(Hypertension. 1995;26:801.)
© 1995 American Heart Association, Inc.
Articles |
Target Organ Status and Serum Lipids in Patients With White Coat Hypertension
From the Centro per lo Studio e la Terapia dell’ Ipertensione Arteriosa, Istituto di Fisiopatologia Medica, University G. D’Annunzio, Chieti, Italy.
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Abstract |
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Abstract Target organ status and serum lipids were investigated in white coat hypertension in comparison with sustained hypertension and normotension. We selected three groups balanced for sex, age, body mass index, and smoking habit: 50 sustained hypertensives (clinical hypertension and 24-hour ambulatory blood pressure >135/85 mm Hg, a cutoff limit obtained from a normotensive population), 25 white coat hypertensives (clinical hypertension and 24-hour ambulatory blood pressure <135/85 mm Hg), and 25 normotensives. Subjects underwent echocardiographic examination to assess left ventricular mass index, carotid ultrasonography to evaluate intima-media thickness and atherosclerotic plaques, venous occlusion plethysmography to record minimum forearm vascular resistance, and determinations of serum lipid profile and 24-hour urinary albumin excretion. Compared with sustained hypertensives, the white coat hypertensives had significantly lower values of left ventricular mass index (125.9±20 versus 97.6±11.5 g/m2, P<.05), intima-media thickness (0.85±0.18 versus 0.71±0.15 mm, P<.05), minimum forearm vascular resistance (2.33±0.11 versus 2.04±0.08 resistance units, P<.05), urinary albumin excretion values (15.1±13.8 versus 4.45±1.48 mg per 24 hours, P<.0001), prevalence of left ventricular hypertrophy (38% versus 4%, P<.002), intima-media thickening (28% versus 4%, P<.015), and microalbuminuria (22% versus 0%, P<.015). No significant difference, however, was observed between the white coat hypertensives and the normotensives. Serum lipid profile was similar in the white coat hypertensives and in the normotensives. In conclusion, our data demonstrate that white coat hypertensives do not show target organ damage and do not present an unfavorable lipid profile, suggesting that they may be counseled on nonpharmacological therapy and that drug treatment could be withheld or delayed.
Key Words: hypertension, white coat • lipids • blood pressure monitoring, ambulatory
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Introduction |
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Some patients have elevated BP in the clinic or physician’s office and normal pressure at other times1 2 3 because of an alarm reaction that triggers a rise in BP.4 This phenomenon is called white coat hypertension1 2 3 and can be reliably identified by ABPM.1 The prognosis for white coat hypertensives is not yet completely clear. To date, there is apparently only one prospective study5 in the literature that deals with prognostic aspects of white coat hypertension investigated with ABPM. While we wait for other, definitive prospective studies on the morbidity and mortality of these patients, the detection of target organ damage remains the main tool with which to evaluate whether or not these patients are at increased cardiovascular risk. In this regard, it has been shown that LV hypertrophy is related to cardiovascular morbidity and mortality.6 7 However, contrasting results have been reported about cardiac involvement in white coat hypertension.2 8 9 10 11 12 Moreover, there are few data on small vessel involvement,3 serum lipids,3 12 13 or microalbuminuria14 (a marker of early renal damage15 that is also related to vascular disease16 and increased mortality17 in nondiabetic subjects). Furthermore, to the best of our knowledge, apparently no study has been devoted to the investigation in white coat hypertensives of the presence of atherosclerotic plaques and IM thickening in the carotid arteries. These represent relevant pathological concerns since they are associated with cerebrovascular disease18 and higher risk of coronary events.19
The present study, therefore, was designed to perform a widespread evaluation of target organ status and serum lipid profile in subjects with white coat hypertension compared with subjects with normotension and those with sustained hypertension.
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Methods |
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Subjects
Two hundred fifty-five untreated research subjects with hypertension according to clinical BP (>140/90 mm Hg) and 100 normotensive control subjects underwent ABPM to evaluate daytime, nighttime, and 24-hour systolic and diastolic BP. Among clinically hypertensive subjects, 201 were defined as sustained hypertensive, and 54 were classified as white coat hypertensive (see below for definition of white coat hypertension). From all these individuals, we selected three groups balanced for sex, age, body mass index, and smoking habit: 50 sustained hypertensive, 25 white coat hypertensive, and 25 normotensive subjects. These groups underwent additional studies. Exclusion criteria for entry in the study were ischemic or valvular heart disease, congestive heart failure, cerebrovascular accidents, diabetes mellitus, chronic renal failure, known secondary hypertension, antihypertensive drug use, and a limited echocardiographic acoustic window. The study was in accordance with the Second Declaration of Helsinki. All participating subjects gave informed consent signing a consent form approved by the Human Ethical Committee of the University of Chieti.
