CARDIOLOGY/ORIGINAL RESEARCH

Subclinical Hypertensive Heart Disease in Black Patients With

Elevated Blood Pressure in an Inner-City Emergency Department
Phillip Levy, MD, MPH, Hong Ye, MS, Scott Compton, PhD, Robert Zalenski, MD, Timothy Byrnes, MD,
John M. Flack, MD, MPH, Robert Welch, MD, MS
From the Department of Emergency Medicine (Levy, Zalenski, Welch), the Division of Cardiology (Byrnes), the Department of Internal Medicine (Flack) and the
Cardiovascular Institute (Levy, Flack, Welch), Wayne State University School of Medicine, Detroit, MI; the Department of Radiation Oncology, William Beaumont
Hospital, Royal Oak, MI (Ye); and the Department of Emergency Medicine, UMDNJ–New Jersey Medical School (Compton), Newark, NJ.

Study objective: We examine the point prevalence of subclinical hypertensive heart disease in a cohort of urban
emergency department (ED) patients with elevated blood pressure.

Methods: A convenience sample of hypertensive (blood pressure ⱖ140/90 mm Hg on 2 measurements)

patients aged 35 years or older with no history of cardiac or renal disease who presented to a single urban ED
and were asymptomatic from a cardiovascular perspective (ie, no symptoms of dyspnea or chest pain) were
enrolled. All patients underwent a standardized evaluation (including echocardiography), and subclinical
hypertensive heart disease was defined by the presence of one or more of the following criterion-based
electrocardiographic findings: left-ventricular hypertrophy, systolic dysfunction, or diastolic dysfunction.

Results: A total of 161 patients were included. Mean age was 49.8 years (SD 8.3 years), 93.8% were black,
and 51.6% were men. Nearly all (93.8%) had a history of hypertension, and many (68.3%) were receiving
antihypertensive therapy at baseline. Mean systolic and diastolic blood pressures were 183.9 mm Hg (SD 25.1
mm Hg) and 109.5 mm Hg (SD 14.4 mm Hg), respectively. Subclinical hypertensive heart disease was found in
146 patients (90.7%; 95% confidence interval [CI] 85.2% to 94.3%), with most (n⫽131) displaying evidence of
diastolic dysfunction (89.7%; 95% CI 83.7% to 93.7%). Left-ventricular hypertrophy was also common (n⫽89;
61.0%; 95% CI 52.9% to 68.5%) and was often (but not exclusively) present in those with diastolic filling
abnormalities (n⫽75; 57.3%; 95% CI 48.7% to 65.4%).

Conclusion: In our largely black cohort of ED patients with elevated blood pressure, subclinical hypertensive
heart disease was highly prevalent, suggesting the need for coordinated efforts to reduce cardiac consequences
of hypertension in such inner-city communities. [Ann Emerg Med. 2012;60:467-474.]

Please see page 468 for the Editor’s Capsule Summary of this article.

A feedback survey is available with each research article published on the Web at www.annemergmed.com.
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0196-0644/$-see front matter
Copyright © 2012 by the American College of Emergency Physicians.
http://dx.doi.org/10.1016/j.annemergmed.2012.03.030

SEE EDITORIAL, P. 475. Importance

INTRODUCTION
Background
Hypertension is commonplace in the United States, affecting
more than 76 million individuals older than 20 years.1 The
burden of hypertension is particularly prominent among blacks,
who experience a higher disease prevalence and, especially for
men, poorer overall blood pressure control than their white and
Hispanic counterparts.1,2 As a result, blacks are at tremendous
risk for pressure-related consequences of hypertension,
particularly premature onset of structural cardiac damage and
functional impairment.3,4
Unfortunately for many, such underlying hypertensive heart
disease is unlikely to be detected until advanced, clinically
apparent manifestations are present.5-8 With appropriate blood
pressure reduction, however, the deleterious effects of
subclinical cardiac disease can be mitigated, symptom onset
(especially heart failure) can be forestalled, and future adverse
events can be prevented.9-11 Early identification of subclinical
cardiac disease has thus emerged as an important aspect of
secondary cardiovascular disease prevention.12
Despite the compelling benefits of directed intervention for
patients with subclinical cardiac disease, the utility of routine
screening in asymptomatic hypertensive patients remains
controversial.12-15 This may be attributable, in part, to uncertainty

