Prevalence and Correlates of Left Ventricular Hypertrophyin the African American Study of Kidney Disease

Cohort StudyGail E. Peterson, Tine de Backer, Avril Gabriel,* Vladimir Ilic, Tudor Vagaonescu, Lawrence J. Appel,

Gabriel Contreras, Cindy Kendrick, Stephen Rostand, Robert A. Phillips; for the African AmericanStudy of Kidney Disease Investigators

Abstract—African Americans with hypertensive renal disease represent a high-risk population for cardiovascular events.Although left ventricular hypertrophy is a strong predictor of adverse cardiac outcome, the prevalence and associatedfactors of left ventricular hypertrophy in this patient population are not well described. The African American Study ofKidney Disease Cohort Study is a prospective, observational study that is an extension of the African American Studyof Kidney Disease randomized clinical trial that was conducted from 1994 to 2001 in African Americans withhypertension and mild-to-moderate renal dysfunction. Echocardiograms and 24-hour ambulatory blood pressuremonitoring were performed at the baseline visit of the cohort. Of 691 patients enrolled in the cohort study, 599 patientshad interpretable baseline echocardiograms and ambulatory blood pressure data. Left ventricular hypertrophy wasdefined using a cut point for left ventricular mass index �49.2 g/m2.7 in men and �46.7 m/m2.7 in women. The majorityof patients had left ventricular hypertrophy (66.7% of men and 73.9% of women). In a multiple regression analysis,higher average day and nighttime systolic blood pressure, younger age, and lower predicted glomerular filtration ratewere associated with left ventricular hypertrophy, but albuminuria was not. These data demonstrate a striking prevalenceof left ventricular hypertrophy in the African American Study of Kidney Disease Cohort and identify potential targetsfor prevention and therapeutic intervention in this high-risk patient population. (Hypertension. 2007;50:1033-1039.)

Key Words: hypertension � hypertrophy � left ventricular � echocardiography � African Americans� kidney failure � chronic � blood pressure monitoring � ambulatory

African Americans with hypertension are at increased riskof cardiovascular morbidity and mortality and have

more frequent progression to end-stage renal disease com-pared with other ethnic groups in the United States.1–5 Inaddition, those patients who develop chronic kidney diseaseare at even greater risk for cardiovascular mortality.6 WhyAfrican Americans are a particularly high-risk group is notfully understood. Left ventricular hypertrophy (LVH) is astrong independent predictor of adverse cardiovascularevents, and several studies have found a higher prevalence forLVH in African Americans compared with whites.7–9

The African American Study of Kidney disease (AASK)cohort involves African American patients with nondiabetic,hypertensive renal disease. The prevalence and associatedfactors of target-organ damage, such as LVH, in this patientpopulation have not been well described previously. In

addition, echocardiographic data in this patient population arevirtually nonexistent; to our knowledge only 1 other study hasspecifically assessed echocardiographic findings in a smallnumber of African Americans with hypertensive renal dis-ease.10 Because this population is at high risk for cardiovas-cular events, the AASK cohort is an ideal group of patients inwhich to evaluate to identify the frequency and correlates ofLVH to help target those patients who may benefit fromaggressive therapy for risk reduction.

MethodsStudy PopulationThe AASK Cohort Study is a prospective, observational study that isan extension of the AASK, which tested the effects of 3 medicationsused as initial antihypertensive therapy (ramipril, metoprolol, andamlodipine) and usual (mean arterial pressure of 102 to 107 mm Hg)

Received March 7, 2007; first decision April 16, 2007; revision accepted September 26, 2007.From the Division of Cardiology (G.E.P.), University of Texas Southwestern Medical Center, Dallas; Cardiovascular Research Foundation (T.d.B.,

V.I., T.V.), New York, NY; Lenox Hill Hospital (A.G.), New York, NY; University of Medicine and Dentistry, New Jersey-Robert Wood JohnsonMedical School (T.V.), New Brunswick, NJ; Johns Hopkins (L.J.A.), Baltimore, Md; University of Miami (G.C.), Fla; Biostatistics and Epidemiology(C.K.), Cleveland Clinic, Ohio; University of Alabama (S.R.), Birmingham; and the University of Massachusetts Memorial Medical Center and MedicalSchool (R.A.P.), Worcester.

