analysis of 9 randomized, placebo-controlled, clinical trials that included 1857 adult patients with a BMI ≥30 kg/m2, treatment with valsartan 80 mg or valsartan 160 mg resulted in mean reductions in SBP ranging from approximately 10 mm Hg to 15 mm Hg.28 More recently, an 8-week trial conducted in 58 overweight or obese patients (BMI ≥25 kg/m2) with mild to moderate hypertension demonstrated that monotherapy with valsartan 160 mg resulted in a mean decrease in SBP/DBP of 15.7/11.7 mm Hg (P<.01 vs baseline), as well as significant improvements in insulin sensitivity.26 A 6-week, forced-titration trial of valsartan has also been conducted recently by Everett and colleagues29 in 1668 patients. Of these patients, 453 patients were overweight (BMI 25 to <30 kg/m2) and 970 were obese (BMI ≥30 kg/m2). Treatment with valsartan 320 mg resulted in a mean reduction in SBP of 16.5 mm Hg in obese patients compared with a mean reduction of 18 mm Hg in the overall study population. Twenty-nine percent of all patients receiving valsartan monotherapy achieved the target BP of <140/90 mm Hg compared with 31% of overweight patients and 26% of obese patients.
The reductions in BP achieved in this study with once-daily, low-dose valsartan are noteworthy, as clinical guidelines for the management of hypertension stress that the initial dosage of antihypertensive agents in children and adolescents should be lower than the initial dosage used in adults, and dosages should be adjusted upwards with great caution.21,22 In phase 1 of this study, the most pronounced mean reductions in BP among non-obese patients were observed in the high-dose group (12.7/9.2 mm Hg at a mean weight-adjusted dose of 3.2 mg/kg) and among obese patients were in the medium-dose group (10.4/7.0 mm Hg at a mean weight-adjusted dose of 1.1 mg/kg). In the latter group (obese patients), there was no further mean reduction in BP with a higher valsartan dose (10.3/5.6 mm Hg at a mean weight-adjusted dose of 2.1 mg/kg).
Once-daily dosing can improve adherence with antihypertensive regimens,30 and adherence is further encouraged among patients (and their parents) if clinically relevant reductions in BP are achieved within a short time after initiating treatment.31 Several studies have shown that adherence rates with ARBs are higher than rates with antihypertensive agents from other classes,32–34 and the efficacy results from this study suggest that adherence rates with valsartan in obese and non-obese children and adolescents could be expected to be high as well.
Adherence has also been shown to be adversely affected by the incidence rate of AEs associated with antihypertensive agents,35–37 and AE profiles vary greatly among the different classes of antihypertensive agents. For example, ACEIs are associated with a high incidence of dry cough, CCBs are associated with the highest incidence of peripheral edema, and β-blockers are associated with the highest incidence of sexual dysfunction in addition to bronchospasm, gastrointestinal disturbances, fatigue, and sleep disorders.38 In contrast, the incidence of AEs with ARB-based therapy has been reported to be substantially lower than the incidence rates with other classes of antihypertensive agents37,39 and mostly limited to mild to moderate dizziness and infrequent cases of hypotension and hyperkalemia.38 Valsartan was well tolerated in this study, and the incidence rates of AEs were generally similar between obese and non-obese patients. In both groups, the most common AE during double-blind treatment was headache (reported in 2.9% and 1.5% of obese patients and 3.4% and 2.7% of non-obese patients during phases 1 and 2, respectively). The most common AEs during the 52-week OLE phase of the study were headache (33%), fever (20%), nasopharyngitis (19%), and cough (18%). Dizziness was reported infrequently (4%). The large majority of AEs did not appear to be related to study medication: headache possibly or probably related to treatment was reported in approximately 6% of obese patients and 5% of non-obese patients, and treatment-related orthostatic hypotension was reported in 1.6% of obese patients and none of the non-obese patients.
