(Hypertension. 2000;35:614.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Attenuation of the "White-Coat Effect" by Antihypertensive Treatment and Regression of Target Organ Damage
From the Clinica Medica, University of Milano-Bicocca and Ospedale S. Gerardo, Monza (G.M.); Centro di Fisiologia Clinica e Ipertensione, IRCCS, Ospedale Maggiore Milano (L.S.); Clinica Medica, University of Padua (P.P.); and the Istituto Scientifico Ospedale S. Luca, IRCCS, Istituto Auxologico Italiano, Milan (G.P., L.U., A.Villani, G.M., A. Vanasia), Italy.
Correspondence to Gianfranco Parati, MD, Ospedale S. Luca, IRCCS, Istituto Auxologico Italiano, via Spagnoletto, 3 20149 Milano, Italy. E-mail gparati{at}mailserver.unimi.it
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Abstract |
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Abstract—This study assessed whether 2 common surrogate measures of the "white-coat effect," namely the clinic-daytime and the clinic-home differences in blood pressure (BP), were attenuated by long-term antihypertensive treatment and whether this attenuation is relevant to the treatment-induced regression of left ventricular hypertrophy, thus having clinical significance. We considered data from 206 patients with essential hypertension (aged 20 to 65 years) who had a diastolic BP between 95 and 115 mm Hg and echocardiographic evidence of left ventricular hypertrophy. In each patient, clinic BP, 24-hour ambulatory BP, and left ventricular mass index were assessed at baseline, after 3 and 12 months of treatment with an angiotensin-converting enzyme inhibitor, and after a final 4-week placebo run-off period. At baseline, the clinic-daytime differences in systolic and diastolic BP were 12.1±15.4 and 6.8±10.1 mm Hg, respectively; the corresponding values for the clinic-home differences were 5.7±10.6 and 2.9±6.1 mm Hg, respectively. These differences were reduced by 57.6% and 77.1% (P<0.01) and by 65.7% and 64.3% (P<0.01), respectively, after 12 months of treatment, with a partial return toward the pretreatment differences after the final placebo period. The observed treatment-induced reductions in left ventricular mass index and those in the clinic-daytime or clinic-home differences for systolic and diastolic BP showed no significant relationship when tested by multiple regression analysis. This provides the first longitudinal evidence that clinic-daytime and clinic-home differences in BP have no substantial value in predicting the regression of target organ damage, such as left ventricular hypertrophy, that has prognostic relevance.
Key Words: blood pressure • hypertension, white-coat • antihypertensive agents
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Introduction |
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Clinic blood pressure (BP) is greater than ambulatory or home BP in most hypertensive patients,1 2 and a major current question is whether the condition in which the former value is elevated when the latter ones are not3 is an innocent phenomenon or if it has an adverse prognostic significance. Some studies reported that in subjects with a high clinic but a normal ambulatory BP, little or no end-organ damage4 5 and no increase in the frequency of cardiovascular morbid or fatal events occurs.5 Other studies, however, have shown that this condition is associated with alterations in organ structure and function or, in subjects with a high clinic and a normal home BP, with metabolic risk factors frequently accompanying hypertension.6 7 8 9 For this reason, guidelines on hypertension have found it difficult to decide whether isolated clinic hypertension (also widely known as white-coat hypertension) requires immediate treatment or just follow-up with no antihypertensive drug administration.10 11 Although some negative data were recently collected,12 no conclusive evidence exists regarding the clinical relevance of another commonly used BP parameter, ie, the surrogate measure of the "white-coat effect" that is quantified as the absolute difference between clinic and ambulatory or home BP, regardless of whether ambulatory of home values are in the normotensive or the hypertensive range.12 13
The present study focused on 3 questions never addressed before on this matter. (1) Does the clinic-daytime BP difference become attenuated with long-term antihypertensive drug administration? (2) What is the relationship between the 2 means commonly used to obtain a surrogate measure of the white-coat effect in the medical practice, ie, the clinic-daytime and the clinic-home BP differences? (3) Does the attenuation of these differences have any relevance to the treatment-induced improvement of end-organ damage and, thereby, carry prognostic significance?
