jnc-7

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The Seventh Report of the JointNational Committee on Prevention,Detection, Evaluation, and Treatmentof High Blood PressureThe JNC 7 ReportAram V. Chobanian, MDGeorge L. Bakris, MDHenry R. Black, MDWilliam C. Cushman, MDLee A. Green, MD, MPHJoseph L. Izzo, Jr, MDDaniel W. Jones, MDBarry J. Materson, MD, MBASuzanne Oparil, MDJackson T. Wright, Jr, MD, PhDEdward J. Roccella, PhD, MPHand the National High BloodPressure Education ProgramCoordinating Committee

FOR MORE THAN 3 DECADES, THE

National Heart, Lung, andBlood Institute (NHLBI) hasadministered the National

High Blood Pressure EducationProgram (NHBPEP) CoordinatingCommittee, a coalition of 39 majorprofessional, public, and voluntaryorganizations and 7 federal agencies.One important function is to issueguidelines and advisories designed toincrease awareness, prevention, treat-ment, and control of hypertension(high blood pressure [BP]). Since thepublication of “The Sixth Report ofthe Joint National Committee on thePrevention, Detection, Evaluation, andTreatment of High Blood Pressure”

( JNC VI) released in 1997,1 manylarge-scale clinical trials have beenpublished.

The decision to appoint a commit-tee for “The Seventh Report of the Joint

Author Affiliations and Financial Disclosures are listedat the end of this article.Corresponding Author and Reprints: Edward J. Roc-cella, PhD, MPH, National Heart, Lung, and Blood In-stitute, National Institutes of Health, 31 Center Dr, MSC2480, Bethesda, MD 20892 (e-mail: [email protected]).

“The Seventh Report of the Joint National Committee on Prevention, De-tection, Evaluation, and Treatment of High Blood Pressure” provides a newguideline for hypertension prevention and management. The following arethe key messages: (1) In persons older than 50 years, systolic blood pres-sure (BP) of more than 140 mm Hg is a much more important cardiovasculardisease (CVD) risk factor than diastolic BP; (2) The risk of CVD, beginningat 115/75 mm Hg, doubles with each increment of 20/10 mm Hg; individu-als who are normotensive at 55 years of age have a 90% lifetime risk fordeveloping hypertension; (3) Individuals with a systolic BP of 120 to 139mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as pre-hypertensive and require health-promoting lifestyle modifications to pre-vent CVD; (4) Thiazide-type diuretics should be used in drug treatment formost patients with uncomplicated hypertension, either alone or combinedwith drugs from other classes. Certain high-risk conditions are compellingindications for the initial use of other antihypertensive drug classes (angio-tensin-converting enzyme inhibitors, angiotensin-receptor blockers, �-block-ers, calcium channel blockers); (5) Most patients with hypertension will re-quire 2 or more antihypertensive medications to achieve goal BP (�140/90mm Hg, or �130/80 mm Hg for patients with diabetes or chronic kidneydisease); (6) If BP is more than 20/10 mm Hg above goal BP, considerationshould be given to initiating therapy with 2 agents, 1 of which usually shouldbe a thiazide-type diuretic; and (7) The most effective therapy prescribed bythe most careful clinician will control hypertension only if patients are mo-tivated. Motivation improves when patients have positive experiences withand trust in the clinician. Empathy builds trust and is a potent motivator.Finally, in presenting these guidelines, the committee recognizes that theresponsible physician’s judgment remains paramount.JAMA. 2003;289:2560-2572 www.jama.com

See also pp 2534 and 2573.

2560 JAMA, May 21, 2003—Vol 289, No. 19 (Reprinted) ©2003 American Medical Association. All rights reserved.

at Indiana University School of Medicine on July 17, 2011jama.ama-assn.orgDownloaded from

http://jama.ama-assn.org/

National Committee on Prevention, De-tection, Evaluation, and Treatment ofHigh Blood Pressure” ( JNC 7) wasbased on 4 factors: publication of manynew hypertension observational stud-ies and clinical trials; need for a newclear and concise guideline that wouldbe useful for clinicians; need to sim-plify the classification of BP; and a clearrecognition that the JNC reports werenot being used to their maximum ben-efit. This JNC report is presented in 2separate publications: this current suc-cinct practical guide and a more com-prehensive report to be published sepa-rately, which will provide a broaderdiscussion and justification for the cur-rent recommendations. In presentingthese guidelines, the committee recog-nizes that the responsible physician’sjudgment is paramount in managing hisor her patients.

METHODSSince publication of the JNC VI report,the NHBPEP Coordinating Committee,chaired by the director of the NHLBI, hasregularly reviewed and discussed the hy-pertension clinical trials at their bian-nual meetings. In many instances, theprincipal investigator of the larger stud-ies has presented the information di-rectly to the Coordinating Committee.The Committee’s presentations and re-views are summarized and posted on the

NHLBI Web site.2 In agreeing to com-mission a new report, the director re-quested that the Coordinating Commit-tee members provide in writing a detailedrationale explaining the necessity to up-date the guidelines and to describe thecritical issues and concepts to be con-sidered for a new report. The JNC 7 chairwas selected in addition to a 9-memberexecutive committee appointed en-tirely from the NHBPEP CoordinatingCommittee membership. The NHBPEPCoordinatingCommittee servedasmem-bers of 5 writing teams, each of whichwere co-chaired by 2 executive commit-tee members.

The concepts identified by the NH-BPEP Coordinating Committee mem-bership were used to develop the re-port outline. A timeline was developedto complete and publish the work in 5months. Based on the identified criti-cal issues and concepts, the executivecommittee identified relevant MedicalSubject Headings (MeSH) terms andkeywords to further review the scien-tific literature. These MeSH terms wereused to generate MEDLINE searchesthat focused on English-language, peer-reviewed scientific literature from Janu-ary 1997 through April 2003. Varioussystems of grading the evidence wereconsidered and the classificationscheme used in JNC VI and otherNHBPEP clinical guidelines was se-

lected,3,4 which classifies studies ina process adapted from Last andAbramson.5

The executive committee met on 6occasions, 2 of which included meet-ings with the entire Coordinating Com-mittee. The writing teams also met byteleconference and used electronic com-munications to develop the report.Twenty-four drafts were created andreviewed in a reiterative fashion. At itsmeetings, the executive committee useda modified nominal group process toidentify and resolve issues. The NHB-PEP Coordinating Committee reviewedthe penultimate draft and providedwritten comments to the executive com-mittee. In addition, 33 national hyper-tension leaders reviewed and com-mented on the document. The NHBPEPCoordinating Committee approved theJNC 7 report.

RESULTSClassification of BP

TABLE 1 provides a classification of BPfor adults aged 18 years or older. Theclassification is based on the mean of2 or more properly measured seated BPreadings on each of 2 or more office vis-its. In contrast with the classificationprovided in the JNC VI report, a newcategory designated prehypertensionhas been added, and stages 2 and 3hypertension have been combined.

Table 1. Classification and Management of Blood Pressure for Adults Aged 18 Years or Older

BPClassification

SystolicBP, mm Hg*

DiastolicBP, mm Hg*

Management*

LifestyleModification

Initial Drug Therapy

Without Compelling Indication With Compelling Indications†

Normal �120 and �80 Encourage

Prehypertension 120-139 or 80-89 Yes No antihypertensive drugindicated

Drug(s) for the compellingindications‡

Stage 1 hypertension 140-159 or 90-99 Yes Thiazide-type diuretics for most;may consider ACE inhibitor,ARB, �-blocker, CCB, orcombination

Drug(s) for the compellingindications

Other antihypertensive drugs(diuretics, ACE inhibitor, ARB,�-blocker, CCB) as needed

Stage 2 hypertension �160 or �100 Yes 2-Drug combination for most(usually thiazide-type diureticand ACE inhibitor or ARB or�-blocker or CCB)§

Drug(s) for the compellingindications

Other antihypertensive drugs(diuretics, ACE inhibitor, ARB,�-blocker, CCB) as needed

Abbreviations: ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker; BP, blood pressure; CCB, calcium channel blocker.*Treatment determined by highest BP category.†See Table 6.‡Treat patients with chronic kidney disease or diabetes to BP goal of less than 130/80 mm Hg.§Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.

THE JNC 7 REPORT

©2003 American Medical Association. All rights reserved. (Reprinted) JAMA, May 21, 2003—Vol 289, No. 19 2561



Patients with prehypertension are at in-creased risk for progression to hyper-tension; those in the 130/80 to 139/89mm Hg BP range are at twice the riskto develop hypertension as those withlower values.6

Cardiovascular Disease RiskHypertension affects approximately 50million individuals in the United Statesand approximately 1 billion individu-als worldwide. As the population ages,the prevalence of hypertension willincrease even further unless broad andeffective preventive measures are imple-mented. Recent data from the Framing-ham Heart Study7 suggest that indi-viduals who are normotensive at 55years of age have a 90% lifetime risk fordeveloping hypertension.

The relationship between BP and riskof cardiovascular disease (CVD) eventsis continuous, consistent, and indepen-dent of other risk factors. The higherthe BP, the greater the chance of myo-cardial infarction, heart failure (HF),stroke, and kidney disease. For indi-viduals aged 40 to 70 years, each in-crement of 20 mm Hg in systolic BP or10 mm Hg in diastolic BP doubles therisk of CVD across the entire BP rangefrom 115/75 to 185/115 mm Hg.8

The classification prehypertension,introduced in this report (Table 1), rec-ognizes this relationship and signals theneed for increased education of healthcare professionals and the public to de-crease BP levels and prevent the devel-opment of hypertension in the generalpopulation.9 Hypertension preven-tion strategies are available to achieve

this goal (see “Lifestyle Modifica-tions” section).

Benefits of Lowering BPIn clinical trials, antihypertensivetherapy has been associated with 35%to 40% mean reductions in stroke in-cidence; 20% to 25% in myocardial in-farction; and more than 50% in HF.10

It is estimated that in patients with stage1 hypertension (systolic BP, 140-159mm Hg and/or diastolic BP, 90-99mm Hg) and additional cardiovascu-lar risk factors, achieving a sustained12-mm Hg decrease in systolic BP for10 years will prevent 1 death for every11 patients treated. In the presence ofCVD or target-organ damage, only 9 pa-tients would require this BP reductionto prevent a death.11

BP Control RatesHypertension is the most common pri-mary diagnosis in the United States with35 million office visits as the primary di-agnosis.12 Current control rates (sys-tolic BP �140 mm Hg and diastolic BP�90 mm Hg), although improved, arestill far below the Healthy People 2010goal of 50%; 30% are still unaware theyhave hypertension (TABLE 2). In the ma-jority of patients, controlling systolic hy-pertension, which is a more importantCVD risk factor than diastolic BP ex-cept in patients younger than 50 years13

and occurs much more commonly inolder persons, has been considerablymore difficult than controlling dias-tolic hypertension. Recent clinical trialshave demonstrated that effective BP con-trol can be achieved in most patients

with hypertension, but the majority willrequire 2 or more antihypertensivedrugs.14,15 When physicians fail to pre-scribe lifestyle modifications, adequateantihypertensive drug doses, or appro-priate drug combinations, inadequate BPcontrol may result.