*Deceased.Correspondence to Gail E. Peterson, Division of Cardiology, University of Texas Southwestern Medical Center, 5909 Harry Hines Blvd, HA9.133,

Dallas, TX 75235-9047. E-mail Gail.Peterson@UTSouthwestern.edu© 2007 American Heart Association, Inc.

Hypertension is available at http://hyper.ahajournals.org DOI: 10.1161/HYPERTENSIONAHA.107.090613

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or lower (mean arterial pressure �93 mm Hg) blood pressure (BP)control. Eligible patients enrolled in the AASK were AfricanAmerican men and women with hypertension, between the ages of18 and 70, diastolic BP of �95 mm Hg, with a glomerular filtrationrate (GFR) of 20 to 65 mL/min per 1.73 m2 and no apparent cause ofrenal insufficiency other than hypertension. The clinical compositeoutcome was reduction in GFR by 50% from baseline, the develop-ment of end-stage renal disease, or death. During the trial, mean BPwas 128/89 mm Hg (�12/8 mm Hg) in the lower BP group and141/85 mm Hg (�12/7 mm Hg) in the usual BP group. There was nodifference in the progression of kidney disease or in the clinicalcomposite outcome between the 2 BP groups. The ramipril grouphad a significant reduction in the composite outcome compared withthe metoprolol and amlodipine groups. Based on the results, in theabsence of contraindications, patients in the cohort phase weretreated with an angiotensin-converting enzyme inhibitor.

All participants in the AASK who had not died or reachedend-stage renal disease were invited to enroll in the cohort study. Thestudy was approved by the institutional review committee at eachparticipating site and adhered to the principles of the Declaration ofHelsinki and Title 45, US Code of Federal Regulations, Part 46,Protection of Human Subjects. All of the subjects gave informedconsent, and procedures followed were in accordance with institu-tional guidelines. Patients enrolled in the AASK Cohort Study hadexcellent BP control during the trial. The average mean BP of cohortparticipants during the trial was 98 mm Hg (�8 mm Hg;93�7 mm Hg in the lower BP group and 104�5 mm Hg in the usualBP group). Details of the study design and inclusion/exclusioncriteria have been reported elsewhere.11

EchocardiographyPatients enrolled in the cohort had an echocardiogram performed attheir baseline visit. M-mode, 2D, and Doppler echocardiographyexaminations were performed at each of the 21 enrolling centersusing commercially available equipment. To ensure data quality,echocardiograms were obtained by trained technologists using astandardized protocol and read centrally at the AASK CardiovascularCore Laboratory. At the core laboratory, echocardiographic tracingswere coded, digitized, and interpreted blindly using the DigiViewDigital/Video System(s), Model DV-DVRS-100 (Digisonics, Inc).An average of 3 measurements was made of each variable. Theend-diastolic (LVIDds) and end-systolic LV internal diameters(LVIDs), interventricular septal thickness, and the posterior wallthickness (PWT) were measured from 2D guided M-mode tracings,according to the American Society of Echocardiography guide-lines.12 When optimal orientation was not possible, measurementswere made using 2D views.13 Left ventricular mass (LVM) wascalculated using an anatomically validated formula14 and normalizedto allometric height.15 LVH as defined according to gender-specificcriterion as LVM index �49.2 g/m2.7 in men and �46.7 g/m2.7

in women.

MethodsRelative wall thickness (RWT) was calculated using the formula(2 PWT)/LVIDd. A concentric remodeling pattern was defined asan RWT � 0.44.16 Left ventricular systolic function was assessedby endocardial fractional shortening [(LVIDd�LVIDDs)/LVIDd]. Echocardiograms were read by 1 of 5 echocardio-graphers. Intraclass correlation statistics showed good agreementbetween measurements (M-mode LVM: 0.72; mitral E wave to Awave ratio: 0.93). Likewise, there was good intrarater variability(eg, mean difference in M-mode LVM was 17.35 g [SD: 27.81],and mean difference of mitral E/A ratio was 0.03 [SD: 0.08]).

BP MeasurementsOffice BP was measured in a standardized method by trained andcertified observers using the Tycos Classic handheld Aneroid device.Two BP measurements were obtained in the seated position and 1 inthe upright position. Patients were encouraged to have their BPmanaged by the AASK cohort staff based as outlined previously.11

Ambulatory BP monitoring (ABPM) was performed over a24-hour period, using the SpaceLabs 90217 Ultralite or SpaceLabs90207 devices. During each 24-hour recording, measurements wereobtained every 30 minutes from which awake and asleep averageswere calculated, along with dipping status. Nighttime BP wasdefined as 12:00 AM to 6:00 AM. A blunted BP at night, the so-callednondipping pattern, was defined as �10% fall in average systolicBP (SBP).