Office BP Measurements
Clinical systolic and diastolic BP
recordings were performed on the same arm, with the subject in
the supine position after 10 minutes of quiet rest, according to a
standard technique.20 Phase V was used to determine
diastolic BP. Measurements were performed in triplicate,
and the average value was used as the BP for the visit.
ABPM
ABPM was performed with a portable noninvasive recorder
(SpaceLabs SL-90207) on a day of typical activity. The accuracy of the
recorder was assessed by taking three simultaneous
readings with a mercury manometer through a Y-tube, as suggested by
Santucci et al.21 The recorder achieved, for both
systolic and diastolic BP, grade B of the British
Hypertension Society protocol and satisfied the accuracy
criteria of the Association for the Advancement of Medical
Instrumentation. Ambulatory BP readings were obtained automatically at
15-minute intervals from 6 AM to midnight, and at 30-minute
intervals from midnight to 6 AM. Each time a reading was
taken, subjects were instructed to remain motionless and to record
their activity on a diary sheet. On completion of ABPM, the data were
analyzed by computer with a program designed to perform editing
and interval statistics. Readings were automatically edited if
systolic BP was >260 or <70 mm Hg or if diastolic
BP was >150 or <40 mm Hg and pulse pressure was >150 or <20 mm Hg.
The following ABPM parameters were evaluated: average
daytime systolic and diastolic BP, average
nighttime systolic and diastolic BP, and average
24-hour systolic and diastolic BP. Average daytime
and nighttime BPs were obtained according to the awake and asleep
periods; thus, these values were recalculated from the single readings
taking into consideration the indications reported in the diary. All
subjects included in the study had recordings of good technical
quality. The recordings were analyzed by the same
physician (T.A.), blinded with respect to the other data.
Definition of White Coat Hypertension
There is no general agreement on the normal limits of ambulatory
BP values, and different upper limits of normalcy have been used in
previous studies.1 2 3 22 23 24 25 26 27 Thus, rather than a previously
reported cutoff point and in light of possible influence of
"geographic" location on BP, we chose the BP values
representing the upper limits (mean+2 SD) of a clinically
normotensive population studied in our geographic area (Chieti,
Abruzzo, Italy). Such a population, which was characterized by a normal
distribution of BP values, was formed by 100 subjects, 60 men and 40
women (age, 46.5±10 years; age range, 20 to 60 years). The resulting
upper limit for average 24-hour BP was 135/85 mm Hg. Thus, subjects
classified as hypertensive according to clinical BP but who had 24-hour
systolic and diastolic BP <135/85 mm Hg were
classified as white coat hypertensive, whereas the remaining
hypertensive subjects were considered to have sustained hypertension.
Because of the relatively small population studied, we could not use
cutoff points stratified for age and sex. In any case, there was no
significant difference among the sustained hypertensive, the white coat
hypertensive, or the normotensive subjects with regard to sex and age,
both for the original groups (201, 54, and 100 subjects, respectively)
and the selected groups (50, 25, and 25 subjects, respectively). Our
reference limit for diastolic BP, however, was the same as
that of Krakoff et al,22 Weber,26 and Khoury
et al.27 When we applied to average daytime BPs of our
clinically hypertensive subjects the cutoff points suggested by
Pickering et al1 (134/90 mm Hg for daytime BP), Verdecchia
et al23 (136/90 mm Hg for daytime BP), and Staessen et
al24 (146/91 mm Hg for daytime BP), the prevalence of
white coat hypertension was 18.4% (95% confidence interval [CI],
13.7% to 23.1%), 19.2% (95% CI, 14.4% to 24%), and 22.7% (95%
CI, 17.6% to 27.1%), respectively.28 These values were
not significantly different from the result obtained with our reference
limit (21%; 95% CI, 16% to 26%).28 We also used the
above-mentioned reference limits reported in the literature to
reclassify the selected sustained hypertension and white coat
hypertension groups.