Accurate BP Measurementin the OfficeThe auscultatory method of BP mea-surement with a properly calibrated andvalidated instrument should be used.16

Patients should be seated quietly for atleast 5 minutes in a chair rather than onan examination table, with feet on thefloor and arm supported at heart level.Measurement of BP in the standing po-sition is indicated periodically, espe-cially in those at risk for postural hypo-tension. An appropriate-sized cuff (cuffbladder encircling at least 80% of thearm) should be used to ensure accu-racy. At least 2 measurements should bemade. Systolic BP is the point at whichthe first of 2 or more sounds is heard(phase 1) and diastolic BP is the pointbefore the disappearance of sounds(phase 5). Physicians should provide topatients, verbally and in writing, theirspecific BP numbers and BP goals.

Ambulatory BP MonitoringAmbulatory BP monitoring17 providesinformation about BP during daily ac-tivities and sleep. Ambulatory BP moni-toring is warranted for evaluation of(white-coat) hypertension in the ab-sence of target-organ injury. It is alsohelpful to assess patients with apparentdrug resistance, hypotensive symptomswith antihypertensive medications, epi-sodic hypertension, and autonomic dys-function. The ambulatory BP values areusually lower thanclinic readings.Awakehypertensive individuals have a mean BPof more than 135/85 mm Hg and dur-ing sleep, more than 120/75 mm Hg. Thelevel of BP using ambulatory BP moni-toring correlates better than office mea-surements with target-organ injury.18

Ambulatory BP monitoring also pro-vides a measure of the percentage of BPreadings that are elevated, the overall BPload, and the extent of BP reduction dur-

Table 2. Trends in Awareness, Treatment, and Control of High Blood Pressure in Adults WithHypertension Aged 18 to 74 Years*

National Health and Nutrition Examination Surveys, Weighted %

II (1976-1980)III (Phase 1,1988-1991)

III (Phase 2,1991-1994) 1999-2000

Awareness 51 73 68 70

Treatment 31 55 54 59

Control† 10 29 27 34

*Data for 1999-2000 were computed (M. Wolz, unpublished data, 2003) from the National Heart, Lung, and BloodInstitute and data for National Health and Nutrition Examination Surveys II and III (phases 1 and 2) are from “The SixthReport of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pres-sure.”1 High blood pressure is systolic blood pressure of at least 140 mm Hg or diastolic blood pressure of at least90 mm Hg or taking antihypertensive medication.

†Systolic blood pressure of less than 140 mm Hg and diastolic blood pressure of less than 90 mm Hg.

THE JNC 7 REPORT




ing sleep. In most individuals, BP de-creases by 10% to 20% during the night;those in whom such decreases are notpresent are at increased risk for cardio-vascular events.

Self-measurement of BPBlood pressure self-measurements maybenefit patients by providing informa-tion on response to antihypertensivemedication, improving patient adher-ence with therapy,19 and in evaluatingwhite-coat hypertension. Individualswith a mean BP of more than 135/85mm Hg measured at home are gener-ally considered to be hypertensive.Home measurement devices should bechecked regularly for accuracy.

Patient EvaluationEvaluation of patients with docu-mented hypertension has 3 objectives:(1) to assess lifestyle and identify othercardiovascular risk factors or concomi-tant disorders that may affect progno-sis and guide treatment (BOX 1); (2) toreveal identifiable causes of high BP(BOX 2); and (3) to assess the presenceor absence of target-organ damage andCVD. The data needed are acquiredthrough medical history, physical ex-amination, routine laboratory tests, andother diagnostic procedures.

The physical examination should in-clude an appropriate measurement of BP,with verification in the contralateral arm;examination of the optic fundi; bodymass index calculated as weight in ki-lograms divided by the square of heightin meters (measurement of waist cir-cumference also may be useful); aus-cultation for carotid, abdominal, andfemoral bruits; palpation of the thyroidgland; thorough examination of the heartand lungs; examination of the abdo-men for enlarged kidneys, masses, andabnormal aortic pulsation; palpation ofthe lower extremities for edema andpulses; and neurological assessment.

Laboratory Tests andOther Diagnostic ProceduresRoutine laboratory tests recom-mended before initiating therapy in-clude an electrocardiogram; urinaly-

sis; blood glucose and hematocrit;serum potassium, creatinine (or the cor-responding estimated glomerular fil-tration rate), and calcium20; and a lipidprofile (after a 9- to 12-hour fast) thatincludes high-density lipoprotein cho-lesterol, low-density lipoprotein cho-lesterol, and triglycerides. Optional testsinclude measurement of urinary albu-min excretion or albumin/creatinineratio. More extensive testing for iden-tifiable causes is not indicated gener-ally unless BP control is not achieved.

TreatmentGoals of Therapy.The ultimate publichealth goal of antihypertensive therapyis the reduction of cardiovascular andrenal morbidity and mortality. Be-cause most patients with hyperten-sion, especially those aged at least 50years, will reach the diastolic BP goalonce systolic BP is at goal, the primaryfocus should be on achieving the sys-tolic BP goal (FIGURE). Treating sys-tolic BP and diastolic BP to targets thatare less than 140/90 mm Hg is associ-

ated with a decrease in CVD compli-cations. In patients with hypertensionwith diabetes or renal disease, the BPgoal is less than 130/80 mm Hg.21,22

Lifestyle Modifications. Adoption ofhealthy lifestyles by all individuals iscritical for the prevention of high BP andan indispensable part of the manage-ment of those with hypertension. Ma-jor lifestyle modifications shown tolower BP include weight reduction in

Box 2. Identifiable Causes ofHypertensionSleep apneaDrug-induced or drug-related

(see Box 3)Chronic kidney diseasePrimary aldosteronismRenovascular diseaseChronic steroid therapy and

Cushing syndromePheochromocytomaCoarctation of the aortaThyroid or parathyroid disease

Box 1. Cardiovascular Risk Factors*

Major Risk FactorsHypertension†Cigarette smokingObesity (BMI �30)†Physical inactivityDyslipidemia†Diabetes mellitus†Microalbuminuria or estimated GFR �60 mL/minAge (�55 years for men, �65 years for women)Family history of premature cardiovascular disease (men �55 years

or women 65 years)

Target-Organ DamageHeart

Left ventricular hypertrophyAngina or prior myocardial infarctionPrior coronary revascularizationHeart failure

BrainStroke or transient ischemic attack

Chronic kidney diseasePeripheral arterial diseaseRetinopathy

*BMI indicates body mass index calculated as weight in kilograms divided by the square ofheight in meters; GFR, glomerular filtration rate.†Components of the metabolic syndrome.

THE JNC 7 REPORT




those individuals who are overweightor obese23,24; adoption of Dietary Ap-proaches to Stop Hypertension eatingplan,25 which is rich in potassiumand calcium26; dietary sodium reduc-tion25-27; physical activity28,29; andmoderation of alcohol consumption

(TABLE 3).30 Lifestyle modifications de-crease BP, enhance antihypertensivedrug efficacy, and decrease cardiovas-cular risk. For example, a 1600-mg so-dium Dietary Approaches to Stop Hy-pertension eating plan has effects similarto single drug therapy.25 Combinations

of 2 or more lifestyle modifications canachieve even better results.

Pharmacologic Treatment. Excel-lent clinical trial outcome data provethat lowering BP with several classesof drugs, including angiotensin-converting enzyme (ACE) inhibitors,angiotensin-receptor blockers (ARBs),�-blockers, calcium channel blockers(CCBs), and thiazide-type diuretics, willall reduce the complications of hyper-tension.10,31-37 TABLE 4 and TABLE 5 pro-vide a list of commonly used antihy-pertensive agents.

Thiazide-type diuretics have been thebasis of antihypertensive therapy in mostoutcome trials.37 In these trials, includ-ing the recently published Antihyper-tensive and Lipid-Lowering Treatmentto Prevent Heart Attack Trial,33 diuret-ics have been virtually unsurpassed inpreventing the cardiovascular compli-cations of hypertension. The exceptionis the Second Australian National BloodPressure trial36 that reported slightly bet-ter outcomes in white men with a regi-men that began with an ACE inhibitorcompared with one starting with a di-uretic. Diuretics enhance the antihyper-tensive efficacy of multidrug regimens,can be useful in achieving BP control, andare more affordable than other antihy-pertensive agents. Despite these find-ings, diuretics remain underused.39

Thiazide-type diuretics should be usedas initial therapy for most patients withhypertension, either alone or in combi-nation with 1 of the other classes (ACEinhibitors, ARBs, �-blockers, CCBs)demonstrated to be beneficial in ran-domized controlled outcome trials. Thelist of compelling indications requiringthe use of other antihypertensive drugsas initial therapy are listed in TABLE 6.If a drug is not tolerated or is contrain-dicated, then1of theother classesprovento reduce cardiovascular events shouldbe used instead.

Achieving BP Control in Indi-vidual Patients. Most patients with hy-pertension will require 2 or more anti-hypertensivemedications toachieve theirBP goals.14,15 Addition of a second drugfrom a different class should be initi-ated when use of a single drug in ad-

Figure. Algorithm for Treatment of Hypertension

Lifestyle Modifications

Initial Drug Choices

Hypertension WithoutCompelling Indications

Hypertension WithCompelling Indications

Optimize Dosages or Add Additional Drugs Until Goal BP Is Achieved

Consider Consultation With Hypertension Specialist

Not at Goal BP(<140/90 mm Hg or <130/80 mm Hg for Those With Diabetes

or Chronic Kidney Disease)

Not at Goal BP

Stage 1 Hypertension(Systolic BP 140-159 mm Hgor Diastolic BP 90-99 mm Hg)

Thiazide-Type Diuretics for Most

May Consider ACE Inhibitor, ARB,β-Blocker, CCB, or Combination

Stage 2 Hypertension(Systolic BP ≥160 mm Hg orDiastolic BP ≥100 mm Hg)

2-Drug Combination for Most(Usually Thiazide-Type Diureticand ACE Inhibitor or ARB orβ-Blocker or CCB)

Drug(s) for theCompelling Indications

(See Table 6)

Other Antihypertensive Drugs(Diuretics, ACE Inhibitor, ARB,β-Blocker, CCB) as Needed

BP indicates blood pressure; ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker; and CCB,calcium channel blocker.