Other MeasurementsUrinary albumin excretion was determined by measuring 24-houralbumin and creatinine levels. A urine albumin: creatinine ratio of�0.22 was used to define albuminuria.

Estimated GFR (eGFR) was calculated from serum creatinine usingan equation developed from baseline data in the AASK trial.17 Specif-ically, eGFR�329�(serum creatinine)�1.096�(age)�0.294�(0.736 forwomen).

Statistical AnalysisBaseline characteristics were summarized as means and SDs forcontinuous variables and as frequencies and percentages for categor-ical variables and were compared between those with and withoutLVH using a 2-sample t test or �2 test, as appropriate. Multiple linearregression analysis was used to relate LVM to the followingprespecified predictor variables: average daytime SBP, averagenighttime SBP, eGFR, age, hematocrit (%), gender, and the log-transformed urine albumin:creatinine ratio. Results of all of thestatistical tests are reported as 2-sided P values, without adjustmentfor multiple comparisons.

ResultsStudy ParticipantsOf the 1094 participants in the AASK, 787 patients were aliveand not on dialysis, and 691 individuals agreed to enrollmentin the cohort study. Baseline echocardiograms were obtainedin 649 patients, of whom 41 lacked ABPM data and 8 lackedmeasurable LVM. Therefore, 599 patients were evaluated forthis report.

Tables 1 to 3 present characteristics of participants overalland stratified by LVH. Overall, the mean age of participantswas 60.1�10.1 years), and 38.4% were women. Averagebody mass index was 31.2�6.98 kg/m2. The mean hematocritwas 38.4�5.3%. eGFR averaged 44.2�16.5 mL/min per 1.73m2, and average serum creatinine was 2.25�1.35 mg/dL.Albuminuria was present in 12.6% of patients. Additionalcharacteristics are shown in Table S1 (please see http://hyper.ahajournals.org).

BP measurements are displayed in Table 2. Average clinicBP was 135�21.5/80�12.4 mm Hg. Average ambulatorydaytime SBP was 138�17 mm Hg, and average nighttimeSBP was 134�21 mm Hg. Average 24-hour pulse pressurewas 56.1�12.5 mm Hg.

Echocardiographic characteristics are shown in Table 3.The majority of patients had normal left ventricular systolicfunction as measured by fractional shortening (average:38�10%). A high proportion of patients had evidence fordiastolic dysfunction, with a median E wave to A wave ratioof 0.92�0.38. Left atrial size was enlarged (mean area:19.2�5.12 cm2. Concentric remodeling was common in thispopulation (mean RWT: 0.53�0.13). Of the patient popula-tion, 69.4% had LVH (66.7% of men and 73.9% of women).The mean LVM index was 60.9�21.6 g/m2.7 overall;60.5�21.0 g/m2.7 in men, and 61.7�22.5 g/m2.7 in women.

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Factors Associated With LVHVariables predictive of LVH were younger age, greater bodymass index, the presence of albuminuria, higher average dayand average nighttime SBP, and higher 24-hour pulse pres-sure. Table 2 shows the correlations between LVH and clinicand ABPM values. Average 24-hour SBP, average day SBP,and average night SBP were all highly predictive of LVH.The difference between daytime and nighttime BP was notsignificantly associated with LVH.

Echocardiographic characteristics associated with the pres-ence of LVH (Table 3) include greater internal diastolic andsystolic dimensions, greater wall thicknesses, larger aorticroot diameter and left atrial size, higher RWT, and higherDoppler stroke volume. Patients with LVH had lower heartrates but a similar cardiac index and fractional shortening.

The Figure shows the joint relationship of daytime andnighttime SBP by quartiles with mean LVM. Independentrelationships were observed between the degree of LVH andprogressive increases in both BP indices as fixed levels of theother index.

Multivariable AssociationsOn multiple regression analysis (adjusted R2�0.10), greateraverage nighttime and daytime SBP, lower estimated eGFR,

and younger age were independent correlates of LVH (Table4). Hematocrit and the presence of microalbuminuria werenot independently associated with LVH.

