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Abstract

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

Young, urban, African American men are at particularly high risk of hypertension and its cardiovascular complications. Left ventricular hypertrophy and renal dysfunction are manifestations of target organ damage from hypertension that predict adverse cardiovascular events. The subjects of this study were 309 African American men, age 18–54 years, with hypertension, residing in inner-city Baltimore. Echocardiograms, electrocardiograms, serum creatinine, and the urinary albumin-creatinine ratio were obtained to evaluate hypertensive target organ damage. Fifty-three percent of the men reported use of antihypertensive medications, of whom 80% were on monotherapy. Calcium channel blockers were used most frequently. The mean echocardiographic left ventricular mass was 211±68 g, with a prevalence of echocardiographic left ventricular hypertrophy of 30%. There were 14 men (5%) with extremely high left ventricular mass, >350 grams. Left ventricular systolic dysfunction was seen in 9% of the men with uncontrolled hypertension, and none of the men with controlled hypertension (p=0.02). Renal dysfunction was found in 12% of the subjects, and microalbuminuria or gross proteinuria in 34%. The authors conclude that there is a high prevalence of cardiac and renal abnormalities in inner-city African American men with hypertension, especially in men on antihypertensive therapy with uncontrolled hypertension. It is imperative that cost-effective medications and culturally acceptable health care delivery programs be developed, tested, and integrated into health systems, with strategies specifically relevant to this high-risk population, to decrease the largely preventable morbidity and mortality associated with hypertension.

Young, urban, African American men are at particularly high risk of developing hypertension1 (HTN) and its cardiovascular complications.2–4 This population has benefited least from nationwide improvements in high blood pressrure (BP) control.5 It is estimated that as many as 30% of all deaths in hypertensive African American men may be attributable to high blood pressure.6 Left ventricular hypertrophy (LVH) and renal dysfunction are manifestations of target organ damage from HTN. LVH is a potent predictor of adverse cardiovascular events,7 and renal dysfunction, measured by urinary albumin excretion8,9 and serum creatinine,10 predicts the future development of renal failure and need for renal dialysis.

We are currently studying, in a randomized clinical trial, the impact of a comprehensive nurse practitioner-based intervention to improve BP control and to prevent progression or foster regression of target-organ damage in a high-risk population of young, African American men. All subjects have undergone an extensive baseline assessment. We have previously reported on the economic, social, and lifestyle barriers to care and control that the young, urban, African American man with HTN experiences.11 This paper describes the high prevalence of target organ damage from HTN found in this cohort at the baseline examination.

Subjects

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

Subjects were eligible for the trial if they were African American men with HTN, aged 18–54 years, resided in inner-city Baltimore, and provided informed consent. HTN was defined as having a systolic BP (SBP) geqslant R: gt-or-equal, slanted140 mm Hg and/or diastolic BP (DBP) geqslant R: gt-or-equal, slanted90 mm Hg on two separate days, or as having been diagnosed with HTN and under treatment with an antihypertensive medication. Subjects were recruited from the nonurgent service of the Johns Hopkins Hospital Emergency Department, advertising, and word-of-mouth. Men receiving renal dialysis were excluded. Data for this analysis were obtained from the baseline visit, prior to randomization in the clinical trial. Three hundred nine men completed the baseline examinations, which occurred in 1996 and 1997.

Clinical Variables

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

BP was measured three times in the sitting position by random zero sphygmomanometry at the randomization visit, after 5 minutes of rest, and the means of the last two measurements were used for SBP and DBP. Controlled HTN was defined as SBP <140 mm Hg and DBP <90 mm Hg. Antihypertensive medication use was evaluated by self-report. Diabetes mellitus was defined as a random serum glucose geqslant R: gt-or-equal, slanted200 mg/dL, or use of oral hypoglycemic agents or insulin. Height and weight were measured, and body mass index was calculated (kg/m2) as a measure of obesity.

Routine 12-lead electrocardiograms (ECGs) were obtained, and the voltages in the various leads were measured by the Marquette computer system. ECG-demonstrated LVH was defined according to the Cornell voltage criteria (RaVL+ SV3geqslant R: gt-or-equal, slanted28 mm).12 The Minnesota Code (MC) was used to classify ST and T wave abnormalities.13 Major ST and T wave changes were defined as MC 4.1 and 4.2 (ST) and 5.1 and 5.2 (T wave), and minor ST and T wave changes as MC 4.3 and 4.4 (ST) and 5.3 and 5.4 (T wave). Left ventricular (LV) strain pattern was defined as MC 4.3 in the presence of T wave abnormalities.