Table 3. Lifestyle Modifications to Manage Hypertension*

Modification RecommendationApproximate Systolic BP

Reduction, Range

Weight reduction Maintain normal body weight (BMI, 18.5-24.9) 5-20 mm Hg/10-kg weightloss23,24

Adopt DASH eatingplan

Consume a diet rich in fruits, vegetables, andlow-fat dairy products with a reducedcontent of saturated and total fat

8-14 mm Hg25,26

Dietary sodiumreduction

Reduce dietary sodium intake to no more than100 mEq/L (2.4 g sodium or 6 g sodiumchloride)

2-8 mm Hg25-27

Physical activity Engage in regular aerobic physical activitysuch as brisk walking (at least 30 minutesper day, most days of the week)

4-9 mm Hg28,29

Moderation of alcoholconsumption

Limit consumption to no more than 2 drinksper day (1 oz or 30 mL ethanol [eg, 24 ozbeer, 10 oz wine, or 3 oz 80-proofwhiskey]) in most men and no more than1 drink per day in women andlighter-weight persons

2-4 mm Hg30

Abbreviations: BMI, body mass index calculated as weight in kilograms divided by the square of height in meters;BP, blood pressure; DASH, Dietary Approaches to Stop Hypertension.

*For overall cardiovascular risk reduction, stop smoking. The effects of implementing these modifications are dose andtime dependent and could be higher for some individuals.

THE JNC 7 REPORT




equate doses fails to achieve the BP goal.When BP is more than 20/10 mm Hgabovegoal, considerationshouldbegivento initiating therapy with 2 drugs, ei-ther as separate prescriptions or in fixed-dose combinations (Figure). The initia-tion of drug therapy with more than 1agent may increase the likelihood ofachieving the BP goal in a more timelyfashion, but particular caution is ad-vised in those at risk for orthostatic hy-potension, such as patients with diabe-tes, autonomic dysfunction, and someolder persons. Use of generic drugs orcombination drugs should be consid-ered to reduce prescription costs.

Follow-up and Monitoring. Once an-tihypertensive drug therapy is initi-ated, most patients should return forfollow-up and adjustment of medica-tions at approximately monthly inter-vals until the BP goal is reached. Morefrequent visits will be necessary for pa-tients with stage 2 hypertension or withcomplicating comorbid conditions. Se-rum potassium and creatinine shouldbe monitored at least 1 to 2 times peryear.60 After BP is at goal and stable, fol-low-up visits can usually be at 3- to6-month intervals. Comorbidities, suchas HF, associated diseases, such as dia-betes, and the need for laboratory testsinfluence the frequency of visits. Othercardiovascular risk factors should betreated to their respective goals, and to-bacco avoidance should be promotedvigorously. Low-dose aspirin therapyshould be considered only when BP iscontrolled, because the risk of hemor-rhagic stroke is increased in patientswith uncontrolled hypertension.61

Special ConsiderationsThe patient with hypertension and cer-tain comorbidities requires special at-tention and follow-up by the clinician.

Compelling Indications. Table 6 de-scribes compelling indications that re-quire certain antihypertensive drugclasses for high-risk conditions. The drugselections for these compelling indica-tions are based on favorable outcomedata from clinical trials. Combination ofagents may be required. Other manage-ment considerations include medica-

tions already in use, tolerability, and de-sired BP targets. In many cases, specialistconsultation may be indicated.

Ischemic Heart Disease. Ischemicheart disease is the most common formof target-organ damage associated withhypertension. In patients with hyper-tension and stable angina pectoris,the first drug of choice is usually a�-blocker; alternatively, long-acting

CCBs can be used.1 In patients withacute coronary syndromes (unstable an-gina or myocardial infarction), hyper-tension should be treated initially with�-blockers and ACE inhibitors,49 withaddition of other drugs as needed forBP control. In patients with postmyo-cardial infarction, ACE inhibitors,�-blockers, and aldosterone antago-nists have proven to be most benefi-

Table 4. Oral Antihypertensive Drugs*

Class Drug (Trade Name)Usual Dose,Range, mg/d

DailyFrequency

Thiazide diuretics Chlorothiazide (Diuril) 125-500 1

Chlorthalidone (generic) 12.5-25 1

Hydrochlorothiazide(Microzide, HydroDIURIL)†

12.5-50 1

Polythiazide (Renese) 2-4 1

Indapamide (Lozol)† 1.25-2.5 1

Metolazone (Mykrox) 0.5-1.0 1

Metolazone (Zaroxolyn) 2.5-5 1

Loop diuretics Bumetanide (Bumex)† 0.5-2 2

Furosemide (Lasix)† 20-80 2

Torsemide (Demadex)† 2.5-10 1

Potassium-sparing diuretics Amiloride (Midamor)† 5-10 1-2

Triamterene (Dyrenium) 50-100 1-2

Aldosterone-receptor blockers Eplerenone (Inspra) 50-100 1-2

Spironolactone (Aldactone)† 25-50 1-2

�-Blockers Atenolol (Tenormin)† 25-100 1

Betaxolol (Kerlone)† 5-20 1

Bisoprolol (Zebeta)† 2.5-10 1

Metoprolol (Lopressor)† 50-100 1-2

Metoprolol extended release(Toprol XL)

50-100 1

Nadolol (Corgard)† 40-120 1

Propranolol (Inderal)† 40-160 2

Propranolol long-acting(Inderal LA)†

60-180 1

Timolol (Blocadren)† 20-40 2

�-Blockers with intrinsic Acebutolol (Sectral)† 200-800 2sympathomimetic activity Penbutolol (Levatol) 10-40 1

Pindolol (generic) 10-40 2

Combined �- and �-blockers Carvedilol (Coreg) 12.5-50 2

Labetalol (Normodyne,Trandate)†

200-800 2

ACE inhibitors Benazepril (Lotensin)† 10-40 1-2

Captopril (Capoten)† 25-100 2

Enalapril (Vasotec)† 2.5-40 1-2

Fosinopril (Monopril) 10-40 1

Lisinopril (Prinivil, Zestril)† 10-40 1

Moexipril (Univasc) 7.5-30 1

Perindopril (Aceon) 4-8 1-2

Quinapril (Accupril) 10-40 1

Ramipril (Altace) 2.5-20 1

Trandolapril (Mavik) 1-4 1(continued)

THE JNC 7 REPORT




cial.50,52,53,62 Intensive lipid manage-ment and aspirin therapy are alsoindicated.

Heart Failure. Heart failure, in theform of systolic or diastolic ventricu-lar dysfunction, results primarily fromsystolic hypertension and ischemicheart disease. Fastidious BP and cho-lesterol control are the primary pre-ventive measures for those at high riskfor HF.40 In asymptomatic individualswith demonstrable ventricular dysfunc-tion, ACE inhibitors and �-blockers arerecommended.52,62 For those with

symptomatic ventricular dysfunction orend-stage heart disease, ACE inhibi-tors, �-blockers, ARBs, and aldoste-rone blockers are recommended alongwith loop diuretics.40,41-48

Diabetic Hypertension. Combina-tions of 2 or more drugs are usuallyneeded to achieve the target BP goal ofless than 130/80 mm Hg.21,22 Thiazidediuretics, �-blockers, ACE inhibitors,ARBs, and CCBs are beneficial in re-ducing CVD and stroke incidence in pa-tients with diabetes.33,54,63 The ACE in-hibitor– or ARB-based treatments

favorably affect the progression of dia-betic nephropathy and reduce albu-minuria,55,56 and ARBs have been shownto reduce progression to macroalbu-minuria.56,57

Chronic Kidney Disease. In pa-tients with chronic kidney disease, de-fined by either (1) reduced excretoryfunction with an estimated glomerularfiltration rate of less than 60 mL/min per1.73 m2 (corresponding approximatelyto a creatinine of �1.5 mg/dL [�132.6µmol/L] in men or �1.3 mg/dL [�114.9µmol/L] in women)20 or (2) the pres-ence of albuminuria (�300 mg/d or 200mg albumin per gram of creatinine),therapeutic goals are to slow deteriora-tion of renal function and prevent CVD.Hypertension appears in the majority ofthese patients and they should receiveaggressive BP management, often with3 or more drugs to reach target BP val-ues of less than 130/80 mm Hg.59,64

The ACE inhibitors and ARBs havedemonstrated favorable effects on theprogression of diabetic and nondia-betic renal disease.55-59,64 A limited in-crease in serum creatinine of as muchas 35% above baseline with ACE in-hibitors or ARBs is acceptable and nota reason to withhold treatment unlesshyperkalemia develops.65 With ad-vanced renal disease (estimated glo-merular filtration rate �30 mL/min per1.73 m2, corresponding to a serum cre-atinine of 2.5-3.0 mg/dL [221-265µmol/L]), increasing doses of loop di-uretics are usually needed in combina-tion with other drug classes.

Cerebrovascular Disease. The risksand benefits of acute lowering of BP dur-ing an acute stroke are still unclear; con-trol of BP at intermediate levels (approxi-mately 160/100 mm Hg) is appropriateuntil the condition has stabilized or im-proved. Recurrent stroke rates are low-ered by the combination of an ACE in-hibitor and thiazide-type diuretic.35

Other Special Situations. MinorityPopulations. Blood pressure control ratesvary in minority populations and arelowest in Mexican Americans and Na-tive Americans.1 In general, the treat-ment of hypertension is similar for alldemographic groups, but socioeco-

Table 4. Oral Antihypertensive Drugs (cont)*

Class Drug (Trade Name)Usual Dose,Range, mg/d

DailyFrequency

Angiotensin II antagonists Candesartan (Atacand) 8-32 1

Eprosartan (Tevetan) 400-800 1-2

Irbesartan (Avapro) 150-300 1

Losartan (Cozaar) 25-100 1-2

Olmesartan (Benicar) 20-40 1

Telmisartan (Micardis) 20-80 1

Valsartan (Diovan) 80-320 1

Calcium channelblockers−non-dihydropyridines

Diltiazem extended release(Cardizem CD,Dilacor XR, Tiazac)†

180-420 1

Diltiazem extended release(Cardizem LA)

120-540 1

Verapamil immediate release(Calan, Isoptin)†

80-320 2

Verapamil long-acting(Calan SR, Isoptin SR)†

120-360 1-2

Verapamil-coer (Covera HS,Verelan PM)

120-360 1

Calcium channel Amlodipine (Norvasc) 2.5-10 1blockers−dihydropyridines Felodipine (Plendil) 2.5-20 1

Isradipine (Dynacirc CR) 2.5-10 2

Nicardipine sustained release(Cardene SR)

60-120 2

Nifedipine long-acting (Adalat CC,Procardia XL)

30-60 1

Nisoldipine (Sular) 10-40 1

�1-Blockers Doxazosin (Cardura) 1-16 1

Prazosin (Minipress)† 2-20 2-3

Terazosin (Hytrin) 1-20 1-2

Central �2-agonists and other Clonidine (Catapres)† 0.1-0.8 2centrally acting drugs Clonidine patch (Catapres TTS) 0.1-0.3 1 weekly

Methyldopa (Aldomet)† 250-1000 2

Reserpine (generic) 0.05-0.25 1‡

Guanfacine (generic) 0.5-2 1

Direct vasodilators Hydralazine (Apresoline)† 25-100 2

Minoxidil (Loniten)† 2.5-80 1-2Abbreviation: ACE, angiotensin-converting enzyme.*Dosages may vary from those listed in the Physicians’ Desk Reference,38 which may be consulted for additional in-

formation.†Are now or will soon become available in generic preparations.‡A 0.1-mg dose may be given every other day to achieve this dosage.