Addressing these questions was made possible by the data collected in the SAMPLE study, which was a prospective, single-blind, noncomparative study aimed at determining the relationship of long-term reductions in clinic, home, and ambulatory BP with the regression of left ventricular hypertrophy in hypertensive patients.14
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Methods |
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Patients
A total of 206 patients with essential hypertension from 11 hypertension centers located in Italy13 were included in the present study using the following criteria: (1) age between 20 and 65 years, (2) a diastolic BP (DBP) between 95 and 115 mm Hg after a 4-week washout from antihypertensive drugs (previously treated patients) or a 3-week observation period (previously untreated patients), and (3) a left ventricular mass index
110 g/m2 in
women and 131 g/m2 in men. Exclusion criteria
were the occurrence of cardiovascular complications or
major cardiovascular or
noncardiovascular diseases besides hypertension and
previous antihypertensive treatment consisting of >2 drugs; these
criteria were used to minimize subsequent drop-out because of a lack of
BP control (see below). All patients consented to the study after being
informed of its nature and purpose. The number of patients dropped
slightly from the initial to the final evaluation after 13 months, but
it always remained higher than the minimum required to ensure adequate
statistical power (158 subjects).14 When patients were
divided into 2 subgroups based on whether their clinic-daytime and
clinic-home BP differences were, respectively, higher or lower than the
median value of the whole group, the number of subjects who dropped out
over time was evenly distributed: 48.5% were in the group with higher
and 51.5% were in the group with lower clinic-daytime or clinic-home
BP differences. The study protocol was approved by the Ethics
Committees of the Centers involved.
BP Measurements
Clinic BP was measured in the morning using a mercury
sphygmomanometer; the first and fifth Korotkoff sounds were used to
identify systolic and diastolic values,
respectively. Two measurements were collected with the patient in the
supine position for 5 and 8 minutes, respectively, and the average of
the 2 values was taken as the clinic BP for inclusion in the study and
for the determination of the efficacy of treatment.
Home BP was measured by a semiautomatic oscillometric device (Model HP 5331, Philips); its accuracy was shown in previous studies.15 The patient was asked to obtain a morning and an evening measurement in the sitting position during the same day in which ambulatory BP monitoring was performed. Morning and evening values were averaged.
Ambulatory BP monitoring was performed by oscillometric SpaceLabs 90202 or 90207 equipment.16 The cuff of the monitoring device was applied to the nondominant arm at the end of the clinic BP measurements, and the device was set to obtain automatic BP readings at 15-minute intervals during the day (from 6 AM to midnight) and at 20-minute intervals during the night (from midnight to 6 AM). The patient was then sent home with instructions to perform his or her usual activities; to hold the arm immobile at the time of the measurements; to note in a diary the occurrence of unusual events, sleep time, and sleep quality; and to return 24 hours later. The BP monitoring was always performed over a working day (Monday through Friday). Before monitoring began, a few BP readings were taken simultaneously with readings provided by a physician using a mercury column to ensure that, on average, the 2 sets of values did not differ by >5 mm Hg.
Ambulatory BP recordings in which BP readings regarded as valid
by the machine software17 were <70% of the expected
number of readings and/or showed no valid readings for 2 hours were
not considered for analysis. In the patients in whom ambulatory
BP data were accepted for further analysis, the number of
daytime readings was, on average, always >96% of the expected number
of readings (which amounted to 72 measures over the 24 hours).
Echocardiography
Left ventricular diameter, septal wall thickness,
and left posterior wall thickness were assessed by M-mode
echocardiography after selecting the measurement
section by B-mode echocardiography. Data were
averaged over 5 cardiac cycles. Left ventricular mass index
was calculated from thickness and diameter values using the Penn
convention formula.18
Study Protocol
The study was conducted using a single-blind, noncomparative,
prospective design. After an initial medical visit, patients were kept
in a no-drug condition for 4 weeks if they were previously treated and
for 3 weeks if they were untreated. This was followed by a second
medical visit and, for patients satisfying recruitment criteria, by the
administration of lisinopril at a morning dose of 20 mg.