Transthoracic echocardiography was performed by a trained sonographer using an HP Sonos 100 machine (Hewlett Packard, Palo Alto, CA). Left ventricular mass (LVM) was calculated off-line by a cardiologist (WSP) blinded to subject characteristics. The two-dimensional 5/6 area-length method was used, due to its potential for greater accuracy and reproducibility than M-mode methods.14–16 Two measurements were made and the mean was used. LVM was indexed to height (meters) raised to the 2.7 power17 and to body surface area (BSA) to adjust for body size. Echocardiographic LVH was defined as LVM/height2.7geqslant R: gt-or-equal, slanted50 g/m2.7 and as LVM/BSA geqslant R: gt-or-equal, slanted131 g/m.2,18 There were seven men who did not have an echocardiogram, and 24 with technically limited echocardiograms. Therefore, there were 278 men (90%) with LVM measurements. The men without LVM measurements were older (44±6 years vs. 41±6 years; p=0.01) and had a higher body mass index (32±9 kg/m2 vs. 27±6 kg/m2; p<0.001) than the men with LVM measurements available.

Pulse-wave Doppler transmitral flow velocity was used to evaluate Doppler indexes of LV diastolic filling by measuring the peak velocity of early flow (e wave) and late flow (a wave) and the deceleration time of early filling. The e to a wave peak velocity ratio was calculated. The LV ejection fraction was calculated using the method of discs. There were seven men who did not have an echocardiogram, and 54 with echocardiograms technically inadequate for accurate measurement of the ejection fraction. The men without ejection fraction measurements had a higher body mass index (31±7 kg/m2 vs. 26±6 kg/m2; p<0.001) than the men with ejection fraction measurements.

A random-spot, afternoon, single-void urine specimen was collected. Urine albumin was measured using an immunonephelometric assay (Boehring Nephelometer II, Deerfield, IL). Urine creatinine was measured (Kodak 700XR Chemistry Analyzer, Rochester, NY) and the albumin to creatinine ratio (ACR) was calculated (expressed as mg of albumin per g of creatinine). Microalbuminuria was defined as ACR 30–300 mg/g, and macroalbuminuria (gross proteinuria) as ACR >300 mg/g. Creatinine clearance (mL/min) was calculated using the Cockcroft-Gault equation: [(140 - age) × weight (kg)]/[72 × serum creatinine(mg/dL)].19 Renal insufficiency was defined as a calculated creatinine clearance <60 mL/min or serum creatinine geqslant R: gt-or-equal, slanted1.6 mg/dL.

This study was approved by the Johns Hopkins Joint Committee on Clinical Investigation. All subjects provided written informed consent.

Statistical Analysis

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

Statistical analyses were performed using SPSS software. Descriptive data are presented as means±standard deviation. Continuous variables were compared with the Student t test and analysis of variance, and categorical variables were compared with the chisquare test. The ACR was log transformed for the parametric analyses, since the distribution was positively skewed. A two-sided p value <0.05 was considered statistically significant.

Baseline Characteristics (Table I)

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

Three hundred nine men completed the baseline examination. The mean age was 41.4±5.6 years. There was a high prevalence of low income (<$10,000/year in 72%), lack of medical insurance (51%), and unemployment/disability (74%). Use of antihypertensive medications was reported by 165 men (53% of the men in the study). BP was “controlled” while on medication (SBP <140 mm Hg and DBP <90 mm Hg) in only 58 men (35% of men on antihypertensive medication and 19% of the men in the study). Men not receiving antihypertensive medications tended to be uninsured, were younger, and had a lower body mass index than the men receiving antihypertensive medications (p<0.005 for each). Diabetes was present in 30 men (10%).

Of the 165 men on antihypertensive therapy, 80% (n=133) reported taking only a single antihypertensive agent. Combination therapy with two different medications was reported by 15% (n=25), and only seven men (4%) reported use of three different antihypertensive agents. BP was “controlled” in two of the seven men on three medications, and in 10 of the 25 men on two medications. Thirty-five percent (46 men) on single antihypertensive therapy had controlled BP.