THE JNC 7 REPORT




nomic factors and lifestyle may be im-portant barriers to BP control in someminority patients. The prevalence, se-verity, and impact of hypertension areincreased in blacks, who also demon-strate somewhat reduced BP responsesto monotherapy with �-blockers, ACEinhibitors, or ARBs compared with di-uretics or CCBs. These differential re-sponses are largely eliminated by drugcombinations that include adequatedoses of a diuretic. Angiotensin-converting enzyme inhibitor–inducedangioedema occurs 2 to 4 times more fre-quently in black patients with hyper-tension than in other groups.33

Obesity and the Metabolic Syndrome.Obesity (body mass index �30) is an in-creasingly prevalent risk factor for thedevelopment of hypertension and CVD.The Adult Treatment Panel III guide-line for cholesterol management de-fines the metabolic syndrome as thepresence of 3 or more of the followingconditions: abdominal obesity (waist cir-cumference �102 cm [�40 in] in menor �89 cm [�35 in] in women), glu-cose intolerance (fasting glucose �110mg/dL [�6.1 mmol/L]), BP of at least130/85 mm Hg, high triglycerides (�150mg/dL [�1.70 mmol/L]), or low high-density lipoprotein cholesterol (�40mg/dL [�1.04 mmol/L] in men or �50mg/dL [�1.30 mmol/L] in women).66

Intensive lifestyle modification shouldbe pursued in all individuals with themetabolic syndrome, and appropriatedrug therapy should be instituted foreach of its components as indicated.

Left Ventricular Hypertrophy. Left ven-tricular hypertrophy is an independentrisk factor that increases the risk of sub-sequent CVD. Regression of left ven-tricular hypertrophy occurs with ag-gressive BP management, includingweight loss, sodium restriction, andtreatment with all classes of antihyper-tensive agents except the direct vasodi-lators, hydralazine and minoxidil.1,67

Peripheral Arterial Disease. Periph-eral arterial disease is equivalent in riskto ischemic heart disease. Any class ofantihypertensive drugs can be used inmost patients with peripheral arterialdisease. Other risk factors should be

managed aggressively and aspirinshould be used.

Hypertension in Older Individuals. Hy-pertension occurs in more than twothirds of individuals after age 65 years.1

This is also the population with the low-

est rates of BP control.68 Treatment rec-ommendations for older individualswith hypertension, including those whohave isolated systolic hypertension,should follow the same principles out-lined for the general care of hyperten-

Table 5. Combination Drugs for Hypertension

Combination Type Fixed-Dose Combination, mg* Trade Name

ACE inhibitors and CCBs Amlodipine/benazepril hydrochloride(2.5/10, 5/10, 5/20, 10/20)

Lotrel

Enalapril maleate/felodipine (5/5) Lexxel

Trandolapril/verapamil (2/180, 1/240,2/240, 4/240)

Tarka

ACE inhibitors and diuretics Benazepril/hydrochlorothiazide (5/6.25,10/12.5, 20/12.5, 20/25)

Lotensin HCT

Captopril/hydrochlorothiazide (25/15,25/25, 50/15, 50/25)

Capozide

Enalapril maleate/hydrochlorothiazide(5/12.5, 10/25)

Vaseretic

Lisinopril/hydrochlorothiazide (10/12.5,20/12.5, 20/25)

Prinzide

Moexipril HCl/hydrochlorothiazide(7.5/12.5, 15/25)

Uniretic

Quinapril HCl/hydrochlorothiazide(10/12.5, 20/12.5, 20/25)

Accuretic

ARBs and diuretics Candesartan cilexetil/hydrochlorothiazide(16/12.5, 32/12.5)

Atacand HCT

Eprosartan mesylate/hydrochlorothiazide(600/12.5, 600/25)

Teveten HCT

Irbesartan/hydrochlorothiazide (75/12.5,150/12.5, 300/12.5)

Avalide

Losartan potassium/hydrochlorothiazide(50/12.5, 100/25)

Hyzaar

Telmisartan/hydrochlorothiazide(40/12.5, 80/12.5)

Micardis HCT

Valsartan/hydrochlorothiazide (80/12.5,160/12.5)

Diovan HCT

�-Blockers and diuretics Atenolol/chlorthalidone (50/25, 100/25) Tenoretic

Bisoprolol fumarate/hydrochlorothiazide(2.5/6.25, 5/6.25, 10/6.25)

Ziac

Propranolol LA/hydrochlorothiazide(40/25, 80/25)

Inderide

Metoprolol tartrate/hydrochlorothiazide(50/25, 100/25)

Lopressor HCT

Nadolol/bendroflumethiazide (40/5,80/5)

Corzide

Timolol maleate/hydrochlorothiazide(10/25)

Timolide

Centrally acting drug and diuretic Methyldopa/hydrochlorothiazide(250/15, 250/25, 500/30, 500/50)

Aldoril

Reserpine/chlorothiazide (0.125/250,0.25/500)

Diupres

Reserpine/hydrochlorothiazide(0.125/25, 0.125/50)

Hydropres

Diuretic and diuretic Amiloride HCl/hydrochlorothiazide (5/50) Moduretic

Spironolactone/hydrochlorothiazide(25/25, 50/50)

Aldactone

Triamterene/hydrochlorothiazide(37.5/25, 50/25, 75/50)

Dyazide, Maxzide

Abbreviations: ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker; CCB, calcium channel blocker;HCl, hydrochloride; HCT, hydrochlorothiazide; LA, long-acting.

*Some drug combinations are available in multiple fixed doses. Each drug dose is reported in milligrams.

THE JNC 7 REPORT




sion. In many individuals, lower ini-tial drug doses may be indicated toavoid symptoms; however, standarddoses and multiple drugs are needed inthe majority of older individuals toreach appropriate BP targets.

Postural Hypotension. A decrease instanding systolic BP of more than 10mm Hg, when associated with dizzi-ness or fainting, is more frequent inolder patients with systolic hyperten-sion, diabetes, and those taking diuret-ics, venodilators (eg, nitrates, �-block-ers, and sildenafil-like drugs), and somepsychotropic drugs. Blood pressure inthese individuals should also be moni-tored in the upright position. Cautionshould be used to avoid volume deple-tion and excessively rapid dose titra-tion of antihypertensive drugs.

Dementia. Dementia and cognitiveimpairment occur more commonly inpatients with hypertension. Reducedprogression of cognitive impairmentmay occur with effective antihyperten-sive therapy.69,70

Hypertension in Women. Oral contra-ceptives may increase BP and the risk ofhypertension increases with duration ofuse. Women taking oral contraceptives

should have their BP checked regu-larly. Development of hypertension is areason to consider other forms of con-traception. In contrast, hormone replace-ment therapy does not raise BP.71

Women with hypertension who be-come pregnant should be followed care-fully because of increased risks to motherand fetus. Methyldopa, �-blockers, andvasodilators arepreferredmedications forthe safety of the fetus.72 Angiotensin-converting enzyme inhibitors and ARBsshould not be used during pregnancy be-cause of the potential for fetal defects andshould be avoided in women who arelikely to become pregnant. Preeclamp-sia, which occurs after the 20th gesta-tion week of pregnancy, is character-ized by new-onset or worseninghypertension, albuminuria, and hyper-uricemia, sometimes with coagulationabnormalities. In some patients, pre-eclampsia may develop into a hyperten-sive urgency or emergency and may re-quire hospitalization, intensivemonitoring, early fetal delivery, and par-enteral antihypertensive and anticon-vulsant therapy.72

Children and Adolescents. In chil-dren and adolescents, hypertension is

defined as BP that is, on repeated mea-surement, at the 95th percentile orgreateradjustedforage,height,andsex.73

The fifth Korotkoff sound is used todefine diastolic BP. Clinicians should bealert to the possibility of identifiablecauses of hypertension in younger chil-dren (ie, kidney disease, coarctation ofthe aorta). Lifestyle interventions arestrongly recommended, with pharma-cologic therapy instituted for higher lev-els of BP, or if there is insufficientresponse to lifestyle modifications.74

Choices of antihypertensive drugs aresimilar in children and adults, but effec-tive doses for children are often smallerand should be adjusted carefully. Angio-tensin-convertingenzymeinhibitorsandARBs should not be used in pregnant orsexually active girls. Uncomplicatedhypertension should not be a reason torestrict children from participating inphysical activities, particularly becauselong-term exercise may lower BP. Useof anabolic steroids should be stronglydiscouraged.Vigorous interventionsalsoshould be conducted for other existingmodifiable risk factors (eg, smoking).