Interestingly, a dose response to valsartan was demonstrated for both MSSBP and MSDBP in non-obese children and adolescents who participated in the current study, but not in obese children and adolescents. The most likely reason for this is that despite the fact that obese patients in the low-, medium-, and high-dose groups received valsartan at levels twice as high as non-obese patients, systemic exposure to valsartan was 58% higher in the non-obese patients (1.9 mg/kg vs 1.2 mg/kg). Thus, the overall systemic exposure to valsartan even among obese patients in the medium- and high-dose groups may have been below the threshold required to demonstrate a dose response. Additionally, although this study enrolled a relatively high number of patients (259 in the ITT population), few were assigned to receive medium-dose valsartan (30 obese patients and 22 non-obese patients), and it is possible that future studies with larger numbers of obese and non-obese patients and a more uniform exposure to valsartan would demonstrate dose-related responses in both groups. Finally, there was evidence of a greater mean increase in BP among non-obese patients who were switched to placebo (MSSBP/MSDBP increased by 5.5/5.3 mm Hg; P<.0001 for both MSSBP and MSDBP) than among obese patients who were switched to placebo (MSSBP/MSDBP increased by 1.8/2.0 mm Hg; P<.05 for MSDBP only). However, an increase in BP is expected on withdrawal of antihypertensive agents, and BP levels at the end of the 2-week withdrawal period did not exceed baseline levels in either group, indicating that abrupt cessation of treatment with valsartan in obese and non-obese children and adolescents did not lead to rapid increases in BP, which could potentially be harmful and result in an increase in the risk for adverse cardiovascular events. The difference in the rebound effect between the obese and non-obese patients in this study may be due to the higher systemic exposure to valsartan in the non-obese group rather than greater accumulation and retention of valsartan in the obese group, as valsartan is hydrophilic in nature,40 has a low volume of distribution (17 L), and does not accumulate with repeat dosing.41
Overall, the results from this study demonstrate that treatment with valsartan is as effective for reducing BP in obese children and adolescents with hypertension as it is in non-obese children and adolescents. Although prospective, long-term, large-scale, comparator-controlled clinical trials will be needed in this population to properly assess the effect of treatment with valsartan on the rates of clinically important outcomes, the result from numerous trials in adults suggest that the benefits of treatment with valsartan may extend beyond that of simple BP lowering, particularly in obese children and adolescents. For example, several studies conducted in healthy, overweight, normotensive patients,42 and obese, hypertensive patients,24,43 as well as in non-obese hypertensive patients,44 have demonstrated that treatment with valsartan significantly improves insulin sensitivity, which is an important cardiovascular risk factor in obese patients, patients with the metabolic syndrome, and patients with type 2 diabetes.
Several studies have also shown that treatment with valsartan improves vascular and cardiac function (eg, reductions in large-artery stiffness, increased small-artery elasticity, increased forearm vasodilation, and reductions in left ventricular mass index)45–50 and has salutary effects on pro-inflammatory cytokine levels,51–53 all of which are implicated in the development of atherosclerosis and other cardiovascular complications. Other studies have demonstrated that treatment with valsartan may slow the progression of chronic kidney disease in patients with hypertension or type 2 diabetes by slowing or reversing persistent microalbuminuria.54–56
Once-daily treatment with valsartan results in statistically significant and clinically relevant reductions in SBP and DBP in both obese and non-obese children and adolescents with hypertension. The mean reductions in MSSBP/MSDBP range from 7/4 mm Hg with valsartan 10 mg to 20 mg to 13/9 mm Hg with valsartan 80 mg to 160 mg and are similar in magnitude between obese and non-obese children and adolescents. Valsartan is well tolerated in this patient population.
Acknowledgments and disclosures: The authors acknowledge all investigators and study coordinators at the participating centers and all patients for their commitment to the study, which was sponsored by Novartis Pharmaceuticals Corporation. The authors acknowledge Jacqueline Bailey, PharmD, and Mary Tom, PharmD, of Oxford PharmaGenesis, Inc, for their editorial support in the development of this manuscript. This support was funded by Novartis Pharmaceuticals Corporation. Kevin E.C. Meyers and Kenneth Lieberman have no conflicts of interest to disclose and all have participated or are participating in other trials sponsored by Novartis. Guangyang Han, Susan Solar-Yohay, and Victor Shi are employees of Novartis Pharmaceuticals Corporation.