Calcium channel antagonists were prescribed for more than one half of the men on medication (56%). Diuretics use was reported by only 19%, and angiotensin-converting enzyme inhibitor use by 16%, of men on medications. Use of centrally acting agents, such as clonidine, was reported by 12%, and 8% were on β blocking agents. There were very few men on a α receptor antagonists, direct vasodilators, or angiotensin II receptor antagonists. The likelihood of having controlled BP was unrelated to the class of medications, except for centrally acting agents, such as clonidine, which had been prescribed more often in men with uncontrolled BP.

Target Organ Damage (Table II)

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

There was a high prevalence of target organ damage in this cohort. The mean echocardiographic LV mass was 211±68g. When LVM was indexed to height2.7, the prevalence of LVH was 30%; and with LVM indexed to BSA, the prevalence of LVH was 25%. There were 14 men (5%) with extremely high LVM, >350 g. Men with uncontrolled HTN who were receiving medication had the highest prevalence of echocardiographic LVH (indexed to height2.7) (37%), compared with men controlled on antihypertensive medication (21%; p=0.05), and did not differ significantly from men not receiving medication (29%; p=NS).

LVM index (LVM/ht2.7) correlated with SBP (r=0.22; p<0.0001), pulse pressure (r=0.17; p<0.005), and DBP (r=0.14; p<0.02), but not with age or body mass index. There was a moderate correlation between the sum of the Cornell voltage criteria and LVM index (r1=0.42; p<0.0001). LVM index also correlated with other measures of target-organ damage, such as serum creatinine (r=0.16; p<0.01) and urine albumin creatinine ratio (natural log, r=0.20; p<0.001). On multiple linear regression analysis, SBP, use of antihypertensive medications, body mass index, and urinary albumin/creatinine ratio (natural log) were all independent predictors of LVM index (Table III).

Twelve percent of subjects had LVH under the Cornell voltage ECG criteria, and 3% had a “strain” pattern on ECG. There was one subject with a right bundle branch block. Major and minor nonspecific T wave abnormalities were present in approximately one third of subjects.

Significant LV systolic dysfunction (EF <50%) was found in 7% of the men. LV systolic dysfunction was most prevalent in men on medication with uncontrolled HTN (10%). None of the men on medication with controlled HTN had LV systolic dysfunction (p=0.02, comparing men on medication with controlled vs. uncontrolled HTN). Diastolic dysfunction was highly prevalent (38% with an e/a wave velocity ratio <1.0 in the entire cohort).

The mean serum creatinine was 1.3±0.9 mg/dL. Ten percent of the men had serum creatinine geqslant R: gt-or-equal, slanted1.6 mg/dL, and 9% had a calculated creatinine clearance <60 mL/min/1.73 m2, suggesting significant renal insufficiency. A creatinine clearance <60 mL/min/1.73 m2 or a serum creatinine geqslant R: gt-or-equal, slanted1.6 mg/dL was found in 12% of the men. The men with decreased creatinine clearance but serum creatinine <1.6 mg/dL tended to be thin (n=5), and those with a normal creatinine clearance and serum creatinine geqslant R: gt-or-equal, slanted1.6 mg/dL tended to be obese (n=9). Proteinuria was highly prevalent. Microalbuminuria was present in 21% of subjects and gross proteinuria in an additional 13%. Men on antihypertensive therapy with uncontrolled HTN were most likely to have gross proteinuria (20%), compared with men not on antihypertensive medications (8%; p<0.005), but the prevalence of gross proteinuria did not differ significantly from that of men with controlled HTN on antihypertensive medications (13%; p=NS)

DISCUSSION

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References

Morbidity and mortality from cardiovascular disease have been decreasing over the past few decades; however, there has been a recent plateau in this trend. The reduction in cardiovascular disease in the United States has been less marked in the African American population.20 African Americans are at particularly high risk for complications related to HTN, due to an increase in the severity of HTN and possibly a greater tendency toward target organ damage, including LVH21,22 and renal dysfunction leading to renal failure.23,24