Hypertensive Urgencies and Emergen-cies. Patients with marked BP eleva-

Table 6. Clinical Trial and Guideline Basis for Compelling Indications for Individual Drug Classes

High-Risk ConditionsWith Compelling

Indication*

Recommended Drugs

Clinical Trial Basis†Diuretic �-BlockerACE

Inhibitor ARB CCBAldosteroneAntagonist

Heart failure ‰ ‰ ‰ ‰ ‰ ACC/AHA Heart Failure Guideline,40

MERIT-HF,41 COPERNICUS,42 CIBIS,43

SOLVD,44 AIRE,45 TRACE,46 ValHEFT,47

RALES48

Post–myocardial infarction ‰ ‰ ‰ ACC/AHA Post-MI Guideline,49 BHAT,50

SAVE,51 Capricorn,52 EPHESUS53

High coronary disease risk ‰ ‰ ‰ ‰ ALLHAT,33 HOPE,34 ANBP2,36 LIFE,32

CONVINCE31

Diabetes ‰ ‰ ‰ ‰ ‰ NKF-ADA Guideline,21,22 UKPDS,54 ALLHAT33

Chronic kidney disease ‰ ‰ NKF Guideline,22 Captopril Trial,55 RENAAL,56

IDNT,57 REIN,58 AASK59

Recurrent stroke prevention ‰ ‰ PROGRESS35

Abbreviations: AASK, African American Study of Kidney Disease and Hypertension; ACC/AHA, American College of Cardiology/American Heart Association; ACE, angiotensin-converting enzyme; AIRE, Acute Infarction Ramipril Efficacy; ALLHAT, Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial; ANBP2, Second AustralianNational Blood Pressure Study; ARB, angiotensin-receptor blocker; BHAT, �-Blocker Heart Attack Trial; CCB, calcium channel blocker; CIBIS, Cardiac Insufficiency BisoprololStudy; CONVINCE, Controlled Onset Verapamil Investigation of Cardiovascular End Points; COPERNICUS, Carvedilol Prospective Randomized Cumulative Survival Study;EPHESUS, Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study; HOPE, Heart Outcomes Prevention Evaluation Study; IDNT, Inbesartan Dia-betic Nephropathy Trial; LIFE, Losartan Intervention For Endpoint Reduction in Hypertension Study; MERIT-HF, Metoprolol CR/XL Randomized Intervention Trial in CongestiveHeart Failure; NKF-ADA, National Kidney Foundation–American Diabetes Association; PROGRESS, Perindopril Protection Against Recurrent Stroke Study; RALES, RandomizedAldactone Evaluation Study; REIN, Ramipril Efficacy in Nephropathy Study; RENAAL, Reduction of Endpoints in Non–Insulin-Dependent Diabetes Mellitus with the Angiotensin IIAntagonist Losartan Study; SAVE, Survival and Ventricular Enlargement Study; SOLVD, Studies of Left Ventricular Dysfunction; TRACE, Trandolapril Cardiac Evaluation Study;UKPDS, United Kingdom Prospective Diabetes Study; ValHEFT, Valsartan Heart Failure Trial.

*Compelling indications for antihypertensive drugs are based on benefits from outcome studies or existing clinical guidelines; the compelling indication is managed in parallel withthe blood pressure.

†Conditions for which clinical trials demonstrate benefit of specific classes of antihypertensive drugs.

THE JNC 7 REPORT




tions and acute target-organ damage(eg, encephalopathy, myocardial in-farction, unstable angina, pulmonaryedema, eclampsia, stroke, head trauma,life-threatening arterial bleeding, or aor-tic dissection) require hospitalizationand parenteral drug therapy.1 Patientswith markedly elevated BP but with-out acute target-organ damage usuallydo not require hospitalization, but theyshould receive immediate combina-tion oral antihypertensive therapy. Theyshould be carefully evaluated and moni-tored for hypertension-induced heartand kidney damage and for identifi-able causes of hypertension (Box 2).

Additional Considerations in Anti-hypertensive Drug Choices. Antihyper-tensive drugs can have favorable or un-favorable effects on other comorbidities.

Potential Favorable Effects. Thiazide-type diuretics are useful in slowing de-mineralization in osteoporosis. �-Block-ers can be useful in the treatment ofatrial tachyarrhythmias/fibrillation, mi-graine, thyrotoxicosis (short-term), es-sential tremor, or perioperative hyper-tension. Calcium channel blockers maybe useful in Raynaud syndrome and cer-tain arrhythmias, and �-blockers maybe useful in prostatism.

Potential Unfavorable Effects. Thia-zide diuretics should be used cau-tiously in patients who have gout orwho have a history of significant hy-ponatremia. �-Blockers should gener-ally be avoided in individuals who haveasthma, reactive airways disease, or sec-ond- or third-degree heart block. An-giotensin-converting enzyme inhibi-tors and ARBs should not be given towomen likely to become pregnant andare contraindicated in those who are;ACE inhibitors should not be used inindividuals with a history of angio-edema. Aldosterone antagonists and po-tassium-sparing diuretics can cause hy-perkalemia and should generally beavoided in patients who have serum po-tassium values of more than 5.0 mEq/Lwhile not taking medications.

Improving Hypertension ControlAdherence to Regimens. Behavioralmodels suggest that the most effective

therapy prescribed by the most carefulclinician will control hypertension onlyif the patient is motivated to take the pre-scribed medication and to establish andmaintain a health-promoting lifestyle.Motivation improves when patients havepositive experiences with and trust intheir clinicians. Empathy builds trustand is a potent motivator.75 Patient at-titudes are greatly influenced by cul-tural differences, beliefs, and previousexperiences with the health care sys-tem.76 These attitudes must be under-stood if the clinician is to build trust andincrease communication with patientsand families.

Failure to titrate or combine medica-tions, despite knowing the patient is notat goal BP, represents clinical inertia andmust be overcome.77 Decision supportsystems (ie, electronic and paper), flowsheets, feedback reminders, and involve-ment of nurse clinicians and pharma-cists can be helpful.78

The patient and clinician must agreeon BP goals. A patient-centered strat-egy to achieve the goal and an estima-tion of the time needed to reach the goalare important.79 When BP is above goal,

alterations in the plan should be docu-mented. Blood pressure self-monitor-ing can also be useful. Patients’ nonad-herence to therapy is increased bymisunderstanding of the condition ortreatment, denial of illness because oflack of symptoms or perception of drugsas symbols of ill health, lack of patientinvolvement in the care plan, or unex-pected adverse effects of medications.The patient should be made to feel com-fortable in telling the clinician all con-cerns and fears of unexpected or dis-turbing drug reactions.

The cost of medications and thecomplexity of care (ie, transportation,patient difficulty with polypharmacy,difficulty in scheduling appointments,and life’s competing demands) areadditional barriers that must be over-come to achieve goal BP. All membersof the health care team (eg, physi-cians, nurse case managers, othernurses, physician assistants, pharma-cists, dentists, registered dietitians,optometrists, and podiatrists) mustwork together to influence and rein-force instructions to improve patients’lifestyles and BP control.80

Box 3. Causes of Resistant HypertensionImproper blood pressure measurementVolume overload and pseudotolerance

Excess sodium intakeVolume retention from kidney diseaseInadequate diuretic therapy

Drug-induced or other causesNonadherenceInadequate dosesInappropriate combinationsNonsteroidal anti-inflammatory drugs; cyclooxygenase 2 inhibitorsCocaine, amphetamines, other illicit drugsSympathomimetics (decongestants, anorectics)Oral contraceptivesAdrenal steroidsCyclosporine and tacrolimusErythropoietinLicorice (including some chewing tobacco)Selected over-the-counter dietary supplements and medicines (eg, ephedra,

ma haung, bitter orange)Associated conditions

ObesityExcess alcohol intake

Identifiable causes of hypertension (see Box 2)

THE JNC 7 REPORT




Resistant Hypertension. Resistanthypertension is the failure to reach goalBP in patients who are adhering to fulldoses of an appropriate 3-drug regi-men that includes a diuretic. After ex-cluding potential identifiable hyper-tension (Box 2), clinicians shouldcarefully explore reasons why the pa-tient is not at goal BP (BOX 3). Particu-lar attention should be paid to di-uretic type and dose in relation to renalfunction (see “Chronic Kidney Dis-ease” section). Consultation with a hy-pertension specialist should be consid-ered if goal BP cannot be achieved.

Public Health Challengesand Community ProgramsPublic health approaches, such as re-ducing calories, saturated fat, and salt inprocessed foods and increasing com-munity and school opportunities forphysical activity, can achieve a down-ward shift in the distribution of a popu-lation’s BP, thus potentially reducingmorbidity, mortality, and the lifetimerisk of an individual becoming hyper-tensive. This becomes especially criti-cal as the body mass index of individu-als in the United States has increased toepidemic levels. Currently, 122 mil-lion adults are overweight or obese,which contributes to the rise in BP andrelated conditions.81 The JNC 7 en-dorses the American Public Health As-sociation resolution that the food manu-facturers and restaurants reduce sodiumin the food supply by 50% during thenext decade. When public health inter-vention strategies address the diversityof racial, ethnic, cultural, linguistic, re-ligious, and social factors in the deliv-ery of their services, the likelihood oftheir acceptance by the community in-creases. These public health ap-proaches can provide an attractive op-portunity to interrupt and prevent thecontinuing costly cycle of managing hy-pertension and its complications.

Author Affiliations: Department of Medicine, Bos-ton University School of Medicine, Boston, Mass (DrChobanian); Department of Preventive Medicine,Rush-Presbyterian-St Luke’s Medical Center, Chi-cago, Ill (Drs Bakris and Black); Veterans Affairs Medi-cal Center, Departments of Preventive Medicine andMedicine, University of Tennessee Health Science Cen-