DiscussionThis study represents the first comprehensive systematicexamination of the prevalence and correlates of LVH inAfrican American patients with hypertensive kidney dysfunc-tion, a population at very high risk for cardiovascular disease.Despite adequate BP control over 5 years before evaluation,there was an extraordinarily high prevalence of LVH in theAASK cohort. In most series, only �30% of patients withhypertension have LVH18 compared with �70% in theAASK Cohort Study.

Our findings point to both direct and potentially indirecteffects of BP on LVH. In particular, ABPM values werehighly correlated with LVH. We found that the most predic-tive value for LVH in this patient population was averagedaytime SBP based on ABPM. Our finding is consistent withother studies that have shown a direct relationship betweenLVH and SBP as measured either by ABPM or office BPaveraged over a 30-year period.19–21 In the Framinghampopulation, a continuous association between SBP and LVH

Table 1. Demographic and Clinical Data: Comparison Between Patients With and Without LVH

VariableAll Patients

(n�599)LVH

(n�416)No LVH(n�183) P

Age, mean�SD 60.1�10.1 59.4�10.1 61.9�10.0 0.0055

Gender, n (%), % female 230.0 (38.4) 170.0 (40.9) 60.0 (32.8) 0.0611

Body mass index, mean�SD, kg/m2 31.2�6.98 32.6�7.09 27.9�5.48 0.0001

Smoking status, n (%) 0.2107

Never smoked 244.0 (40.8) 176.0 (42.4) 68.0 (37.2)

Currently smoking 105.0 (17.6) 76.0 (18.3) 29.0 (15.8)

Past smoker 249.0 (41.6) 163.0 (39.3) 86.0 (47.0)

Hematocrit, mean�SD, % 38.4�5.27 38.2�5.12 38.9�5.59 0.193

eGFR, mean�SD, mL/min/1.73 m2 44.2�16.5 43.4�16.3 46.1�17.0 0.0734

Serum creatinine, mean�SD, mg/dL 2.25�1.35 2.30�1.48 2.14�1.00 0.1164

Serum cholesterol, mean�SD, mg/dL 201.0�45.5 202.0�45.8 199.0�44.7 0.3787

Albuminuria, n (%), UACR �0.22 75.0 (12.6) 66.0 (15.9) 9.0 (4.9) 0.0002

UACR indicates urinary albumin:creatinine ratio.

Table 2. Association of BP Measurements with LVH

Variable, mm HgAll Patients (n�599),

Mean�SDLVH (n�416),

Mean�SDNo LVH (n�183),

Mean�SD P

Baseline clinic SBP 135.0�21.5 138.0�21.1 131.0�21.6 0.0003

Baseline clinic DBP 80.7�12.4 81.6�12.8 78.8�11.3 0.0068

Baseline clinic pulse pressure 54.6�16.6 55.9�16.5 51.8�16.7 0.0057

24-h pulse pressure 56.1�12.5 58.0�12.5 51.6�11.4 0.0001

24-h average SBP 136.0�18.0 139.0�18.0 130.0�16.6 0.0001

24-h average DBP 80.0�11.2 80.7�11.5 78.3�10.3 0.0126

Average day SBP 138.0�17.0 140.0�16.8 132.0�16.2 0.0001

Average day DBP 82.6�10.8 83.2�10.9 81.3�10.5 0.0388

Average night SBP 134.0�21.0 137.0�21.1 128.0�19.2 0.0001

Average night DBP 77.3�13.0 78.2�13.6 75.4�11.6 0.01

Average day-night SBP 3.26�12.8 2.80�12.9 4.31�12.7 0.1818

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was found even at BP levels considered to be in the normal ornear-reference range.22 Most investigators have found thatSBP is better correlated with LVH than diastolic BP19,20 andthat ABPM is a better predictor of LVH than clinic BP.20

Average nighttime SBP was also strongly predictive ofLVH. Although average daytime SBP was reasonably wellcontrolled in our population, average nighttime SBP waselevated. In other studies, African Americans have beenshown to have higher nighttime BP than whites despitesimilar daytime BP.23,24 The majority of patients with uncom-plicated hypertension experience a fall in their nighttime BPof �10% of the daytime mean arterial BP. The absence of afall in nocturnal BP has been linked to target organ damage,such as carotid artery structural alterations and LVH in somestudies25–29 but not others.30,31 Observational studies haveshown that hypertensive patients with elevated nighttime BPare at greater risk for experiencing cardiovascular outcomesand stroke compared with hypertensive patients with anormal decrease in nocturnal BP.25,32 In our patient popula-

tion there was an additive relationship between nighttime anddaytime SBP, with the greater LVM occurring in patient inthe upper quartiles of both night and day SBP.

