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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.
A podcast for this article is available at www.annemergmed.com.
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


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

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Hypertension in the Emergency Department Levy et al

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

previously undetected subclinical cardiac disease. Moreover, mortality.37,38 Thus, knowledge of the subclinical hypertensive
although our intent was to evaluate the point prevalence of heart disease prevalence in our target population has therapeutic
subclinical hypertensive heart disease in a cohort of predominantly meaning that may help reduce the likelihood of adverse outcome.39
black, urban-dwelling patients, such an approach precludes Although racial differences in cardiac remodeling have been
extrapolation of our data to other racial or ethnic subgroups and previously demonstrated with an increased prevalence of left-
other clinical settings. Additionally, those included in the study ventricular hypertrophy across all age ranges in blacks with
experienced extremely poor blood pressure control, and our data hypertension,4,40 the unique aspect of our study is the sheer
may not apply to populations (irrespective of race) with better magnitude of previously unrecognized subclinical hypertensive
chronic hypertension management. As shown by comparison of heart disease. That a sizable proportion of our patients had
study subjects with a consecutive series of hypertensive individuals advanced abnormalities with diastolic and, in some cases, frank
evaluated in our ED, findings are, at the least, generalizable to systolic dysfunction provides some insight into the underlying
urban black patients in our geographic region. To some degree, this substrate that contributes to existing disparities in hypertension-
may reflect the relatively high rate of uninsured patients with mediated morbidity and mortality. Blacks progress from
hypertension in our community, and the applicability of our results asymptomatic to symptomatic stages of left-ventricular dysfunction
to more affluent but racially similar communities is unclear. more rapidly, and the mean age of blacks who are admitted to the
Although such a consideration would appear amenable to suggested hospital with heart failure is much lower than that of whites (63.6
improvements in outpatient management (especially efforts to [SD 15.4] versus 75.2 [SD 12.7] years; P⬍.001).41,42 Given that
enhance medication compliance and clinician adherence to existing the median life expectancy after an incident hospital admission for
guidelines), we are unable to project quantifiable benefits because heart failure is less than 2.5 years,43,44 there is remarkable potential
we did not collect data on existing primary care relationships. Last, for prevention of subsequent cardiovascular events12,45,46 in this
we did not include a control population of normotensive vulnerable population. Though generalizability may be limited by
individuals, making it difficult to determine how much race alone the included cohort, our data are applicable to the majority of
may have contributed to underlying cardiac structure and function individuals (ie, urban black patients with poorly controlled chronic
in study subjects. However, large-scale epidemiologic studies such hypertension) who, according to previously published reports,
as the Coronary Artery Disease Risk Development in Young Adults
typically present to EDs in the United States with elevated blood
have shown a low prevalence of left-ventricular hypertrophy in
pressure.34,47 Because hypertension contributes more than any
nonhypertensive black men (5%) and women (3%).19
other factor (⬇15%) to the overall racial difference in years of life
Furthermore, this study and the Dallas Heart Study, a probability-
lost to cardiovascular disease,28 initiatives targeting improved care
based random sample of Dallas County that included 1,335 blacks,
for those most at risk (especially within racially disparate locations)
found prevalent left-ventricular hypertrophy to be mostly mediated
are likely to be a high-yield endeavor.
by variation in blood pressure,19,35 suggesting that our results do
What are the specific implications of this research for
indeed reflect an independent relationship between blood pressure
emergency medicine? First and foremost, it highlights the
and subclinical cardiac disease.
unavoidable confluence of primary and acute care in the ED
DISCUSSION setting and suggests a need to be more proactive in the
In this study of asymptomatic, predominantly black individuals identification and referral of patients with uncontrolled or
who presented to our urban ED with elevated blood pressure, untreated hypertension. Since 2006, this approach has been
subclinical hypertensive heart disease was detected in 9 of every 10 endorsed in an official clinical policy on asymptomatic
patients. These data, which to our knowledge are the first to be hypertension by the American College of Emergency
compiled in such a population, greatly exceeded our estimated Physicians,31 yet according to a recent survey of ED directors,
point prevalence and underscore the disproportionate population- only 50% of US EDs routinely provide such a service.48 The
attributable risk of cardiovascular disease that hypertension imparts point is not to add further screening activities to the ED load
on the inner-city black community.28,36 Beyond epidemiologic but to enhance responsiveness to tasks that we currently carry
implications, the presence of subclinical hypertensive heart disease out (ie, check a blood pressure on every patient). Elevated blood
heralds an important branch point in clinical management because, pressure is common in the ED setting, even among patients
according to recently published guidelines by the International who lack overt evidence of end-organ damage, and knowing
Society of Hypertension in Blacks, such patients should be treated that up to 90% are at increased risk over time for death or other
in a manner that targets more aggressive blood pressure goals adverse events is actionable information. To be most effective,
(⬍130/80 mm Hg) than current guidelines based on the 7th however, the ED should function as a point at which a
Report of the Joint National Committee on Prevention, Detection, coordinated transition to enhanced outpatient management can
Evaluation, and Treatment of High Blood Pressure (⬍140/90 mm be initiated, not a destination for definitive care. Even then,
Hg).36 Appropriate antihypertensive therapy contributes clinician and patient inertia is common, and espousing a role
substantially to regression of left-ventricular remodeling and, in within the larger context of accountable care is important.
patients with subclinical hypertensive heart disease, decreases the Empowering patients for success through education, including
likelihood of subsequent cardiovascular disease morbidity and diet (especially sodium intake) and exercise advice, smoking

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Levy et al Hypertension in the Emergency Department

cessation counseling, encouragement of medication compliance, Presented at the Society for Academic Emergency Medicine
and provision of information regarding blood pressure goals, is a annual meeting, May/June 2008, Washington, DC; and the
simple activity that can be accomplished during a relatively brief Society for Academic Emergency Medicine annual meeting,
May 2009, New Orleans, LA.
interaction. In patients with persistently poor blood pressure
control, up-titration of antihypertensive therapy from the ED or Address for correspondence: Phillip Levy, MD, MPH, E-mail
referral to a subspecialty hypertension clinic may be needed. plevy@med.wayne.edu.
Our data also serve as a reminder that, in general, ED
patients with chronic disease are a high-risk subset, a finding
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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)

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