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Hypertension in the Emergency Department
Editor’s Capsule Summary
What is already known on this topic
Emergency physicians treat many patients who have
suboptimally controlled hypertension.
What question this study addressed
Whether patients with asymptomatic hypertension
have subclinical heart disease.
What this study adds to our knowledge
In a largely black 161-patient sample, the majority
(91%; 95% confidence interval 85% to 94%) of
patients with asymptomatic hypertension had
underlying cardiac dysfunction, most commonly
diastolic dysfunction.
How this is relevant to clinical practice
The recognition that in some emergency
departments most patients with asymptomatic
hypertension have underlying cardiac dysfunction
should lead to improved vigilance in developing
coordinated care pathways to prevent further
deterioration.
about the prevalence of subclinical hypertensive heart disease,
which, depending on operational definitions and the population
studied, can vary from 0.9% to 50%.4,16-21 Such data, however,
were compiled almost exclusively with community-based sampling
methods and may not accurately depict the level of risk that exists
for the many millions of patients who present with moderate or
severely elevated blood pressure each year to emergency
departments (EDs) across the United States.22,23 Of particular
concern, they may underestimate the prevalence of subclinical
hypertensive heart disease in inner-city blacks, an especially high-
risk subset who, for lack of an alternative, rely on the ED for
detection or ongoing management of primary care amenable
conditions such as hypertension.24-27
Goals of This Investigation
Because hypertension contributes more than any other factor to
racial differences in cardiovascular disease survival,28 much can be
gained through enhanced understanding of subclinical hypertensive
heart disease (a potentially modifiable preclinical disease state) in
at-risk hypertensive patients. Accordingly, the objective of this
study was to estimate the point prevalence of echocardiographically
defined subclinical hypertensive heart disease in a cohort of
predominantly black, inner-city ED patients with asymptomatic
yet profoundly elevated blood pressure.
MATERIALS AND METHODS
Study Design and Setting
This was designed as a prospective cross-sectional study of
patients who presented to the ED of a single medical center
468 Annals of Emergency Medicine
Levy et al
(Detroit Receiving Hospital, Detroit, MI) between April 2006
and July 2007 with elevated blood pressure. Detroit Receiving
Hospital is a tertiary care facility operating within a large urban
environment and is affiliated with the Wayne State University
School of Medicine. The hospital ED has a total annual census
of approximately 98,000 adult patients, the majority of whom
(⬇85%) are black. Study approval was obtained from the
Human Investigations Committee of Wayne State University
before patient recruitment.
Selection of Participants
The purpose of this study was to evaluate the point prevalence
of subclinical hypertensive heart disease in ED patients who had
elevated blood pressure but were asymptomatic from the
perspective of potential acute or chronic end-organ cardiac damage.
As such, we targeted enrollment of patients aged 35 years or older
who met validated criteria for stage 1 or greater hypertension
(blood pressure ⱖ140/90 mm Hg on initial ED triage vital sign
assessment and at repeated measurement 1 hour later, both of
which were obtained with an automated, adult-sized blood pressure
cuff27,29-31) and had neither a primary nor secondary presenting
complaint potentially attributable to an acute hypertensive
emergency or underlying cardiac disease (ie, chest pain,
palpitations, dyspnea, syncope, focal neurologic deficits, and altered
mental status). To avoid conflict with patient care needs and to
minimize the potential influence of acute physiologic perturbations
on echocardiographic findings, patients who required hospital
admission for any reason were excluded from the study. Moreover,
patients with a known cardiac condition (ie, heart failure, coronary
artery disease, cardiomyopathy [dilated, idiopathic, or
hypertrophic], or valvular heart disease), those at risk for heart
disease from a cause other than hypertension (ie, renal failure), and
those with previously documented evidence of abnormal cardiac
structure or function on echocardiography or other cardiovascular
imaging study (ie, computed tomography, magnetic resonance
imaging, or cardiac catheterization), whether hypertensive in cause
or not, were also excluded. Patients with diabetes mellitus, however,
were eligible for inclusion.
Screening was performed in the ED by dedicated research
personnel. Written informed consent was obtained from
patients who met eligibility criteria and were willing to
participate. Our initial intent was to recruit 24 hours a day, 7
days a week; however, we encountered difficulty in having
patients return for study procedures once they were discharged
from the ED. To account for this, we adjusted our approach so
that the entire study protocol (described in greater detail in the
following section) could be completed in the ED at enrollment.
To accommodate this change, recruitment had to be
coordinated with the availability of key personnel (specifically,
the study’s echocardiographic technician), limiting screening to
“usual” business hours (Monday through Friday, 9 AM to 4 PM).
Subjects included in the study cohort thus represent a
convenience sample of ED patients.
To evaluate for potential bias in our sample, we compared
patients who were enrolled in the study with a consecutive series
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Levy et al Hypertension in the Emergency Department

of ED patients treated for hypertension during a Patients initially

contemporaneous period. Patients included in this consecutive consented for
series (n⫽742) were culled by applying study eligibility criteria participation in study
to a larger group identified by primary discharge diagnosis n=200