Unlike previous studies, we found that younger age wasassociated with greater LVM in this cohort population. TheAASK cohort population is derived from a high-risk, olderpopulation followed through the 5-year AASK and is com-posed of survivors who had not died or reached end-stagerenal disease. Therefore, this unexpected finding may representa survival bias; those patients who were older with lower LVMand those who were younger (with or without high LVM) mayhave been less likely to reach an outcome in the trial, and,therefore, were eligible for enrollment in the cohort study.

We did not find an independent relationship between thepresence of albuminuria and LVH. This observation contrastswith some33,34 but not other35,36 studies where albuminuriacorrelated with LVM. Many of these studies measured clinicrather than ambulatory BP.33 ABPM values (particularlyambulatory SBP) have been shown to have a closer associa-tion with LVM compared with office measurements.35,37–39

The use of ABPM data in our analysis may be one reason forthe lack of an independent association between urinaryalbumin excretion and LVH. Other studies using ABPM intheir analysis have also found a lack of independent associ-ation between albuminuria and LVH.35,36 Unlike other studiesevaluating albuminuria, the vast majority of patients (75%) inthe AASK cohort were treated with angiotensin-convertingenzyme inhibitors. Increased renin-angiotensin activity hasbeen associated with the presence of microalbuminuria andtarget organ damage,40 and it is possible that the widespreaduse of angiotensin-converting enzyme inhibitors in our pa-tient population accounted in part for the lack of associationin our study. Previous studies also excluded patients withrenal insufficiency,33–35 whereas all of the AASK cohortpatients had established hypertensive renal dysfunction.

Table 3. Echocardiographic Data: Comparison Between Patients With and Without LVH

Variable All Patients (n�599) LVH (n�416) No LVH (n�183) P

LVIDd, mean�SD, mm 48.4�6.70 50.1�6.49 44.3�5.30 0.0001

LVIDs, mean�SD, mm 28.8�6.85 30.1�7.04 25.8�5.34 0.0001

IVST, mean�SD, mm 13.4�2.91 14.2�2.81 11.6�2.30 0.0001

PWT, mean�SD, mm 12.7�2.46 13.4�2.39 11.1�1.81 0.0001

Aortic root diameter, mean�SD, mm 34.2�5.10 34.8�5.04 33.0�5.03 0.0001

Left atrium diameter, mean�SD, mm 41.2�6.95 43.0�6.55 37.2�6.08 0.0001

Left atrial area, mean�SD, cm2 19.2�5.12 20.4�5.21 16.6�3.72 0.0001

LV mass index, mean�SD, g/m2.7 60.9�21.6 70.0�19.6 40.2�6.07 0.0001

RWT, mean�SD 0.53�0.13 0.55�0.14 0.51�0.11 0.0003

RWT�0.44, n (%) 467.0 (78.0) 329.0 (79.1) 138.0 (75.4) 0.3173

Fractional shortening, mean�SD, % 0.38�0.10 0.38�0.10 0.38�0.10 0.8899

Doppler SV, mean�SD, mL 98.9�58.9 103.0�60.2 89.8�55.0 0.0124

Doppler cardiac index, mean�SD, L/min/m2 3.03�1.67 3.08�1.72 2.92�1.54 0.3413

SV/PP ratio, mean�SD 1.72�1.12 1.73�1.12 1.69�1.14 0.6902

SV/PP ratio, mean�SD, 24-h pulse pressure 1.83�1.14 1.84�1.12 1.81�1.17 0.7632

Heart rate, mean�SD 67.0�13.4 66.1�13.0 69.5�13.9 0.0117

IVST indicates intraventricular wall thickness; PWT, posterior wall thickness; SV, stroke volume; SV/PP ratio, stroke volume:pulsepressure ratio.

0

50

100

150

200

250

300

Day SBP>149

Day SBP136-149

Day SBP126-136

Day SBP< 126

Night SBP < 120

Night SBP 120-133

Night SBP 133-147

Night SBP > 147

Figure. Joint association of mean LVM with quartiles of day andnight SBP.