ter, Memphis (Dr Cushman); Department of FamilyMedicine, University of Michigan, Ann Arbor (DrGreen); Department of Medicine and Pharmacology,State University of New York at Buffalo School of Medi-cine, Buffalo (Dr Izzo); Department of Medicine andCenter for Excellence in Cardiovascular-Renal Re-search, University of Mississippi Medical Center, Jack-son (Dr Jones); Department of Medicine, Universityof Miami School of Medicine, Miami, Fla (Dr Mater-son); Department of Medicine, Physiology, and Bio-physics, Division of Cardiovascular Disease, Univer-sity of Alabama at Birmingham (Dr Opari l);Departments of Medicine, University Hospitals ofCleveland and the Louis Stokes Cleveland VeteransAffairs Medical Center, Cleveland, Ohio (Dr Wright);and National High Blood Pressure Education Pro-gram, National Heart, Lung, and Blood Institute, Na-tional Institutes of Health, Bethesda, Md (Dr Roccella).Additional Authors/National High Blood Pressure Edu-cation Program Coordinating Committee Partici-pants:ClaudeLenfant,MD, chair (NationalHeart, Lung,and Blood Institute, Bethesda, Md); George L. Bakris,MD, Henry R. Black, MD (Rush Presbyterian-St Luke’sMedical Center, Chicago, Ill); Barry L. Carter, PharmD(University of Iowa, Iowa City); Jerome D. Cohen, MD(St Louis University School of Medicine, St Louis, Mo);Pamela J. Colman, DPM (American Podiatric MedicalAssociation, Bethesda, Md); William C. Cushman, MD(VeteransAffairsMedicalCenter,Memphis,Tenn);MarkJ.Cziraky,PharmD(HealthCore, Inc,Newark,Del); JohnJ. Davis, PA-C (American Academy of Physician Assis-tants, Memphis, Tenn); Keith Copelin Ferdinand, MD(Heartbeats Life Center, New Orleans, La); Ray W. Gif-ford, Jr,MD(ClevelandClinicFoundation,FountainHills,Ariz); Michael Glick, DMD (UMDNJ, New Jersey Den-tal School, Newark); Lee A. Green, MD, MPH (Univer-sityofMichigan,AnnArbor); StephenHavas,MD,MPH,MS (University of Maryland School of Medicine, Bal-timore); Thomas H. Hostetter, MD (National InstituteofDiabetesandDigestiveandKidneyDiseases,Bethesda,Md); Joseph L. Izzo, Jr, MD (State University of NewYork at Buffalo School of Medicine, Buffalo); Daniel W.Jones, MD (University of Mississippi Medical Center,Jackson); Lynn Kirby, RN, NP, COHNS (Sanofi-Synthelabo Research, Malvern, Pa); Kathryn M. Kolasa,PhD, RD, LDN (Brody School of Medicine at East Caro-lina University, Greenville, NC); Stuart Linas, MD (Uni-versity of Colorado Health Sciences Center, Denver);William M. Manger, MD, PhD (New York UniversityMedical Center, New York); Edwin C. Marshall, OD,MS, MPH (Indiana University School of Optometry,Bloomington); Barry J. Materson, MD, MBA (Univer-sity of Miami, Miami, Fla); Jay Merchant, MHA (Cen-ters for Medicare and Medicaid Services, Washington,DC); Nancy Houston Miller, RN, BSN (Stanford Uni-versity School of Medicine, Palo Alto, Calif ); MarvinMoser, MD (Yale University School of Medicine,Scarsdale,NY);WilliamA.Nickey,DO(PhiladelphiaCol-legeofOsteopathicMedicine,Philadelphia,Pa); SuzanneOparil,MD(UniversityofAlabamaatBirmingham);Ote-lio S. Randall, MD (Howard University Hospital, Wash-ington, DC); James W. Reed, MD (Morehouse SchoolofMedicine,Atlanta,Ga); Edward J.Roccella,PhD,MPH(National Heart, Lung, and Blood Institute, Bethesda,Md); Lee Shaughnessy (National Stroke Association,Englewood, Colo); Sheldon G. Sheps, MD (Mayo Clinic,Rochester, Minn); David B. Snyder, RPh, DDS (HealthResources and Services Administration, Rockville, Md);James R. Sowers, MD (SUNY Health Science Center atBrooklyn, Brooklyn, NY); Leonard M. Steiner, MS, OD(Eye Group, Oakhurst, NJ); Ronald Stout, MD, MPH(Procter and Gamble, Mason, Ohio); Rita D. Strick-land, EdD, RN (New York Institute of Technology,Springfield Gardens, NY); Carlos Vallbona, MD (Bay-lorCollegeofMedicine,Houston,Tex);HowardS.Weiss,MD, MPH (Georgetown University Medical Center,Washington Hospital Center, Walter Reed Army Medi-cal Center, Washington, DC); Jack P. Whisnant, MD

(Mayo Clinic and Mayo Medical School, Rochester,Minn); Gerald J. Wilson, MA, MBA (Citizens for PublicAction on High Blood Pressure and Cholesterol, Inc,Potomac,Md);MaryWinston,EdD,RD(AmericanHeartAssociation, Dallas, Tex); Jackson T. Wright, Jr, MD,PhD(CaseWesternReserveUniversity,Cleveland,Ohio);Staff: Joanne Karimbakas, MS, RD (American Insti-tutes for Research Health Program, Silver Spring, Md).Financial Disclosures: The following authors have re-ceived honoraria for serving as a speaker: Dr Choba-nian (Monarch, Wyeth, Astra-Zeneca, Solvay, Bristol-Myers Squibb); Dr Bakris (Astra-Zeneca, Abbott,Alteon, Biovail, Boerhinger-Ingelheim, Bristol-MyersSquibb, Forest, GlaxoSmithKline, Merck, Novartis, Sa-nofi, Sankyo, Solvay); Dr Black (Astra-Zeneca, Bristol-Myers Squibb, Novartis, Pfizer, Pharmacia, Wyeth-Ayerst); Dr Izzo (Boehringer-Ingelheim, Merck, Pfizer,Astra-Zeneca, Solvay, Novartis, Forest, Sankyo); DrSowers (Med Com Vascular Biology Working Group,Joslin Clinic Foundation); Dr Wright (Astra, Aventis,Bayer, Bristol-Myers Squibb, Forest, Merck, Norvar-tis, Pfizer, Phoenix Pharmaceuticals, GlaxoSmith-Kline, Solvay/Unimed).

The following authors have received funding/grantsupport for research projects: Dr Bakris (National Insti-tutes of Health, Astra-Zeneca, Abbott, Alteon, Boer-hinger-Ingelheim, Forest, GlaxoSmithKline, Merck,Novartis, Sankyo, Solvay); Dr Black (Bristol-MyersSquibb, Boehringer-Ingelheim, Merck, Pfizer, Pharma-cia); Dr Cushman (Astra-Zeneca, Merck, Pfizer, Kos,Aventis Pharma, King Pharmaceuticals, GlaxoSmith-Kline, Boehringer-Ingelheim); Dr Izzo (Boehringer-Ingelheim, Merck, Astra-Zeneca, Novartis, GlaxoSmith-Kline, Biovail); Dr Oparil (Abbott Laboratories, Astra-Zeneca, Aventis, Boehringer-Ingelheim, Bristol-MyersSquibb, Eli Lilly, Forest, GlaxoSmithKline, Monarch,Novartis [Ciba], Merck, Pfizer, Sanofi/BioClin, Scher-ing Plough, Schwarz Pharma, Scios Inc, GD Searle, Wy-eth-Ayerst, Sankyo, Solvay, Texas Biotechnology Cor-poration); Dr Sowers (Novartis, Astra-Zeneca); Dr Wright(Astra, Aventis, Bayer, Biovail, Bristol-Myers Squibb, For-est, Merck, Norvartis, Pfizer, Phoenix Pharmaceuti-cals, GlaxoSmithKline, Solvay/Unimed).

The following authors have served as a consultant/advisor: Dr Bakris (Astra-Zeneca, Abbott, Alteon,Biovail, Boerhinger-Ingelheim, Bristol-Myers Squibb,Forest, GlaxoSmithKline, Merck, Novartis, Sanofi, San-kyo, Solvay); Dr Black (Abbott, Astra-Zeneca, Biovail,Bristol-Myers Squibb, GlaxoSmithKline, Merck, Pfizer,Pharmacia); Dr Carter (Bristol-Myers Squibb); Dr Cush-man (Bristol-Myers Squibb, Sanofi, GlaxoSmithKline,Novartis, Pfizer, Solvay, Pharmacia, Takeda, Sankyo,Forest, Biovail); Dr Izzo (Merck, Astra-Zeneca, Novar-tis, Intercure, Sankyo, Nexcura); Dr Jones (Pfizer, Bristol-Myers Squibb, Merck, Forest, Novartis); Dr Manger(NHBPEP Coordinating Committee); Dr Materson(Unimed, Merck, GlaxoSmithKline, Novartis, Reliant,Tanabe, Bristol-Myers Squibb, Pfizer, Pharmacia, No-ven, Boehringer-Ingelheim, Solvay); Dr Oparil (Bristol-Myers Squibb, Merck, Pfizer, Sanofi, Novartis, The SaltInstitute, Wyeth-Ayerst).

The following author has stock holdings: Dr Izzo (In-tercure, Nexcura).

Dr Oparil is also on the Board of Directors for theTexas Biotechnology Corporation.The NHBPEP Coordinating Committee Thanks the Fol-lowing Reviewers: William B. Applegate, MD, MPH(Wake Forest University School of Medicine, Wins-ton Salem, NC); Jan N. Basile, MD (Veterans Admin-istration Hospital, Charleston, SC); Robert Carey, MD(University of Virginia Health System, Charlottes-ville, Va); Victor Dzau, MD (Brigham and Women’sHospital, Boston, Mass); Brent M. Egan, MD (Medi-cal University of South Carolina, Charleston, SC); Bo-nita Falkner, MD ( Jefferson Medical College, Phila-delphia, Pa); John M. Flack, MD, MPH (Wayne StateUniversity School of Medicine, Detroit, Mich); Ed-ward D. Frohlich, MD (Ochsner Clinic Foundation, New

THE JNC 7 REPORT




Orleans, La); Haralambos Gavras, MD (Boston Uni-versity School of Medicine, Boston, Mass); Martin Grais,MD (Feinberg School of Medicine, Northwestern Uni-versity, Chicago, Ill); Willa A. Hsueh, MD (David Gef-fen School of Medicine, University of California at LosAngeles); Kenneth A. Jamerson, MD (University ofMichigan Medical Center, Ann Arbor); Norman M.Kaplan, MD (University of Texas Southwestern Medi-cal Center, Dallas); Theodore A. Kotchen, MD (Medi-cal College of Wisconsin, Milwaukee); Daniel Levy,MD (National Heart, Lung, and Blood Institute,Framingham, Mass); Michael A. Moore, MD (WakeForest University School of Medicine and Dan RiverRegion Cardiovascular Health Initiative Program, Dan-ville, Va); Thomas J. Moore, MD (Boston UniversityMedical Center, Boston, Mass); Vasilios Papademe-triou, MD (Veterans Administration Medical Center,Washington, DC); Carl J. Pepine, MD (University ofFlorida, College of Medicine, Gainesville, Fla); Rob-ert A. Phillips, MD, PhD (New York University, LenoxHill Hospital, New York); Thomas G. Pickering, MD,DPhil (Mount Sinai Medical Center, New York, NY);L. Michael Prisant, MD (Medical College of Georgia,Augusta); C. Venkata S. Ram, MD (University of TexasSouthwestern Medical Center and Texas Blood Pres-sure Institute, Dallas); Elijah Saunders, MD (Univer-sity of Maryland School of Medicine, Baltimore); Ste-phen C. Textor, MD (Mayo Clinic, Rochester, Minn);Donald G. Vidt, MD (Cleveland Clinic Foundation,Cleveland, Ohio); Myron H. Weinberger, MD (Indi-ana University School of Medicine, Indianapolis); PaulK. Whelton, MD, MSc (Tulane University Health Sci-ences Center, New Orleans, La).Funding/Support: This work was supported entirelyby the National Heart, Lung, and Blood Institute. Theexecutive committee, writing teams, and reviewersserved as volunteers without remuneration.The NHBPEP Coordinating Committee Includes Rep-resentatives From the Following Member Organiza-tions: American Academy of Family Physicians; Ameri-can Academy of Neurology; American Academy ofOphthalmology; American Academy of Physician Assis-tants; American Association of Occupational HealthNurses; American College of Cardiology; American Col-lege of Chest Physicians; American College of Occu-pational and Environmental Medicine; American Col-legeofPhysicians-AmericanSocietyof InternalMedicine;American College of Preventive Medicine; AmericanDental Association; American Diabetes Association;American Dietetic Association; American Heart Asso-ciation; American Hospital Association; American Medi-cal Association; American Nurses Association; Ameri-can Optometric Association; American OsteopathicAssociation; American Pharmaceutical Association;American Podiatric Medical Association; American Pub-lic Health Association; American Red Cross; AmericanSociety of Health-System Pharmacists; American Soci-ety of Hypertension; American Society of Nephrology;Association of Black Cardiologists; Citizens for PublicAction on High Blood Pressure and Cholesterol, Inc;Hypertension Education Foundation, Inc; Interna-tional Society on Hypertension in Blacks; National BlackNurses Association, Inc; National Hypertension Asso-ciation, Inc; National Kidney Foundation, Inc; NationalMedical Association; National Optometric Associa-tion; National Stroke Association; NHLBI Ad Hoc Com-mittee on Minority Populations; Society for NutritionEducation; The Society of Geriatric Cardiology. Fed-eralAgencies:AgencyforHealthcareResearchandQual-ity;Centers forMedicareandMedicaidServices;Depart-ment of Veterans Affairs; Health Resources and ServicesAdministration; National Center for Health Statistics;National Heart, Lung, and Blood Institute; National Insti-tute of Diabetes and Digestive and Kidney Diseases.Acknowledgment: We appreciate the assistance ofCarol Creech, MILS, and Gabrielle Gessner, BS, fromAmerican Institutes for Research Health Program, Sil-ver Spring, Md.