Echocardiography
Echocardiograms were recorded with a Hewlett-Packard 77030A
ultrasound imaging system equipped with a 2.5- or 3.5-MHz transducer.
All studies were performed by the same echocardiographer
(S.D.P.), who was unware of the subjects’ characteristics.
Two-dimensionally guided M-mode echocardiograms of the LV were
taken at the cordal level with the patient in the partial left lateral
decubitus position, and three to five measurements were averaged.
End-systolic and end-diastolic measurements
of interventricular septal thickness, LV internal
diameter, and posterior wall thickness were made according to the
American Society of Echocardiography
recommendations.29 LV mass was calculated using the
formula introduced by Devereux et al30 based on necropsy
validation studies. Individual values for LV mass were indexed by body
surface area (LV mass index). LV hypertrophy was defined as
reported by Devereux et al.31 The reproducibility of
measurements was studied by performing a repeat examination 3 days
later in a randomly drawn subsample of 30 subjects. The coefficient of
variation and the repeatibility coefficient32 for
end-diastolic LV wall thickness measurements were 3.7%
and 0.85 mm, respectively, and for end-diastolic LV
internal diameter measurements were 2.3% and 2.1 mm, respectively.
Carotid Ultrasonography
Ultrasonographic scanning was performed with a Hewlett-Packard
model 77030A ultrasound imaging system with a 7.5-MHz transducer. All
studies were performed by a trained sonographer (M.D.G.) who was
blinded with regard to the subjects’ characteristics. Subjects were
examined in the supine position with a slight hyperextension of the
neck, and then the common carotid artery, carotid bulb, and
extracranial internal and external carotid arteries were identified.
The carotid arteries were explored with longitudinal and transverse
scans. Measurements of lumen diameter and IM thickness were made in
both right and left common carotid arteries at least 1 cm below the
carotid bifurcation, at end diastole by
electrocardiographic triggering. Lumen diameter was defined as the
distance between the leading edges of the intima-lumen interface of
the near wall and the lumen-intima interface of the far wall. IM
thickness was defined as the distance from the leading edge of the
lumen-intima interface of the far wall to the leading edge of the
media-adventitia interface of the far wall.33 34 The
mean of six measurements was used to derive an estimate of the overall
IM thickness of common carotid arteries. IM thickening was defined as
IM thickness >1 mm.19 35 The atherosclerotic lesion was
defined as a plaque when a distinct area could be identified either
with mineralization (bright echo, often producing a typical echogenic
shadow) or with focal protrusion into the lumen. A plaque was defined
as stenotic if it obstructed >20% of the lumen diameter in
the projection with the greatest diameter
obstruction19 The reproducibility of the measurements of
IM thickness was studied by performing a repeat scan 1 week later in a
randomly drawn subsample of 30 subjects. The coefficient of variation
and the repeatibility coefficient32 were 6.7% and 0.11
mm, respectively.
Forearm Plethysmography
All subjects were studied in the supine position in a quiet room
at a temperature of approximately 22°C (72°F). The dominant arm was
slightly elevated above the level of the heart, and a
mercury-filled silicone elastomer (Silastic) strain gauge was
placed approximately 7 cm below the olecranon.36 This
gauge was connected to a plethysmograph (Hokanson EC-5R). A BP cuff was
placed on the upper arm and intermittently inflated to 40 mm Hg with a
rapid cuff inflator (Hokanson E-10) to occlude venous outflow from the
extremity. A wrist BP cuff was inflated to suprasystolic
pressure 1 minute before any recording was made, to exclude the
hand circulation.37 The sequential inflation and deflation
of the cuff on the upper arm were timed to give four FBF measurements
each minute, under basal conditions. BP was recorded in the
contralateral arm by sphygmomanometry. FBF (in mL/100 mL forearm volume
per minute) was calculated from the mean vertical deflection per minute
on the tracings divided by the 1% electrical calibration signal.