(International Classification of Diseases, Ninth Revision code Failed to return for

401.9 — unspecified essential hypertension) with billing data. outpatient echo
Once patients were enrolled, baseline data (demographics, n=20

medical and family history, and use of pharmaceutical agents)

were collected by trained research assistants, ECG was
Found to have prior
performed, urine was collected for dipstick testing, and serum documented history of
samples were obtained for measurement of blood urea nitrogen, cardiac disease
creatinine, and b-type natriuretic peptide (Biosite Incorporated, n=19
San Diego, CA). Echocardiograms were subsequently obtained
at the point of care in the ED by a single, certified
echocardiographic technician using a Phillips iE333 ultrasound
machine (Phillips Heathcare US, Andover, MA) with a 2.5-
MHz cardiac transducer and interpreted by one of 2 board- Included in final
certified cardiologists who were blinded to all demographic and study cohort
n=161
historical information, as well as ECG, urine dipstick, blood
urea nitrogen, creatinine, and b-type natriuretic peptide data. Figure. Flow chart outlining derivation of study cohort.
Echocardiography in enrolled subjects was performed expressly
for purposes of this study, and results were not used to inform Table 1. Breakdown of subclinical hypertensive heart disease
by left-ventricular dysfunction criterion in patients with and
clinical management.
without left-ventricular hypertrophy.
Left-Ventricular
Outcome Measures Hypertrophy
Left-Ventricular Total, No.
Subclinical hypertensive heart disease, the primary outcome of Dysfunction Yes No (%)*
interest, was determined by demonstration of one or more of the
following externally validated 2-dimensional and Doppler None 12 0 12 (8.2)
Diastolic dysfunction alone 60 49 109 (74.7)
echocardiographic criteria32,33: left-ventricular hypertrophy, Systolic dysfunction alone 2 1 3 (2.1)
defined by left-ventricular mass indexed to height2.7 greater than or Systolic and diastolic 15 7 22 (15.1)
equal to 46 g/m2.7 for women or greater than or equal to 49 g/m2.7 dysfunction
for men; left-ventricular systolic dysfunction determined by Total, No. (%)* 89 (61.0) 57 (39.0) 146 (100)
Simpson’s biplane method, defined by an ejection fraction less than *Percentage of patients with subclinical hypertensive heart disease (n⫽146).
or equal to 50%; or left-ventricular diastolic dysfunction, defined
by diastolic velocity measured at the medial mitral annulus by tissue
Doppler imaging (e=) less than 8 cm/second. RESULTS
Two hundred patients were enrolled and echocardiograms
Primary Data Analysis were successfully obtained for 180 (90%). Despite contradictory
The primary purpose of this study was to provide a precise self-report, 19 (10.6%) patients were found on subsequent
estimate of the point prevalence of subclinical hypertensive heart comprehensive chart review to have a history of heart failure or
disease among asymptomatic, hypertensive ED patients. To coronary artery disease and were thus excluded, resulting in a
provide a sufficient sample population for an a priori prevalence final study cohort of 161 patients. A flow chart of study cohort
estimate of 10% with a 95% confidence interval (CI) of 6.5% to derivation is provided in the Figure.
13.5% (3.5%), screening of 254 patients was needed. Although enrollment fell short of our projected target,
Groupwise descriptive data were compiled, and proportions analysis of study echocardiograms revealed the presence of
or means and medians with corresponding measures of variance subclinical hypertensive heart disease in 146 patients, yielding a
(SD and interquartile range, respectively) were calculated. point prevalence that was far greater (90.7%; 95% CI 85.2% to
All data were entered into a Microsoft Office 2007 Access 94.3%) than our a priori estimate. The majority of patients with
program (Microsoft, Bellevue, WA) and subsequently analyzed subclinical hypertensive heart disease (Table 1) had diastolic
with SPSS (version 16.0; SPSS Inc, Chicago, IL). To ensure dysfunction (n⫽131; 89.7%; 95% CI 83.7% to 93.7%), a
data integrity, double entry was performed for all patients finding that was associated with concurrent left-ventricular
included in the final analysis, with adjudication by the principal hypertrophy in most but not all patients (n⫽75; 57.3%; 95%
investigator (P.L.) of any variables with demonstrated CI 48.7% to 65.4%). Twenty-five individuals (15.5%; 95% CI
discrepancy. 10.7% to 21.9%) had evidence of systolic dysfunction with an

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Hypertension in the Emergency Department Levy et al

Table 2. Baseline data.