In this study, we documented a high prevalence of cardiac and renal abnormalities in a young cohort of African American men with HTN residing in innercity Baltimore. Echocardiographic LVH was present in 25%–30% of the men, and a relatively high proportion of these men had severe LVH, with an LVM >350 g. LVH is a potent predictor of adverse cardiovascular events.7 We also found that one third of subjects had major or minor T wave abnormalities on their ECGs, which is also associated with an increased risk of cardiovascular disease events25. LV systolic dysfunction was present in 8%–10% of the men who had uncontrolled HTN. HTN is the most common risk factor for congestive heart failure,26 especially in African Americans.27 Once LV systolic dysfunction has devel-oped, African Americans are more likely than whites to suffer progressive heart failure and death.28

The prevalence of LVH varies, depending on the method used and the partition value chosen. This has been described in previous studies.29 In general, LVM indexed to height2.7 is more likely to detect LVH in obese people, and LVM indexed to BSA identifies LVH in lean subjects.29 We used a two-dimensional method to measure LVM, rather than the M-mode method, due to its potential for greater accuracy and reproducibility than M-mode methods.14–16 Although the partition values for the definition of LVH may be somewhat arbitrary, the finding of severe LVH (LVM >350 g) in 5% of our population documents the severity of LVH in this population.

Renal dysfunction documented by elevated serum creatinine or reduced estimated creatinine clearance was found in 12% of the men, and microalbuminuria or gross proteinuria in 34% of the men in this population. These findings are especially significant, given the young age of our cohort. Lower socioeconomic status and higher BP increase the likelihood of renal failure.30 African Americans are 3.5 times more likely than whites to require renal dialysis,31 and rapid progression toward end-stage renal failure is most common in young, hypertensive, African American men.32 The need for adequate BP control is paramount in the population of young, African American men with HTN, who are otherwise destined for renal dialysis.

It is interesting to note that most men reporting use of medical therapy for HTN were only on monotherapy and that few men were receiving low-dose diuretics, which are known to be beneficial in lowering BP in this population.33 The importance of adding low-dose diuretics as one component of combination therapy should be emphasized to physicians caring for African American patients. The men with uncontrolled HTN who had been prescribed antihypertensive therapy tended to have more target organ damage (both cardiac and renal) than the untreated hypertensive men and those controlled on antihypertensive theraphy. It is possible that these men had the most severe and long standing HTN.

The lack of a comparison group is a limitation of this study. It is difficult to compare our results with other studies, due to variations in measurement techniques and differences in the populations studied. However, the degree of target organ damage in our cohort appears to be consistent with or slightly greater than that of other reports in hypertensive African American men. The mean LV mass in African American hypertensive men with a mean age of 51 (±10) years in a study reported by Arnett et al.34 was 204 (±52) g, or 44.6 (±11.6) g/ht2.7, which is slightly lower than in our cohort. The mean serum creatinine in African American hypertensive men 20–60 years old in the Third National Health and Nutrition Examination Survey (NHANES III)35 was 1.3 mg/dL, which is similar to our data. However, the NHANES III did not exclude men on dialysis, which our study did. Therefore, the mean serum creatinine in the nondialysis population would be lower than that of our cohort. Both the study by Arnett et al.34 and NHANES III35 document greater degrees of LVH and renal dysfunction in African Americans than in Caucasians.

The importance of primary prevention is especially salient in this high-risk population. We have documented a high prevalence of target organ damage in this young cohort of African American inner-city hypertensive men. This study is unique, since there are no identified studies focusing on cardiovascular abnormalities associated with HTN in this hard-to-reach population. We are currently studying the effects of our comprehensive clinic- and community based intervention, delivered by a nurse practitioner and community health worker, which includes initial treatment with an angiotensin receptor antagonist with or without a diuretic, on BP control and target organ damage. It is imperative that cost-effective medications and culturally acceptable health care delivery programs be devel-oped, tested, and integrated into health systems, with strategies specifically relevant to this high-risk population, to decrease the largely preventable morbidity and mortality associated with HTN.

The obstacles to BP control in this population are varied and include significant social, economic, and lifestyle problems.11 They also include health care policies and practices that systematically affect disadvantaged and underserved groups.36 Thus, understanding and addressing racial disparities in health care will require recognition of institution- and society-level interventions, including moving “beyond tampering with what doesn't work and to begin learning how to exploit what does work.”37

Acknowledgments: This work is supported by grants from NINR-NIH #RO1NR04119, Johns Hopkins GCRC NIH-NCRR #5M01RR00052, and Merck & Co.