Forearm vascular resistance, expressed as resistance units, was
calculated as the mean arterial pressure
(diastolic pressure plus one-third pulse pressure)
divided by the FBF. To evaluate the hyperemic response to
ischemia, the BP cuff on the upper arm was inflated to 250 mm
Hg, thereby occluding the circulation in the forearm. A period of 12
minutes of ischemia coupled with exercise in the last 2 minutes
of the ischemia was adopted.38 On completion of
the ischemic period, the occluding cuff was rapidly deflated to
0 mm Hg, then reinflated to 40 mm Hg with maximum FBF measurements
determined from the mean of the six highest curves during the 60 to 90
seconds immediately after the ischemic release. mFVR was
calculated as the ratio of mean arterial pressure to
maximum FBF. As previously reported by Folkow,39 mFVR can
be taken as a hemodynamic index of the arteriolar
structural changes in hypertension. All examinations were performed by
one investigator (C.S.) who was unaware of the subjects’
characteristics. In 20 patients, the intraday and interday coefficients
of variation for mFVR were 8.1% and 10.8%, respectively.
Biochemical Analyses
Blood samples for total serum cholesterol, HDL-C,
triglycerides, glucose, and creatinine were
drawn after a fasting period of 12 hours. Total cholesterol
and triglyceride levels were determined by an enzymatic
technique. HDL-C was measured similarly after precipitation of the
non-HDL fraction with phosphotungstate-magnesium.
Low-density-lipoprotein cholesterol was calculated
as described by Friedewald et al.40 Plasma glucose and
creatinine were determined by an oxidase method. Subjects
made a 24-hour complete urine collection for determination of
creatinine and UAE on 3 consecutive days of similar
physical activity. UAE was evaluated by immunonephelometric
technique41 and reported as an average value of the three
samples. Microalbuminuria was defined as UAE >30 mg
per 24 hours and <300 mg per 24 hours42 in at least two
of the three samples. Creatinine clearance was also
calculated.
Statistical Analysis
Data are expressed as mean±SD. Groups were compared with
one-way ANOVA followed by Scheffè’s test for multiple
comparisons regarding continuous variables and the Kruskal-Wallis
test followed by the Mann-Whitney U test for multiple
comparisons regarding noncontinuous variables.43
Frequency distribution was analyzed with Fisher’s exact test
and 
2 test where appropriate.43 All
analyses were made with the use of SYSTAT package
implemented on an Apple Macintosh SE/30 personal computer. Statistical
significance was defined as P<.05.
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Results |
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Characteristics of the study population are reported in Table 1. Age, sex distribution, body mass index, and smoking habits did not differ among the three groups. Table 2 shows clinical and ambulatory BP values in the sustained hypertension, white coat hypertension, and normotension groups.
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Cardiac and Vascular Findings
Cardiac and vascular findings in the three groups are given in
Table 3. LV mass index, IM thickness, mFVR, and
prevalence of LV hypertrophy and IM thickening were
significantly higher in the sustained hypertension group than in the
other two groups; there was no difference, however, between the white
coat hypertension and the normotension groups. Only one subject with
white coat hypertension showed mild LV hypertrophy, and one
white coat hypertensive and one normotensive subject presented
with IM thickening. The prevalence of atherosclerotic plaques was
higher in the sustained hypertensive than in the white coat
hypertensive and the normotensive subjects but did not attain
statistical significance (P=.08) when the latter two groups
were analyzed separately. However, since there was no
difference between the white coat hypertensive and the normotensive
subjects, we have also considered these two groups as a whole. With the
use of this approach the sustained hypertensive subjects had a
significantly higher prevalence (P=.03) of atherosclerotic
plaques.
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Laboratory Findings
Table 4 summarizes laboratory data. Total
cholesterol was higher in the sustained hypertensive than
in the normotensive subjects, but there was no difference between the
sustained hypertensive and the white coat hypertensive subjects or
between the white coat hypertensive and the normotensive subjects.
Triglyceride values and prevalence of
hypertriglyceridemia were greater in the
sustained hypertension group than in the white coat hypertension and
normotension groups; however, there was no difference between the white
coat hypertensive and the normotensive subjects. UAE values and
prevalence of microalbuminuria were higher in the
sustained hypertension group than in the other two groups, and there
was no difference between the white coat hypertensive and the
normotensive subjects. All the other laboratory parameters
reported were similar among the three groups.