Subclinical Hypertensive No Subclinical Hypertensive
Overall, Heart Disease, Heart Disease,
Variable nⴝ161 nⴝ146 nⴝ15
Mean Age, y (SD) 49.8 (8.3) 50.0 (8.3) 47.3 (8.3)
Sex, No. (%)
Male 83 (51.6) 77 (52.7) 6 (40.0)
Female 78 (48.4) 69 (47.3) 9 (60.0)
Race, No. (%)
Black 151 (93.8) 137 (93.8) 14 (93.3)
White 6 (3.7) 6 (4.1) 0
Body mass index, kg/m2 (SD) 29.8 (7.1) 30.2 (7.0) 26.3 (6.7)
Insured, No. (%) 93 (57.8) 86 (58.9) 7 (46.7)
Reason for ED visit, No. (%)
High blood pressure 37 (23.0) 33 (22.6) 4 (26.7)
Headache 11 (6.8) 10 (6.9) 1 (6.7)
Epistaxis 3 (1.9) 3 (2.1) 0
Acute injury 13 (8.1) 12 (8.2) 1 (6.7)
Chronic pain 19 (11.8) 16 (11.0) 3 (20.0)
Acute infection 20 (12.4) 19 (13.0) 1 (6.7)
GI or GU complaint 32 (20.0) 30 (20.6) 2 (13.3)
Neurologic or psychiatric complaint 17 (10.6) 15 (10.3) 2 (13.3)
Metabolic issue 10 (6.2) 9 (6.2) 1 (6.7)
History of hypertension, No. (%) 151 (93.8) 137 (93.8) 14 (93.3)
Receiving antihypertensive therapy, No. (%) 110 (68.3) 98 (67.1) 12 (80.0)
Antihypertensive class, No. (%)
ACEI or ARB 25 (15.5) 21 (14.4) 4 (26.7)
␤-Blocker 20 (12.4) 16 (11.0) 4 (26.7)
Clonidine 30 (18.6) 30 (20.6) 0
Diuretic 35 (21.7) 30 (20.6) 5 (33.3)
Calcium-channel blocker 31 (19.3) 27 (18.5) 4 (26.7)
Other 9 (5.6) 8 (5.5) 1 (6.7)
Unknown 51 (31.7) 48 (32.9) 3 (20.0)
History of diabetes, No. (%) 30 (18.6) 26 (17.8) 4 (26.7)
Receiving diabetic medication, No. (%) 23 (14.3) 20 (13.7) 3 (20.0)
Insulin 11 (6.8) 9 (6.2) 2 (13.3)
Oral agents 12 (7.5) 11 (7.5) 1 (6.7)
History of stroke, No. (%) 15 (9.3) 15 (10.3) 0
Other medications, No. (%)
Statin 11 (6.8) 10 (6.9) 1 (6.7)
Aspirin 24 (14.9) 22 (15.1) 2 (13.3)
NSAID 22 (13.7) 18 (12.3) 4 (26.7)
Social history, No. (%)
Active cigarette smoker 78 (48.5) 72 (49.3) 6 (40.0)
Drinks alcohol 76 (47.2) 67 (45.9) 9 (60.0)
Uses cocaine 14 (8.7) 11 (7.5) 3 (20.0)
Uses heroin 8 (5.0) 8 (5.0) 0
Smokes marijuana 30 (18.6) 29 (19.9) 1 (6.7)
Physical examination findings, No. (%)
Elevated jugular venous pressure 1 (0.6) 1 (0.7) 0
Lower extremity edema 6 (3.7) 6 (4.1) 0
Ascites 1 (0.6) 1 (0.7) 0
S3 gallop 0 0 0
Pulmonary rales 0 0 0
Initial vital signs, mean (SD)
Systolic blood pressure, mm Hg 183.9 (25.1) 184.4 (25.3) 179.0 (23.0)
Diastolic blood pressure, mm Hg 109.5 (14.4) 109.7 (14.4) 108.3 (15.3)
Pulse rate, beats/min 85.1 (16.0) 84.6 (15.3) 89.9 (21.7)
Repeated vital signs, mean (SD)
Systolic blood pressure, mm Hg 175.1 (23.4) 174.9 (23.7) 177.7 (20.7)
Diastolic blood pressure, mm Hg 105.1 (15.1) 104.6 (14.7) 110.1 (18.6)
Pulse rate, beats/min 80.1 (14.4) 79.5 (14.1) 85.5 (17.2)

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Levy et al Hypertension in the Emergency Department