References

  1. Top of page
  2. Abstract
  3. METHODS
  4. Subjects
  5. Clinical Variables
  6. Statistical Analysis
  7. RESULTS
  8. Baseline Characteristics ()
  9. Target Organ Damage ()
  10. DISCUSSION
  11. References
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    Bianchi S, Bigazzi R, Campese VM. Microalbuminuria in essential hypertension: significance, pathophysiology, and therapeutic implications. Am J Kidney Dis. 1999;34:973995.
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    Obialo CI, Hewan-Lowe K. Rapid progression to end-stage renal disease in young hypertensive African Americans with proteinuria. J Natl Med Assoc. 1998;90:649655.
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    Shulman NB, Ford CE, Hall WD, et al. Prognostic value of serum creatinine and effect of treatment of hypertension on renal function. Results from the hypertension detection and follow-up program. The Hypertension Detection and Follow-up Program Cooperative Group. Hypertension. 1989;13:I80I93.
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    Hill MN, Bone LR, Kim MT, et al. Barriers to hypertension care and control in young urban black men. Am J Hypertens. 1999;12:951958.
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    Casale N, Devereux RB, Alonso DR, et al. Improved sex-specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: validation with autopsy findings. Circulation. 1987;75:565572.
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    Rose GA, Blacburn H. Classification of the electrocardiogram for population studies. In: WHO Monograph Series #56. New York , NY : Cardiovascular Survey Methods. 1968;137151.
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    Devereux RB, Pini R, Aurigemma GP, et al. Measurement of left ventricular mass: methodology and expertise. J Hypertens. 1997;15:801809.
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    Reichek N, Helak J, Plappert T, et al. Anatomic validation of left ventricular mass estimates from clinical two-dimensional echocardiography: initial results. Circulation. 1983;67:348352.
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    Collins HW, Kronenberg MW, Byrd BF III. Reproducibility of left ventricular mass measurements by two-dimensional and M-mode echocardiography. J Am Coll Cardiol. 1989;14(3):672676.
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    de Simone G, Daniels SR, Devereux RB, et al. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol. 1992;20:12511260.
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    Levy D, Savage DD, Garrison RJ, et al. Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol. 1987;59:956960.
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    Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron. 1976;16:3141.
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    Gillum RF. Trends in acute myocardial infarction and coronary heart disease death in the United States. J Am Coll Cardiol. 1993;23:12731277.
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    Hammond IW, Devereux RB, Alderman MH, et al. The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension. J Am Coll Cardiol. 1986;7:639650.
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    Devereux RB, Okin PM, Roman MJ. Pre-clinical cardiovascular disease and surrogate end-points in hypertension: does race influence target organ damage independent of blood pressure? Ethn Dis. 1998;8:138148.
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    Coresh J, Jaar B. Further trends in the etiology of end-stage renal disease in African-Americans. Curr Opin Nephrol Hypertens. 1997;6:243249.
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    Feldman HI, Klag MJ, Chiapella AP, et al. End-stage renal disease in US minority groups. Am J Kidney Dis. 1992;19:397410.
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    Daviglus ML, Liao Y, Greenland P, et al. Association of nonspecific minor ST-T abnormalities with cardiovascular. mortality: the Chicago Western Electric Study. JAMA. 1999;281:530536.