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When the selected sustained hypertension and white coat hypertension groups were reclassified according to the cutoff points suggested by Pickering et al1 and Verdecchia et al,23 one subject with white coat hypertension was reclassified as sustained hypertensive; and when the reference limit suggested by Staessen et al24 was applied, one subject with sustained hypertension was reclassified as white coat hypertensive. However, this slight redistribution of the subjects did not change the results previously reported.
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Discussion |
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Measurement of clinical BP has been until recently the cornerstone for diagnosing arterial hypertension. However, the introduction of ABPM among clinically hypertensive patients has allowed physicians to identify the subgroup of white coat hypertensive patients, ie, those patients with high clinical BP but normal pressure at other times. Little is known about the prognosis of these patients and whether they should be treated with antihypertensive drugs. To date, there is apparently only one prospective report5 that deals with prognostic aspects of white coat hypertension investigated with ABPM; this study is indicative of low cardiovascular morbidity in white coat hypertension. While we await other, definitive prospective trials on morbidity and mortality in white coat hypertension, the determination of target organ status appears to be a helpful tool in the clinic management of white coat hypertensive patients.
Some authors2 8 9 have reported that white coat hypertensive patients do not show cardiac damage, whereas others10 11 12 have suggested that white coat hypertension should not be considered an entirely innocuous condition. In our study, the white coat hypertension group showed LV structural characteristics significantly different from those in the sustained hypertension group and similar to those in the normotension group. Thus, our data are in agreement with those by White et al,2 Hoegholm et al,8 and Gosse et al,9 whereas there are some differences between our findings and those by Cardillo et al10 and Kuwajima et al.11 In light of the relevance of ambulatory BP in determining LV mass,44 the discrepancies may be explained by the difference in ambulatory BP values between the normotensive and the white coat hypertension groups. In fact, in both these studies10 11 the white coat hypertensive subjects showed higher ambulatory BP values than the normotensive subjects, whereas there was no difference in ambulatory BP values between the white coat hypertensive and the normotensive subjects in our study. The present findings are consistent with the hypothesis that the white coat effect is specifically related to the clinical setting rather than reflecting a generalized hyperreactivity.45 Moreover, Kuwajima et al11 have studied elderly subjects in whom the increase in LV mass may be due in part to some intrinsic age-related factors. Cardillo et al10 and Kuwajima et al11 have reported a mild increase of LV mass in white coat hypertensive subjects compared with normotensive subjects, the prognostic significance of which is still unknown; the authors, however, did not report in the white coat hypertensive subjects the prevalence of LV hypertrophy, which is clearly related to cardiovascular morbidity and mortality.6 7 Weber at al12 recently reported that LV mass index tended to be higher in white coat hypertensive subjects than in normotensive subjects, but this difference did not reach statistical significance, so their results cannot be considered effectively different from our findings; moreover, they did not report data regarding the prevalence of LV hypertrophy in white coat hypertension. In addition, it should be noted that Weber et al12 used a cutoff point only for 24-hour diastolic BP and not for 24-hour systolic BP, so it cannot be ruled out that a mild elevation of systolic BP in their subjects, classified as white coat hypertensives, could have influenced LV mass index values. Indeed, 24-hour systolic BPs of their white coat hypertensive subjects are apparently higher than those of our white coat hypertensive subjects. Our findings are also supported by previous studies in which target organ damage44 46 and cardiovascular morbidity and mortality47 were more strongly associated with ambulatory rather than clinical BPs.
Julius et al3 reported that white coat hypertensive and sustained hypertensive subjects show similar BP-related arteriolar structural changes; conversely, in the present study, forearm vascular characteristics in the white coat hypertensive subjects were significantly different from those in the sustained hypertensive subjects but similar to those in the normotensive subjects. These differences may be related to various factors. First, the different methods used to define white coat hypertension, ie, home BP recording versus ABPM, could have influenced the classification of subjects; second, in our study there was no difference in ambulatory BP values between the white coat hypertensive and the normotensive subjects, whereas in the study by Julius et al3 a significant difference in home BP values was observed between the white coat hypertensive subjects and the normotensive subjects; and third, the sustained hypertensive population (borderline hypertensive subjects) studied by Julius et al3 bears little resemblance to our sustained hypertensive subjects, who showed higher BP values.