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Therefore, in patients with established renal dysfunction, theadditional presence of albuminuria may be less stronglyassociated with LVH.

We found GFR to be a predictor of LVH independent ofBP (measured at the time of enrollment in the cohort) and thehemodynamic effects of anemia. An association betweenrenal dysfunction and LVH has been described by others inrecent studies. Data from the Framingham Study, a predom-inately white population, has shown that patients with evenmild renal impairment have twice the prevalence of coronarydisease, heart failure, ischemic stroke, and LVH,41 althoughthe results were not adjusted for BP. In an exclusively whitepopulation with normal serum creatinine, abnormal renalfunction as defined by GFR �60 mL/min per 1.73 m2 or thepresence of microalbuminuria was associated with increasedLVM.42 The only other study to date identifying a relation-ship between GFR and LVH in an African American popu-lation is the Atherosclerosis Risk in Communities Study. Inthis population study of 1968 African Americans, those withmoderately reduced kidney function (32 patients) had greaterLVM after adjusting for age, sex, BP, and hemoglobin.10 Ourstudy of a large group of African Americans with moderaterenal dysfunction confirms the Atherosclerosis Risk in Com-munities Study findings.

The association between renal dysfunction and LVH mayexplain in part the high cardiovascular morbidity and mortal-ity observed in African Americans with hypertensive kidneydisease. Although the mechanism of this association is notfully understood, factors associated with renal impairment,including increased calcium-phosphorus product,43 hyper-phosphoremia,44 parathormone,43,45 sympathetic nervous sys-tem activity,46,47 and activation of the renin-angiotensin-aldo-sterone system,48 may contribute to the target-organ damageand cardiovascular risk in these patients as well. The rela-tionship of reduced eGFR with LVH in this population mayalso represent an indirect effect of sustained BP elevationover time. Our results emphasize the importance of earlyidentification of renal impairment in targeting those at greaterrisk for cardiovascular events. In conclusion, in AfricanAmericans with hypertension and chronic kidney disease,LVH is strongly associated with both higher average daytimeand nighttime SBP and lower eGFR.

PerspectivesWe documented an extremely high prevalence of LVH inAfrican Americans with hypertensive kidney disease, despite

excellent BP control, as measured by office BP, during thepreceding 5 years. The high prevalence of LVH is likelymultifactorial but may relate in part to a genetic predisposi-tion in African Americans. Recently identified candidategenes that are more common in African Americans and alsoseem to be associated with higher LVM or inappropriateLVH include a variant of the corin gene,49 a polymorphism inthe calcineurin gene,50 and the 894T allele of endothelial NOsynthase gene.51

The high prevalence of LVH in this population raises thequestion of whether LVH itself should be a therapeutic target.Regression of LVM with effective BP reduction has beendemonstrated in �400 clinical studies, but �10% have beendouble-blind, placebo-controlled studies.52 Data indicate thatLVM regression reduced adverse clinical outcomes in hyper-tensive patients. In a prospective cohort study, a decreasedrisk of cardiac events with LVM regression was foundindependent of baseline LVM, BP, and the degree of BPreduction.53 In the Losartan Intervention for Endpoint Reduc-tion Trial, patients who had LVM regression with treatmenthad significantly less cardiac morbidity and mortality.54 Amechanism that might explain these findings is that midwallfractional shortening, a sensitive measure of intrinsic myo-cardial systolic performance, improves with LV mass regres-sion.55 Our own findings that LVH and LVM were signifi-cantly associated with daytime and nighttime SBP provide astrong rationale for additional research, particularly clinicaltrials, that test whether reduction in ambulatory BP andtargeted treatment of nighttime BP reduce LVM and preventclinical cardiovascular events.

Sources of FundingThis work was supported by cooperative agreements from NationalInstitute of Diabetes and Digestive and Kidney Disease5U01DK045388 and the National Center for Minority Health andHealth Disparities (5M01RR00071), National Institutes of Health.Support was also provided by King Pharmaceuticals, Pfizer Inc, andAstra Zeneca Pharmaceuticals. The following National Institutes ofHealth institutional grants also provided support: RR-00080, RR-00071, RR-00032, RR-00827, RR-11145, RR-11104, RR 00052, RR00095, and DK 2818.

DisclosuresS.R. has ownership interest in Merck and Pfizer. The remainingauthors report no conflicts.