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    Levy D, Larson MG, Vasan RS, et al. The progression from hypertension to congestive heart failure. JAMA. 1996;275:15571562.
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    Matthew J, Davidson S. Narra L, et al. Etiology and characteristics of congestive heart failure in blacks. Am J Cardiol. 1996;78:14471450.
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    Dries DL, Exner DV, Gersh BJ, et al. Racial differences in the outcome of left ventricular dysfunction. N Engl J Med. 1999;340:609616.
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    Wachtell K, Bella JN, Liebson PR, et al. Impact of different partition values on prevalences of left ventricular hypertrophy and concentric geometry in a large hypertensive population: the LIFE study. Hypertension. 2000;35:612.
  • 30
    Klag MJ, Whelton PK, Randall BL, et al. End-stage renal disease in African-American and white men. 16-year MRFIT findings. JAMA. 1997;277:12931298.
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    Feldman HI, Klag MJ, Chiapella AP, et al. End-stage renal disease in US minority groups. Am J Kidney Dis. 1992;19:397410.
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    Arnett DK, Hong Y, Bella JN, et al. Sibling correlation of left ventricular mass and geometry in hypertensive African Americans and whites. The HyperGEN Study. Am J Hypertens. 2001;14:12261230.
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Table I.  Baseline Demographics
 Entire Cohort (N=309)Not On Medication at Baseline (N=144)On Medication at Baseline: Not Controlled (N=107)On Medication at Baseline: Controlled (N=58)
 Mean (SD)Mean (SD)Mean (SD)Mean (SD)
Age (years)41.4 (5.6)40.5 (5.6)42.1 (5.3)42.6 (5.9)
BMI (kg/m2)27.1 (6.4)26.0 (5.5)28.2 (7.5)27.8 (6.0)
Systolic BP (mm Hg)147 (20)155 (19)149 (16)125 (10)
Diastolic BP (mm Hg)99 (15)106 (12)100 (12)80 (7)
Pulse pressure (mm Hg)48 (13)49 (15)48 (13)45 (9)
Income <$10,00072%73%70%74%
No health insurance51%67%38%35%
Unemployed or disabled74%72%75%74%
BP=blood pressure; BMI=body mass index
Table II.  Target Organ Abnormalities
 Entire CohortNot On Medication at BaselineOn Medication at Baseline: Not ControlledOn Medication at Baseline: Controlled
 Mean (SD)Mean (SD)Mean (SD)Mean (SD)
Left ventricular hypertrophy (n=278 for echo; n=301 for ECG)
  Echo LVM (g)211 (68)210 (67)223 (73)192 (58)
  Echo LVM/ht2.745.9 (14.6)45.3 (13.7)48.0 (15.2)43.6 (15.4)
  Echo LVM/BSA108 (35)108 (35)112 (36)100 (31)
  Echo LVH % (LVM/ht2.7)30%29%37%21%
  Echo LVH % (LVM/BSA)25%26%30%14%
  ECG sum Cornell voltage18.4 (9.0)18.0 (8.3)20.2 (9.1)15.7 (9.7)
  ECG LVH Cornell voltage %12%11%18%4%
  ECG strain pattern3%4%5%0
Nonspecific T wave abnormality
  Major15%16%17%9%
  Minor18%13%26%16%
Diastolic function (n=284)
  E wave velocity (cm/sec)69 (16)69 (14)68 (17)70 (16)
  A wave velocity (cm/sec)64 (13)62 (13)65 (14)65 (12)
  E/A wave ratio1.1 (0.3)1.15 (0.33)1.08 (0.29)1.10 (0.30)
  Deceleration time (msec)202 (68)198 (68)202 (71)211 (62)
  E/A ratio <1.038%33%45%39%
  Deceleration time >240 msec25%21%27%29%
Systolic function (n=248)
  Ejection fraction69 (13)68 (13)68 (14)71 (8)
  Ejection fraction <50%7%8%10%0%
Renal function (n=298 for serum; n=281 for urine)
  Serum creatinine (mg/dL)1.3 (0.9)1.2 (0.8)1.4 (0.9)1.3 (1.0)
  Creatinine >1.6 (mg/dL)10%7%14%11%
  Urine Cr Cl (mL/min/1.73 m2)102 (37)102 (34)103 (42)99 (32)
  Cr Cl <60 (mL/min/1.73 m2)9%7%10%11%
  Urine albumin/creatinine ratio187 (569)125 (451)262 (697)210 (571)
  Microalbuminuria (%)21%21%24%15%
  Gross proteinuria (%)13%8%20%13%
  Proteinuria (%)34%29%42%28%
echo=echocardiography; LVM=left ventricular mass; ECG=electrocardiography; BSA=body surface area; LVH=left ventricular hypertrophy; Cr Cl=creatinine clearance
Table III.  Multiple Linear Regression, With Echocardiographic Left Ventricular Mass Index* as the Dependent Variable
VariableBeta±SDStandardized Betap Value
Systolic BP0.20±0.070.270.004
Medication Use4.1±2.00.140.05
Ln urine ACR1.4±0.50.160.01
Body mass index0.33±0.160.130.04
Serum creatinine1.4±1.20.080.24
Diastolic BP0.004±0.090.0050.96
Age0.008±0.170.0030.96
BP=blood pressure; Ln=natural log; ACR=albumin-creatine ratio; *LV mass/ht2.7; r2=0.13; n=250