Table 2. Continued.
Subclinical Hypertensive No Subclinical Hypertensive
Overall, Heart Disease, Heart Disease,
Variable nⴝ161 nⴝ146 nⴝ15
Renal function, No. (%) or mean (SD)
Proteinuria 94 (61.0) 86 (58.9) 8 (53.3)
Blood urea nitrogen, g/dL 13.5 (5.7) 13.4 (5.6) 15.0 (6.6)
Serum creatinine, g/dL 1.0 (0.3) 1.0 (0.3) 1.1 (0.8)
eGFR, mL/min 90.8 (25.9) 91.2 (26.0) 86.7 (25.8)
b-Type natriuretic peptide, mean (SD), pg/dL 56.2 (84.0) 56.0 (84.8) 57.9 (78.5)
Electrocardiography, mean (SD)
Cornell criteria, mV* 25.5 (11.8) 25.6 (12.1) 24.2 (8.6)
Cornell product, msec⫻mV* 2275.9 (1199.6) 2307.7 (1244.4) 1977.5 (584.6)
GI, Gastrointestinal; GU, genitourinary; ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; NSAID, nonsteroidal anti-inflammatory agent;
eGRF, estimated glomerular filtration rate (calculated with the Modification of Diet in Renal Disease formula).
*Criterion for determination of left-sided ventricular hypertrophy: Cornell criteria⫽R in aVL⫹S in V3 (⫹8 mV if female); indicative of hypertrophy if greater than or equal
to 28 mV; Cornell product⫽Cornell criteria⫻QRS duration; indicative of hypertrophy if greater than or equal to 2,440 msec⫻mV.

Table 3. Echocardiographic measurements. had a history of hypertension and were aware of this diagnosis,
No
though not all (68.3%) were receiving antihypertensive therapy.
Subclinical Subclinical Diabetes (18.6%), cigarette smoking (48.5%), and at least
Hypertensive Hypertensive occasional alcohol use (47.2%) were frequently observed as well.
Heart Heart The most common reason for visiting the ED was elevated
Overall, Disease, Disease, blood pressure (23%) and, at triage, mean systolic and diastolic
Variable, Mean (SD) nⴝ161 nⴝ146 nⴝ15
blood pressures were 183.9 mm Hg (SD 25.1 mm Hg) and
Left atrial diameter, cm 3.7 (0.7) 3.7 (0.7) 3.3 (0.6) 109.5 mm Hg (SD 14.4 mm Hg), respectively. Proteinuria was
LV systolic diameter, cm 2.7 (0.6) 2.8 (0.7) 2.5 (0.3)
observed in 61% but renal function as assessed by estimated
LV diastolic diameter, cm 4.7 (0.7) 4.7 (0.7) 4.1 (0.5)
LV end-diastolic volume, mL 94.1 (33.0) 96.4 (33.2) 71.5 (20.2) glomerular filtration rate was normal (mean 90.8 mL/min [SD
LV end-systolic volume, mL 29.2 (13.8) 29.9 (14.0) 22.7 (10.4) 25.9 mL/min]). Despite the frequency with which subclinical
Stroke volume, mL 65.6 (27.0) 67.4 (27.5) 48.9 (14.7) hypertensive heart disease was encountered, mean brain
IVSD, cm 1.3 (0.3) 1.3 (0.3) 1.0 (0.2) natriuretic peptide was not elevated, at 56.2 pg/mL (SD 84.0
LVPWD, cm 1.2 (0.3) 1.2 (0.3) 1.0 (0.2)
pg/mL), and there was no electrocardiographic evidence of left-
Ejection fraction, % 62.4 (12.9) 61.9 (13.1) 67.2 (10.1)
E, cm/s 73.5 (19.9) 72.4 (19.4) 83.7 (22.2) ventricular hypertrophy by Cornell voltage or Cornell product
A, cm/s 77.9 (21.2) 79.2 (21.1) 65.6 (18.4) criteria. Mean systolic and diastolic blood pressures at the time
E/A 1.0 (0.4) 0.9 (0.3) 1.3 (0.4) echocardiography was performed were 167.4 mm Hg (SD 27.0
e=, cm/s 6.5 (1.8) 6.2 (1.5) 9.7 (1.6) mm Hg) and 101.1 mm Hg (SD 15.5 mm Hg), respectively. As
E/e= 11.8 (3.7) 12.1 (3.8) 8.9 (1.8)
shown in Table 3, echocardiographic findings reflect the
E deceleration time, ms 248.5 (80.5) 250.6 (82.3) 227.8 (58.7)
LV mass, g 223.2 (95.3) 231.8 (95.1) 139.6 (42.0) ubiquitous presence of subclinical hypertensive heart disease in
LV mass indexed to BSA, 112.1 (46.6) 116.2 (46.6) 71.9 (18.5) the overall study population and, by group, the operational
g/m2 definitions used in our study design.
LV mass indexed to 52.4 (23.8) 54.7 (23.8) 39.7 (6.9)
height2.7, g/m2.7
Relative wall thickness 0.52 (0.14) 0.52 (0.14) 0.49 (0.13) LIMITATIONS
LV, Left-ventricular; IVSD, interventricular septal diameter; LVPWD, left-ventricu- Our results were derived from a convenience sample of ED
lar posterior wall diameter; BSA, body surface area. patients in a single center and may have been influenced by
misclassification bias, particularly as it pertains to identification of a
truly asymptomatic state. More stringent exclusion criteria could
ejection fraction less than 50%, nearly all of whom (n⫽22) also have eliminated patients with subtle clinical manifestations but, in
had diastolic filling abnormalities. the absence of acute symptoms, it would be inherently difficult
Baseline data for the enrolled cohort are displayed in Table (and potentially erroneous) to attribute intermittent, nonspecific
2. Comparison of these individuals with the aforementioned features such as dyspnea, chest pain, or fatigue to underlying
consecutive series of nonenrolled hypertensive patients can be hypertensive heart disease without definitive (ie, echocardiographic)
found in the accompanying Appendix E1 (available online at assessment. In addition, because we sought to target
http://www.annemergmed.com). Mean age of patients enrolled undifferentiated, asymptomatic hypertensive patients in the ED, a
was 49.8 years (SD 8.3 years), 93.8% were black, 51.6% were subpopulation typically neglected by the medical community,34 an
men, and 57.8% had health insurance. Most patients (93.8%) inclusive approach was needed to provide an accurate estimate of