Table 4. Multiple Regression Analysis Relating the LVM Index to SelectedPredictor Variables

Independent Variable Parameter Estimate SE t Value Pr�t

Average nighttime SBP 0.13823 0.06680 2.07 0.0390

Average daytime SBP 0.19316 0.08302 2.33 0.0203

eGFR �0.13166 0.05799 �2.27 0.0236

Age �0.30420 0.08689 �3.50 0.0005

Hematocrit �0.17322 0.18656 �0.93 0.3535

Female gender 0.25347 1.89215 0.13 0.8935

Log(Ualb/Ucr) 0.12408 0.51417 0.24 0.8094

Log(Ualb/Ucr) indicates log-transformed urine albumin:creatinine ratio.

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Peterson et al Left Ventricular Hypertrophy in African Americans 1039

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Prevalence and Correlates of Left Ventricular Hypertrophy in the African American Study of Kidney Disease Cohort Study

Gail E. Peterson, MD1, Tine de Backer, MD2, Avril Gabriel*3, Vladimir Ilic, MD2, Tudor

Vagaonescu, MD2,4, Lawrence J Appel, MD, MPH5, Gabriel Contreras, MD, MPH6,

Cindy Kendrick7, Stephen Rostand, MD8, and Robert A. Phillips, MD, PhD9, for the

AASK investigators.

1 UT Southwestern Medical Center, Dallas, TX; 2Cardiovascular Research Foundation, New York, NY; 3Lenox Hill Hospital, New York, NY; 4UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ; 5Johns Hopkins, Baltimore, MD; 6University of Miami, Miami, FL; 7Biostatistics and Epidemiology, Cleveland Clinic, Cleveland, OH; 8University of Alabama, Birmingham, AB, 9UMASS Memorial Medical Center and Medical School, Worcester, MA.

*deceased Word Count: Abstract 233 words, Manuscript 5988 words. Corresponding author: Gail Peterson, MD

Division of Cardiology

University of Texas Southwestern Medical Center

5909 Harry Hines Blvd, HA9.133

Dallas,Texas 75235-9047

214-645-7500

Fax 214-645-7501

Gail.Peterson@UTSouthwestern.edu

Table S1. Supplemental demographic and clinical data: comparison between patients with and without LVH

All patients

(n=599)

LVH

(n=416)

No LVH

(n=183)

Variable n(%) or mean

+/- s.d.

n(%) or

mean +/- s.d.

n(%) or mean

+/- s.d.

p

Income 0.5865

<$15,000 243 (40.6%) 175 (42.1%) 68 (37.2%)

$15,000-39,999 163 (27.2%) 110 (26.4%) 53 (29%)

$40,000+ 64 (10.7%) 41 (9.9%) 23 (12.6%0

Declines to answer 129 (21.5%) 90 (21.6%) 39 (21.3)

Education (from trial) 0.6528

Not a HS graduate 235 (39.3%) 161 (38.7%) 74 (40.7%)

HS Graduate 190 (31.8%) 137 (32.9%) 53 (29.1%)

College or beyond 173 (28.9%) 118 (28.4%0 55 (30.2%)

C-reactive protein (CRP)

(mg/dL)

0.80 +/- 1.22 0.80 +/- 0.98 0.81 +/- 1.65 0.9217

Appendix. African American Study of Kidney Disease Cohort Investigators

Case Western Reserve University: Principal Investigators – Jackson T. Wright, Jr.,

Mahboob Rahman, Study Coordinator - Renee Dancie, Louise Strauss. Emory

University: Principal Investigator - Janice Lea, Study Coordinators - Beth Wilkening,

Arlene Chapman and Diane Watkins. Harbor-UCLA Medical Center: Principal

Investigator - Joel D. Kopple, Study Coordinators - Linda Miladinovich, Jooree Choi,

and Patricia Oleskie, Connie Secules. Harlem Hospital Center: Principal Investigator -

Velvie Pogue, Study Coordinators - Donna Dowie, Herman Anderson, Leroy Herbert,

Robeta Locko, Hazeline Nurse, Jen-Tse. Cheng, G Darkwa, Victoria Dowdy, Beverly

Nicholas. Howard University: Principal Investigators - Otelio Randall, Tamrat Retta,

Study Coordinators - Shichen Xu, Muluemebet Ketete, Debra Ordor, Carl Tilghman.