Furthermore, Julius et al3 suggested that white coat hypertensive patients may be characterized by a lipid profile similar to that in sustained hypertensive patients, which includes low HDL-C and high triglyceride values that could increase their cardiovascular risk. These findings were not duplicated in the present study. In fact, global lipid profile was similar in the white coat hypertensive and the normotensive subjects. These discrepancies may depend on different populations studied, dietetic and smoking habits, sample size, and the exclusion of diabetic patients from our study. Our data about HDL-C and triglycerides, however, are in agreement with those reported by Weber et al.12
It has been reported that hypertensive individuals tend to be heavier and more frequently overweight than normotensive individuals,3 48 although there may be geographic and ethnic variations to this issue. Body mass index per se may influence the normal variability of cardiovascular structure, as well as some metabolic features. Thus, we have also balanced the groups for the aforementioned variable, so it is possible that potential disparities between our study and some other investigations may be related to such a methodological approach.
Microalbuminuria has been shown to be positively correlated with BP values in nondiabetic, hypertensive individuals49 50 and may represent a marker of early hypertension-related target organ damage in the kidney.15 Moreover, microalbuminuria has been reported to be associated with vascular disease16 and increased mortality17 in nondiabetic subjects. Hoegholm et al14 showed that white coat hypertensive subjects display less renal involvement than sustained hypertensive subjects, even though they are characterized by slightly higher UAE values than normotensive subjects. In our study, microalbuminuria was not found in either the white coat hypertensive subjects or the normotensive subjects. These discrepancies may be explained by the different methods used to detect UAE, ie, a single early morning urine sample versus 24-hour urine collection on 3 consecutive days (our study), which could have influenced the definition of microalbuminuric subjects, and by the different upper limits of BP used to identify white coat hypertension, which could have influenced subject classification. In fact, Hoegholm et al14 used a cutoff point only for diastolic BP and not for systolic BP; considering the correlation reported by these authors between UAE and systolic BP, it is not clear whether a mild elevation of systolic BP in some patients classified as white coat hypertensive could have influenced UAE values.
Atherosclerotic plaques and IM thickening of carotid arteries are associated with cerebrovascular disease18 and a higher risk of coronary events.19 In the present study, the prevalence of atherosclerotic plaques was significantly higher (P=.03) in the sustained hypertensive than in the white coat hypertensive and the normotensive subjects when these latter two groups were considered as a whole. Furthermore, the characteristics of atherosclerotic plaques (number, percentage of lumen obstruction, and prevalence of complicated lesions) indicated a more severe vascular disease in the sustained hypertensive subjects. More importantly, in the present study there was no difference between the white coat hypertension and the normotension groups concerning the presence of atherosclerotic plaques. IM thickness was significantly higher in the sustained hypertension group than in the white coat hypertension and the normotension groups, without any difference between these latter two groups. Ultrasonic B-mode imaging did not allow us to discriminate between the media and the intima, so we do not know whether IM thickening is related to the thickening of intima and/or media in the sustained hypertension group. Our findings on IM thickness in the sustained hypertension and the normotension groups are in agreement with Roman et al51 and Gariepy et al.52 To the best of our knowledge, however, the present study apparently reports for the first time some data about carotid artery characteristics in white coat hypertension, showing that in these subjects the prevalence of atherosclerotic plaques and IM thickening was similar to that in the normotensive subjects.
In conclusion, our data indicate that white coat hypertensive subjects do not show target organ damage and present a lipid profile similar to that in normotensive persons. In light of the recognized prognostic significance of LV hypertrophy, microalbuminuria, atherosclerotic plaques, and IM thickening, we suggest that white coat hypertensive patients are at low cardiovascular risk. Thus, they should be counseled regarding nonpharmacological therapy, whereas drug treatment could be withheld or delayed. Prospective studies on morbidity and mortality in treated and untreated white coat hypertensive patients seem to be needed to clarify this issue.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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We thank Domenico De Cesare and Giuliano Ciofani for their technical assistance and Franca Daniele, MD, for her help in preparing the manuscript.
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Footnotes |
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Reprint requests to Sante D. Pierdomenico, MD, Istituto di Patologia Medica, c/o Ospedale S.S. Annunziata, via PA Valignani, 66100 Chieti, Italy.
Received March 1, 1995; accepted August 10, 1995.
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