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Hypertension in the Emergency Department
previously undetected subclinical cardiac disease. Moreover,
although our intent was to evaluate the point prevalence of
subclinical hypertensive heart disease in a cohort of predominantly
black, urban-dwelling patients, such an approach precludes
extrapolation of our data to other racial or ethnic subgroups and
other clinical settings. Additionally, those included in the study
experienced extremely poor blood pressure control, and our data
may not apply to populations (irrespective of race) with better
chronic hypertension management. As shown by comparison of
study subjects with a consecutive series of hypertensive individuals
evaluated in our ED, findings are, at the least, generalizable to
urban black patients in our geographic region. To some degree, this
may reflect the relatively high rate of uninsured patients with
hypertension in our community, and the applicability of our results
to more affluent but racially similar communities is unclear.
Although such a consideration would appear amenable to suggested
improvements in outpatient management (especially efforts to
enhance medication compliance and clinician adherence to existing
guidelines), we are unable to project quantifiable benefits because
we did not collect data on existing primary care relationships. Last,
we did not include a control population of normotensive
individuals, making it difficult to determine how much race alone
may have contributed to underlying cardiac structure and function
in study subjects. However, large-scale epidemiologic studies such
as the Coronary Artery Disease Risk Development in Young Adults
have shown a low prevalence of left-ventricular hypertrophy in
nonhypertensive black men (5%) and women (3%).19
Furthermore, this study and the Dallas Heart Study, a probability-
based random sample of Dallas County that included 1,335 blacks,
found prevalent left-ventricular hypertrophy to be mostly mediated
by variation in blood pressure,19,35 suggesting that our results do
indeed reflect an independent relationship between blood pressure
and subclinical cardiac disease.
DISCUSSION
In this study of asymptomatic, predominantly black individuals
who presented to our urban ED with elevated blood pressure,
subclinical hypertensive heart disease was detected in 9 of every 10
patients. These data, which to our knowledge are the first to be
compiled in such a population, greatly exceeded our estimated
point prevalence and underscore the disproportionate population-
attributable risk of cardiovascular disease that hypertension imparts
on the inner-city black community.28,36 Beyond epidemiologic
implications, the presence of subclinical hypertensive heart disease
heralds an important branch point in clinical management because,
according to recently published guidelines by the International
Society of Hypertension in Blacks, such patients should be treated
in a manner that targets more aggressive blood pressure goals
(⬍130/80 mm Hg) than current guidelines based on the 7th
Report of the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure (⬍140/90 mm
Hg).36 Appropriate antihypertensive therapy contributes
substantially to regression of left-ventricular remodeling and, in
patients with subclinical hypertensive heart disease, decreases the
likelihood of subsequent cardiovascular disease morbidity and
472 Annals of Emergency Medicine
Levy et al
mortality.37,38 Thus, knowledge of the subclinical hypertensive
heart disease prevalence in our target population has therapeutic
meaning that may help reduce the likelihood of adverse outcome.39
Although racial differences in cardiac remodeling have been
previously demonstrated with an increased prevalence of left-
ventricular hypertrophy across all age ranges in blacks with
hypertension,4,40 the unique aspect of our study is the sheer
magnitude of previously unrecognized subclinical hypertensive
heart disease. That a sizable proportion of our patients had
advanced abnormalities with diastolic and, in some cases, frank