Johns Hopkins University: Principal Investigators - Edgar Miller, Brad Astor,

Study Coordinators - Charalett Diggs, Jeanne Charleston, Charles Harris, Thomas

Shields. Charles R. Drew University: Principal Investigators - Keith Norris, David

Martins, Study Coordinators - Melba Miller, Holly Howell, Laurice Pitts.

Medical University of South Carolina: Principal Investigator - DeAnna Cheek, Study

Coordinator - Deborah Brooks. Meharry Medical College: Principal Investigators -

Marquetta Faulkner, Olufemi Adeyele, Study Coordinators - Karen Phillips, Ginger

Sanford, Cynthia Weaver. Morehouse School of Medicine: Principal Investigatos -

William Cleveland, Kimberly Chapman, Study Coordinators - Winifred Smith, Sherald

Glover. Mount Sinai School of Medicine and University of Massachusetts: Principal

Investigators - Robert Phillips, Michael Lipkowitz, Mohammed Rafey Study

Coordinators - Avril Gabriel, Eileen Condren, Natasha Coke. Ohio State University:

Principal Investigators - Lee Hebert, Ganesh Shidham, Study Coordinators - Leena

Hiremath, Stephanie Justice. University of Chicago, Chicago: Principal Investigators -

George Bakris, James Lash, Study Coordinators - Linda Fondren, Louise Bagnuolo,

Janet Cohan, Anne Frydrych. University of Alabama, Birmingham: Principal

Investigators - Stephen Rostand, Denyse Thornley-Brown, Study Coordinator - Beverly

Key. University of California, San Diego: Principal Investigators - Francis B. Gabbai,

Daniel T. O'Connor; Study Coordinator - Brenda Thomas. University of Florida:

Principal Investigators - C. Craig Tisher, Geraldine Bichier, Study Coordinators -

Cipriano Sarmiento, Amado Diaz, Carol Gordon. University of Miami: Principal

Investigators - Gabriel Contreras, Jacques Bourgoignie, Dollie Florence-Green, Study

Coordinator - Jorge Junco, Jacqueline Vassallo. University of Michigan: Principal

Investigators - Kenneth Jamerson, Akinlou Ojo, Tonya Corbin, Study Coordinators -

Denise Cornish-Zirker, Tanya Graham, Wendy Bloembergen. University of Southern

California: Principal Investigators - Shaul Massry, Miroslav Smogorzewski, Study

Coordinators - Annie Richardson, Laurice Pitts. University of Texas Southwestern

Medical Center, Dallas: Principal Investigators - Robert Toto, Gail Peterson, Ramesh

Saxena, Study Coordinators - Tammy Lightfoot, Sherry-Ann Blackstone, Carlos Loreto.

Vanderbilt University: Principal Investigators - Julie Lewis, Gerald Schulman, Study

Coordinators - Mo Sika, Sandy McLeroy. National Institute of Diabetes and Digestive

and Kidney Diseases: Lawrence. Y. Agodoa, Josephine. P. Briggs, John. W. Kusek;

Steering Committee Chair - Lawrence. Appel. Data Coordinating Center (Cleveland

Clinic Foundation): Jennifer Gassman, Gerald Beck, Tom Greene, Bo Hu, Study

Coordinators – Karen Brittain, Susan Sherer, Laurie Tuason, Cynthia Kendrick, Sharon

Bi, Harvey Litowitz, Xianyou Liu, Xuelei Wang, Kimberly Wiggins, Cheryl A. Tatum.

Central Biochemistry Laboratory: Frederick Van Lente, Joan Waletzky, Cathy

O'Laughlin, LaChauna Burton. External Advisory Committee: William McClellan,

Lucile Adams-Campbell, Kathy Faber-Langendoen, Bryce Kiberd, Elisa Lee, Timothy

Meyer, David Nathan, John Stokes, Herman Taylor, Peter W. Wilson. Cardiovascular

Research Foundation: Tine deBacker, Alexandra Lansky, Steve Slack.

for the African American Study of Kidney Disease InvestigatorsAppel, Gabriel Contreras, Cindy Kendrick, Stephen Rostand and Robert A. Phillips

Gail E. Peterson, Tine de Backer, Avril Gabriel, Vladimir Ilic, Tudor Vagaonescu, Lawrence J.Study of Kidney Disease Cohort Study

Prevalence and Correlates of Left Ventricular Hypertrophy in the African American

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