REFERENCES

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14. Cushman WC, Ford CE, Cutler JA, et al. Successand predictors of blood pressure control in diverseNorth American settings: The Antihypertensive andLipid-Lowering Treatment to Prevent Heart Attack Trial(ALLHAT). J Clin Hypertens (Greenwich). 2002;4:393-404. Ra15. Black HR, Elliott WJ, Neaton JD, et al. Baselinecharacteristics and elderly blood pressure control inthe CONVINCE trial. Hypertension. 2001;37:12-18.Ra16. World Hypertension League. Measuring yourblood pressure. Available at: http://www.mco.edu/org/whl/bloodpre.html. Accessed April 1, 2003.17. Pickering T. Recommendations for the use of home(self ) and ambulatory blood pressure monitoring. AmJ Hypertens. 1996;9:1-11. Pr18. Verdecchia P. Prognostic value of ambulatoryblood pressure. Hypertension. 2000;35:844-851. Pr19. American Heart Association. Home monitoring ofhigh blood pressure. Available at: http://www.americanheart.org/presenter.jhtml?identifier=576. Ac-cessed April 1, 2003.20. Calculators and modeling aids. GFR/1.73 M2 byMDRD (±SUN and SAlb). Available at: http://www.hdcn.com/calcf/gfr.htm. Accessed April 1, 2003.21. American Diabetes Association. Treatment of hy-pertension in adults with diabetes. Diabetes Care. 2003;26(suppl 1):S80-S82. Pr22. National Kidney Foundation Guideline. K/DOQIclinical practice guidelines for chronic kidney disease:Kidney Disease Outcome Quality Initiative. Am J Kid-ney Dis. 2002;39(suppl 2):S1-S246. Pr23. The Trials of Hypertension Prevention Collabo-rative Research Group. Effects of weight loss andsodium reduction intervention on blood pressure andhypertension incidence in overweight people with high-normal blood pressure. Arch Intern Med. 1997;157:657-667. Ra24. He J, Whelton PK, Appel LJ, Charleston J, KlagMJ. Long-term effects of weight loss and dietary so-dium reduction on incidence of hypertension. Hyper-tension. 2000;35:544-549. F25. Sacks FM, Svetkey LP, Vollmer WM, et al, for theDASH-Sodium Collaborative Research Group. Ef-fects on blood pressure of reduced dietary sodium andthe Dietary Approaches to Stop Hypertension (DASH)diet. N Engl J Med. 2001;344:3-10. Ra26. Vollmer WM, Sacks FM, Ard J, et al. Effects ofdiet and sodium intake on blood pressure. Ann In-tern Med. 2001;135:1019-1028. Ra27. Chobanian AV, Hill M. National Heart, Lung, andBlood Institute Workshop on Sodium and Blood Pres-sure: a critical review of current scientific evidence.Hypertension. 2000;35:858-863. Pr

Scheme Used for Classification of the EvidenceM Meta-analysis; use of statistical methods to combine the results from clinical

trialsRa Randomized controlled trials; also known as experimental studiesRe Retrospective analyses; also known as case-control studiesF Prospective study; also known as cohort studies, including historical or pro-

spective follow-up studiesX Cross-sectional survey; also known as prevalence studiesPr Previous review or position statementsC Clinical interventions (nonrandomized)

These symbols are appended to the citations in the reference list. The studies thatprovided evidence supporting the recommendations of this report were classifiedand reviewed by the staff and the executive committee. The classification schemeis from the JNC VI report.1

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28. Kelley GA, Kelley KS. Progressive resistance ex-ercise and resting blood pressure. Hypertension. 2000;35:838-843. M29. Whelton SP, Chin A, Xin X, He J. Effect of aero-bic exercise on blood pressure. Ann Intern Med. 2002;136:493-503. M30. Xin X, He J, Frontini MG, et al. Effects of alcoholreduction on blood pressure. Hypertension. 2001;38:1112-1117. M31. Black HR, Elliott WJ, Grandits G, et al. Principalresults of the Controlled Onset Verapamil Investiga-tion of Cardiovascular End Points (CONVINCE) trial.JAMA. 2003;289:2073-2082. Ra32. Dahlof B, Devereux RB, Kjeldsen SE, et al. Car-diovascular morbidity and mortality in the Losartan In-tervention For Endpoint Reduction in HypertensionStudy (LIFE). Lancet. 2002;359:995-1003. Ra33. The ALLHAT Officers and Coordinators for the ALL-HAT Collaborative Research Group. Major outcomes inhigh-risk hypertensive patients randomized to angio-tensin-converting enzyme inhibitor or calcium channelblocker vs diuretic. JAMA. 2002;288:2981-2997. Ra34. The Heart Outcomes Prevention Evaluation StudyInvestigators. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular eventsin high-risk patients. N Engl J Med. 2000;342:145-153. Ra35. PROGRESS Collaborative Group. Randomised trialof a perindopril-based blood-pressure-lowering regi-men among 6105 individuals with previous stroke ortransient ischaemic attack. Lancet. 2001;358:1033-1041. Ra36. Wing LMH, Reid CM, Ryan P, et al, for SecondAustralian National Blood Pressure Study Group. Acomparison of outcomes with angiotensin-converting-enzyme inhibitors and diuretics for hypertension in theelderly. N Engl J Med. 2003;348:583-592. Ra37. Psaty BM, Smith NL, Siscovick DS, et al. Healthoutcomes associated with antihypertensive therapiesused as first-line agents. JAMA. 1997;277:739-745.M38. Physicians’ Desk Reference. 57th ed. Oradell, NJ:Medical Economics; 2003.39. Psaty BM, Manolio TA, Smith NL, et al. Time trendsin high blood pressure control and the use of antihy-pertensive medications in older adults. Arch Intern Med.2002;162:2325-2332. X40. Hunt SA, Baker DW, Chin MH, et al. ACC/AHAguidelines for the evaluation and management of chronicheart failure in the adult. J Am Coll Cardiol. 2001;38:2101-2113. Pr41. Tepper D. Frontiers in congestive heart failure:effect of metoprolol CR/XL in chronic heart failure.Congest Heart Fail. 1999;5:184-185. Ra42. Packer M, Coats AJ, Fowler MB, et al. Effect ofcarvedilol on survival in severe chronic heart failure.N Engl J Med. 2001;344:1651-1658. Ra43. CIBIS Investigators and Committees. A random-ized trial of beta-blockade in heart failure: the Car-diac Insufficiency Bisoprolol Study (CIBIS). Circula-tion. 1994;90:1765-1773. Ra44. The SOLVD Investigators. Effect of enalapril onsurvival in patients with reduced left ventricular ejec-tion fractions and congestive heart failure. N EnglJ Med. 1991;325:293-302. Ra45. The Acute Infarction Ramipril Efficacy (AIRE) StudyInvestigators. Effect of ramipril on mortality and mor-bidity of survivors of acute myocardial infarction withclinical evidence of heart failure. Lancet. 1993;342:821-828. Ra46. Kober L, Torp-Pedersen C, Carlsen JE, et al, forTrandolapril Cardiac Evaluation (TRACE) Study Group.A clinical trial of the angiotensin-converting-enzymeinhibitor trandolapril in patients with left ventricular

dysfunction after myocardial infarction. N Engl J Med.1995;333:1670-1676. Ra47. Cohn JN, Tognoni G. A randomized trial of theangiotensin-receptor blocker valsartan in chronic heartfailure. N Engl J Med. 2001;345:1667-1675. Ra48. Pitt B, Zannad F, Remme WJ, et al, for Random-ized Aldactone Evaluation Study Investigators. Theeffect of spironolactone on morbidity and mortalityin patients with severe heart failure. N Engl J Med.1999;341:709-717. Ra49. Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA 2002 guideline update for the management ofpatients with unstable angina and non-ST-segmentelevation myocardial infarction. J Am Coll Cardiol.2002;40:1366-1374. Pr50. �-Blocker Heart Attack Trial Research Group. Arandomized trial of propranolol in patients with acutemyocardial infarction, I: mortality results. JAMA. 1982;247:1707-1714. Ra51. Hager WD, Davis BR, Riba A, et al, for the Sur-vival and Ventricular Enlargement (SAVE) Investiga-tors. Absence of a deleterious effect of calcium chan-nel blockers in patients with left ventricular dysfunctionafter myocardial infarction: the SAVE Study Experi-ence. Am Heart J. 1998;135:406-413. Ra52. The Capricorn Investigators. Effect of carvedilolon outcome after myocardial infarction in patients withleft-ventricular dysfunction: the CAPRICORN ran-domised trial. Lancet. 2001;357:1385-1390. Ra53. Pitt B, Remme W, Zannad F, et al. Eplerenone, aselective aldosterone blocker, in patients with left ven-tricular dysfunction after myocardial infarction. N EnglJ Med. 2003;348:1309-1321. Ra54. UK Prospective Diabetes Study Group. Efficacy ofatenolol and captopril in reducing risk of macrovas-cular and microvascular complications in type 2 dia-betes: UKPDS 39. BMJ. 1998;317:713-720. Ra55. Lewis EJ, Hunsicker LG, Bain RP, Rohde RD. Theeffect of angiotensin-converting-enzyme inhibition ondiabetic nephropathy: The Collaborative Study Group.N Engl J Med. 1993;329:1456-1462. Ra56. Brenner BM, Cooper ME, de Zeeuw D, et al. Ef-fects of losartan on renal and cardiovascular out-comes in patients with type 2 diabetes and nephropa-thy. N Engl J Med. 2001;345:861-869. Ra57. Lewis EJ, Hunsicker LG, Clarke WR, et al. Reno-protective effect of the angiotensin-receptor antago-nist irbesartan in patients with nephropathy due to type2 diabetes. N Engl J Med. 2001;345:851-860. Ra58. The GISEN (Gruppo Italiano di Studi Epidemio-logici in Nefrologia) Group. Randomised placebo-controlled trial of effect of ramipril on decline in glo-merular filtration rate and risk of terminal renal failurein proteinuric, non-diabetic nephropathy. Lancet. 1997;349:1857-1863. Ra59. Wright JT Jr, Agodoa L, Contreras G, et al. Suc-cessful blood pressure control in the African Ameri-can Study of Kidney Disease and Hypertension. ArchIntern Med. 2002;162:1636-1643. Ra60. Bakris GL, Weir MR, for the Study of Hyperten-sion and Efficacy of Lotrel in Diabetes (SHIELD) In-vestigators. Achieving goal blood pressure in pa-tients with type 2 diabetes. J Clin Hypertens(Greenwich). 2003;5:201-210. Ra61. Antithrombotic Trialist Collaboration. Collabora-tive meta-analysis of randomised trials of antiplatelettherapy for prevention of death, myocardial infarc-tion, and stroke in high risk patients. BMJ. 2002;324:71-86. M62. Pfeffer MA, Braunwald E, Moye LA, et al, for theSAVE Investigators. Effect of captopril on mortality andmorbidity in patients with left ventricular dysfunc-tion after myocardial infarction. N Engl J Med. 1992;327:669-677. Ra