systolic dysfunction provides some insight into the underlying
substrate that contributes to existing disparities in hypertension-
mediated morbidity and mortality. Blacks progress from
asymptomatic to symptomatic stages of left-ventricular dysfunction
more rapidly, and the mean age of blacks who are admitted to the
hospital with heart failure is much lower than that of whites (63.6
[SD 15.4] versus 75.2 [SD 12.7] years; P⬍.001).41,42 Given that
the median life expectancy after an incident hospital admission for
heart failure is less than 2.5 years,43,44 there is remarkable potential
for prevention of subsequent cardiovascular events12,45,46 in this
vulnerable population. Though generalizability may be limited by
the included cohort, our data are applicable to the majority of
individuals (ie, urban black patients with poorly controlled chronic
hypertension) who, according to previously published reports,
typically present to EDs in the United States with elevated blood
pressure.34,47 Because hypertension contributes more than any
other factor (⬇15%) to the overall racial difference in years of life
lost to cardiovascular disease,28 initiatives targeting improved care
for those most at risk (especially within racially disparate locations)
are likely to be a high-yield endeavor.
What are the specific implications of this research for
emergency medicine? First and foremost, it highlights the
unavoidable confluence of primary and acute care in the ED
setting and suggests a need to be more proactive in the
identification and referral of patients with uncontrolled or
untreated hypertension. Since 2006, this approach has been
endorsed in an official clinical policy on asymptomatic
hypertension by the American College of Emergency
Physicians,31 yet according to a recent survey of ED directors,
only 50% of US EDs routinely provide such a service.48 The
point is not to add further screening activities to the ED load
but to enhance responsiveness to tasks that we currently carry
out (ie, check a blood pressure on every patient). Elevated blood
pressure is common in the ED setting, even among patients
who lack overt evidence of end-organ damage, and knowing
that up to 90% are at increased risk over time for death or other
adverse events is actionable information. To be most effective,
however, the ED should function as a point at which a
coordinated transition to enhanced outpatient management can
be initiated, not a destination for definitive care. Even then,
clinician and patient inertia is common, and espousing a role
within the larger context of accountable care is important.
Empowering patients for success through education, including
diet (especially sodium intake) and exercise advice, smoking
Volume , .  : October 
Levy et al
cessation counseling, encouragement of medication compliance,
and provision of information regarding blood pressure goals, is a
simple activity that can be accomplished during a relatively brief
interaction. In patients with persistently poor blood pressure
control, up-titration of antihypertensive therapy from the ED or
referral to a subspecialty hypertension clinic may be needed.
Our data also serve as a reminder that, in general, ED
patients with chronic disease are a high-risk subset, a finding
consistent with a recent analysis of National Health and
Nutrition Examination Survey data that showed a 4-fold greater
odds of adverse cardiovascular outcome for hypertensive
patients who either lack a usual source of primary care or rely on
the ED for ongoing management of their blood pressure.49
Simply put, because the ED functions as a site at which initial
contact with a health care provider is often made (particularly in
the inner city) and blood pressures are measured at every
encounter, emergency physicians are uniquely positioned to
lessen the overall effect of chronic hypertension in at-risk
communities. By rendering current screening activities more
effective (ie, not just taking in new information but also acting
on it), we can substantively contribute to much-needed
secondary disease prevention efforts.34
In summary, the point prevalence of subclinical hypertensive
heart disease in this cohort of asymptomatic, predominantly
black ED patients with elevated blood pressure is substantial.
Efforts that seek to mitigate the adverse cardiovascular effects of
hypertension, especially subclinical structural and functional
cardiac abnormalities, in this and demographically similar
patient settings are warranted.
Supervising editor: Judd E. Hollander, MD
Author contributions: PL conceived the study, designed the
trial, obtained research funding, supervised the conduct of the
trial, oversaw data collection, and directed all data analyses.
HY, SC, RZ, and RW assisted with design of the trial, provided
statistical advice on study design, and assisted with analysis
of the data. TB oversaw interpretation of study
echocardiograms. PL drafted the article, and all authors
contributed substantially to its revision. PL takes responsibility
for the paper as a whole.
Funding and support: By Annals policy, all authors are required
to disclose any and all commercial, financial, and other
relationships in any way related to the subject of this article
as per ICMJE conflict of interest guidelines (see
www.icmje.org). The authors have stated that no such
relationships exist. Funding for this study was provided by the
Blue Cross Blue Shield of Michigan Foundation (BCBSM
Foundation grant 1072.ii). Design of the study, data
interpretation, and development of the final article were
conducted independent of the funding agency.
Publication dates: Received for publication February 7, 2012.
Revision received March 17, 2012. Accepted for publication
March 30, 2012. Available online May 31, 2012.
Volume , .  : October 
Hypertension in the Emergency Department
Presented at the Society for Academic Emergency Medicine
annual meeting, May/June 2008, Washington, DC; and the
Society for Academic Emergency Medicine annual meeting,
May 2009, New Orleans, LA.
Address for correspondence: Phillip Levy, MD, MPH, E-mail
plevy@med.wayne.edu.
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Appendix E1. Comparison of study subjects with consecutive series of nonenrolled hypertensive patients.
Hypertensive Patients
Study Cohort Not Enrolled,
Variable nⴝ161 nⴝ742 Diff (95% CI)
Mean age, y (SD) 49.8 (8.3) 49.5 (11.9) 0.3 (⫺1.6 to 2.2)
Sex, No. (%)
Male 83 (51.6) 395 (53.2) ⫺1.6 (⫺10.1 to 6.7)
Female 78 (48.4) 347 (46.8) 1.6 (⫺6.7 to 10.1)
Race, No. (%)
Black 151 (93.8) 703 (94.7) ⫺0.9 (⫺6.0 to 2.4)
White 6 (3.7) 21 (2.8) 0.9 (⫺1.6 to 5.2)
Insured, No. (%) 93 (57.8) 442 (59.6) ⫺1.8 (⫺10.3 to 6.4)
Reason for ED visit, No. (%)
Blood pressure high 37 (23.0) 453 (61.1) ⫺38.1 (⫺44.8 to ⫺30.1)
Headache 11 (6.8) 185 (24.9) ⫺18.1 (⫺22.5 to ⫺12.3)
History of hypertension, No. (%) 151 (93.8) 635 (85.6) 8.2 (2.8 to 12.1)
Receiving antihypertensive medication, No. (%) 110 (68.3) 466 (62.8) 5.5 (⫺2.8 to 13.1)
Antihypertensive medication class, No. (%)
Angiotension converting enzyme inhibitors 25 (15.5) 188 (25.3) ⫺9.8 (⫺15.6 to ⫺2.8)
or angiotension receptor blockers
Beta-blockers 20 (12.4) 134 (18.1) ⫺5.7 (⫺10.8 to 0.9)
Clonidine 30 (18.6) 147 (19.8) ⫺1.2 (⫺7.2 to 6.1)
Diuretic 35 (21.7) 208 (28.0) ⫺6.3 (⫺12.8 to 2.4)
Calcium-channel blockers 31 (19.3) 122 (16.4) 2.8 (⫺3.2 to 10.0)
Other 9 (5.6) 28 (3.8) 1.8 (⫺1.3 to 6.7)
History of diabetes, No. (%) 30 (18.6) 105 (14.2) 4.5 (⫺1.4 to 11.6)
Receiving diabetic medication, No. (%) 23 (14.3) 78 (10.5) 3.8 (⫺1.4 to 10.3)
Insulin 11 (6.8) 30 (4.0) 2.8 (⫺0.6 to 7.9)
Oral agents 12 (7.5) 48 (6.5) 1.0 (⫺2.7 to 6.3)
History of stroke, No. (%) 15 (9.3) 37 (5.0) 4.3 (0.3 to 10.0)
Social history, No. (%)
Active cigarette smoker 78 (48.5) 342 (46.1) 2.4 (⫺6.1 to 10.8)
Drinks alcohol 76 (47.2) 217 (29.2) 18.0 (9.7 to 26.3)
Uses cocaine 14 (8.7) 52 (7.0) 1.7 (⫺2.3 to 7.3)
Mean initial blood pressure, mm Hg (SD)
Systolic 183.9 (25.1) 194.0 (23.5) ⫺10.1 (⫺14.2 to ⫺6.0)
Diastolic 109.5 (14.4) 110.1 (14.6) ⫺0.6 (⫺3.1 to 1.9)

Volume , .  : October  Annals of Emergency Medicine 474.e1