63. Lindholm LH, Ibsen H, Dahlof B, et al. Cardio-vascular morbidity and mortality in patients with dia-betes in the Losartan Intervention For Endpoint re-duction in hypertension study (LIFE). Lancet. 2002;359:1004-1010. Ra64. Bakris GL, Williams M, Dworkin L, et al, for Na-tional Kidney Foundation Hypertension and Diabe-tes Executive Committees Working Group. Preserv-ing renal function in adults with hypertension anddiabetes. Am J Kidney Dis. 2000;36:646-661. Pr65. Bakris GL, Weir MR. Angiotensin-converting en-zyme inhibitor-associated elevations in serum creati-nine. Arch Intern Med. 2000;160:685-693. M66. National Cholesterol Education Program. Third Re-port of the National Cholesterol Education Program(NCEP) Expert Panel on Detection, Evaluation, andTreatment of High Blood Cholesterol in Adults (AdultTreatment Panel III) final report. Circulation. 2002;106:3143-3421. Pr67. Kjeldsen SE, Dahlof B, Devereux RB, et al. Ef-fects of losartan on cardiovascular morbidity and mor-tality in patients with isolated systolic hypertension andleft ventricular hypertrophy: a Losartan Interventionfor Endpoint Reduction (LIFE) substudy. JAMA. 2002;288:1491-1498. Ra68. Hyman DJ, Pavlik VN. Characteristics of patientswith uncontrolled hypertension in the United States.N Engl J Med. 2001;345:479-486. X69. Staessen JA, Wang J. Blood-pressure lowering forthe secondary prevention of stroke [commentary]. Lan-cet. 2001;358:1026-1027.70. Di Bari M, Pahor M, Franse LV, et al. Dementiaand disability outcomes in large hypertension trials:lessons learned from the Systolic Hypertension in theElderly Program (SHEP) trial. Am J Epidemiol. 2001;153:72-78. Ra71. Writing Group for the Women’s Health InitiativeInvestigators. Risks and benefits of estrogen plus pro-gestin in healthy postmenopausal women. JAMA. 2002;288:321-333. Ra72. National High Blood Pressure Education Pro-gram. Report of the National High Blood Pressure Edu-cation Program Working Group on high blood pres-sure in pregnancy. Am J Obstet Gynecol. 2000;183:S1-S22. Pr73. National High Blood Pressure Education Pro-gram Working Group on Hypertension Control in Chil-dren and Adolescents. Update on the 1987 Task ForceReport on high blood pressure in children and ado-lescents. Pediatrics. 1996;98:649-658. Pr74. Barlow SE, Dietz WH. Obesity evaluation andtreatment: expert committee recommendations.Pediatrics. 1998;102:E29. Pr75. Barrier PA, Li JT, Jensen NM. Two words to im-prove physician-patient communication: what else?Mayo Clin Proc. 2003;78:211-214. Pr76. Betancourt JR, Carrillo JE, Green AR. Hyperten-sion in multicultural and minority populations. Curr Hy-pertens Rep. 1999;1:482-488.77. Phillips LS, Branch WT, Cook CB, et al. Clinicalinertia. Ann Intern Med. 2001;135:825-834.78. Balas EA, Weingarten S, Garb CT, et al. Improv-ing preventive care by prompting physicians. ArchIntern Med. 2000;160:301-308. C79. Boulware LE, Daumit GL, Frick KD, et al. An evi-dence-based review of patient-centered behavioral in-terventions for hypertension. Am J Prev Med. 2001;21:221-232. Pr, M80. Hill MN, Miller NH. Compliance enhancement: acall for multidisciplinary team approaches. Circula-tion. 1996;93:4-6.81. Flegal KM, Carroll MD, Ogden CL, Johnson CL.Prevalence and trends in obesity among US adults,1999-2000. JAMA. 2002;288:1723-1727. X

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Each child donated a deciduous superior incisor, lost in theprevious months. Donated teeth were washed and organic wash-ing was assayed to ascertain contamination from external nico-tine.Subsequently,nicotineandcotininewereextractedfrompow-deredteethbyorganicsolventandanalyzedbygaschromatographyand mass spectrometry.5 The homogeneity of nicotine and coti-nine content were verified in those cases in which the donatedteeth were pairs of 2 superior incisors (n=3). A univariate linearregression analysis was conducted to assess a dose-response rela-tionship between childhood exposure to ETS and log-transformedvaluesofnicotineandcotinineconcentrations inteeth.

Results. Teeth from 35 children (mean [SD] age, 7.4 [0.6] years)from nonsmoking and smoking parents were examined. Exter-nal nicotine contamination was negligible, and the concentra-tions of analytes were similar (difference, �5%) in the 3 matchedpairs of superior incisors. Nicotine concentration in teeth (TABLE)statistically discriminated between children exposed and not ex-posed to parental smoking even during pregnancy, as measuredby questionnaire, by the average value of parental daily consump-tion of nicotine and by average levels of exposure to tobacco smokeduring childhood. Cotinine concentrations in teeth, althoughshowing a trend similar to those of nicotine, did not have a sta-tistically significant relationship to ETS.

Comment. Aligne et al6 recently reported an association be-tween ETS and risk of dental caries among children. The au-thors speculated that levels of serum cotinine might provide agood estimate of exposure to tobacco smoke in infancy. Thereis no biomarker, however, that accounts for cumulative expo-sure to ETS during the whole childhood. Our data suggest thatconcentrations of nicotine in teeth may be a promising nonin-vasive tool for monitoring and categorizing cumulative expo-sure to environmental tobacco smoke during the entirety of child-hood. It is possible that nicotine reaches the inside of the toothby systemic circulation and can be accumulated together withlesser amounts of its metabolite, cotinine, during fetal life.

Oscar Garcia-Algar, MD, PhDOriol Vall, MD, PhDPaediatric ServiceHospital del MarBarcelona, Spain

Jordi Segura, PhDJose Antonio Pascual, PhDDavid Diaz, BScUnit of PharmacologyLaura Munoz, BScInstitut Municipal d’Investigacio Medica (IMIM)Pompeu Fabra UniversityBarcelonaPiergiorgio Zuccaro, PhDRoberta Pacifici, PhDSimona Pichini, PhDIstituto Superiore di Sanita (ISS)Rome, Italy

Funding/Support: This study was supported in part by Progetto N. 1 “Area Pro-getto Droga” from Istituto Superiore di Sanita, Rome, Italy, and Fondo de Inves-tigaciones Sanitarias (FIS-00/0021-01), Spain.Acknowledgment: We thank the Gianni Rodari primary school of Rome, Italy, forhelp with recruitment of children for this study.

1. Jaakkola MS, Jaakkola JJ. Assessment of exposure to environmental tobaccosmoke. Eur Respir J. 1997;10:2384-2397.2. Pichini S, Basagana X, Pacifici R, et al. Cord serum cotinine as a biomarker offetal exposure to cigarette smoke at the end of pregnancy. Environ Health Per-spect. 2000;108:1079-1083.3. Pichini S, Altieri I, Pellegrini M, Pacifici R, Zuccaro P.The analysis of nicotine ininfants’ hair for measuring exposure to environmental tobacco smoke: prelimi-nary results. Forensic Sci Int. 1997;84:253-258.4. Ostrea EM, Knapp K, Romero A, Montes M, Ostrea AR. Meconium analysis toassess fetal exposure to nicotine by active and passive maternal smoking. J Pedi-atr. 1994;124:471-476.5. Shin HS, Kim JG, Shin YJ, Jee SH. Sensitive and simple method for the deter-mination of nicotine and cotinine in human urine, plasma and saliva by gas chro-matography-mass spectrometry. J Chromatogr B Analyt Technol Biomed Life Sci.2002;769:177-183.6. Aligne CA, Moss ME, Auinger P, Weitzman M. Association of pediatric dentalcaries with passive smoking. JAMA. 2003;289:1258-1264.

CORRECTION

Incorrect Drug Trade Names: In the Special Communication entitled “The Sev-enth Report of the Joint National Committee on Prevention, Detection, Evalua-tion, and Treatment of High Blood Pressure: the JNC 7 Report” published in theMay 21, 2003, issue of THE JOURNAL (2003;289:2560-2572), there were incorrectdrug trade names in TABLE 4 and TABLE 5. On page 2566, in Table 4, the tradename “Tevetan” should have read “Teveten” and on page 2567, in Table 5, thetrade name “Aldactone” should have read “Aldactazide.” In addition, on page2565, in column 1, the first full sentence should have read “When BP is more than20 mm Hg above the systolic BP goal or 10 mm Hg above the diastolic BP goal,consideration should be given to initiating therapy with 2 drugs, either as sepa-rate prescriptions or in fixed-dose combinations (Figure).”

LETTERS

©2003 American Medical Association. All rights reserved. (Reprinted) JAMA, July 9, 2003—Vol 290, No. 2 197



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