Lisinopril was selected because the administration of an
angiotensin-converting enzyme inhibitor
guarantees the regression of left ventricular
hypertrophy,19 which was necessary to compare
the relative importance of the effect of treatment on clinic, home, and
ambulatory BP in relation to regression of target organ damage. A
morning dose of 12.5 or 25 mg of hydrochlorothiazide
was added during subsequent visits in nonresponders, ie, in patients in
whom clinic DBP at trough had not fallen below 90 mm Hg or by
10 mm Hg. Treatment was continued for an overall period of 12
months; after this time, antihypertensive drugs were substituted, in a
single-blind fashion, with placebo tablets, which were administered for
an additional 4-week period. Home BP, ambulatory BP, and
echocardiographic data were collected before the
beginning of treatment, after 3 and 12 months of treatment, and at the
end of the final placebo period.
Data Analysis
Data obtained in the longitudinal study were analyzed
retrospectively. In each patient, the differences between clinic and
home and clinic and average daytime systolic BP (SBP) were
computed for the data obtained before treatment, after 3 and 12 months
of treatment, and at the end of the final placebo period. Daytime SBP
was defined as the average value obtained for the hours in which the
subjects reported in their diary as being awake. These waking hours
were selected within the time interval ranging from 6 AM to
midnight. Results from individual subjects were expressed as means±SEM
for the group as a whole. Similar calculations were made for the
differences between clinic and home or daytime average DBP. The
reproducibility of these differences was assessed by computing the
correlation coefficients between the data obtained in the initial and
subsequent periods.
Echocardiographic data were obtained for pretreatment and drug treatment conditions. Both univariate and multivariate linear regression analyses were applied to the changes in left ventricular mass index after 12 months of treatment and the corresponding treatment-induced changes in clinic BP, home BP, and clinic-home or clinic-daytime average BP differences. When multiple regression analysis was performed, the treatment-induced changes in average daytime or home BP and treatment-induced changes in clinic-daytime or clinic-home BP differences were included in the model as independent variables; these data were separated into SBPs and DBPs. Treatment-induced changes in left ventricular mass index or in left ventricular wall thickness (average of septal and left posterior wall thickness) were taken as dependent variables.
The statistical significance of the treatment-induced changes was assessed by ANOVA and by Student’s t test for paired observations, with Bonferroni’s correction for repeated comparisons when necessary, after the determination of the normality of the data distribution by the Shapiro Wilk nonparametric test.20 P<0.05 was the level of statistical significance.
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Results |
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Clinic-Daytime BP Difference Before and During Treatment
Figure 1 shows that before treatment, the average clinic SBP was higher than the average daytime SBP; both measures fell after 3 and 12 months of treatment and returned toward the initial high values after the final placebo period. In all 4 conditions, the clinic-daytime SBP difference showed large between-patient variability. Compared with the pretreatment condition, however, the mean difference decreased after 3 and 12 months of treatment (P<0.01), with a return toward the initial higher mean value after the final placebo period (Table 1; Figure 2, top left). Similar findings were obtained for DBP (Figure 2, top right). As shown in Table 2, the clinic-daytime BP differences before treatment were, in general, significantly related to the corresponding differences after the final off-treatment period. This was also the case for the clinic-daytime BP differences after 3 and 12 months of treatment. In no instance, however, were the correlation coefficients >0.45.
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Clinic-Home BP Differences Before and During Treatment
Figure 1 shows that before treatment, home SBP and
DBP values were lower than the corresponding clinic values but higher
than the corresponding average daytime BP values; the pretreatment
clinic-home BP differences were, thus, smaller than the clinic-daytime
BP differences. The clinic-home BP differences decreased after 3 and 12
months of treatment (more after 12 than 3 months), with a partial
return toward the pretreatment values after the final placebo period;
this return was less evident than that observed for the clinic-daytime
BP differences (Table 1; Figure 2, bottom). The
clinic-home BP differences observed in the periods without treatment
(pretreatment and final placebo values) were also usually related (but
only to a limited extent and with 1 exception) to those during
treatment (3 and 12 months of treatment) (Table 2). Before
treatment, the clinic-home BP differences showed a limited, although
significant, relationship with the clinic-daytime BP differences. This
also occurred when the changes in these 2 measurements induced by
treatment were considered (Figure 3); the
relationship was closer for SBP than DBP values.
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Clinic-Daytime or Clinic-Home BP Differences and Left
Ventricular Mass Index
As shown in Figure 1, the left ventricular mass
index was reduced by 3 months and even more so by 12 months of
treatment, with a significant increase after the final placebo
period.14 The change in left ventricular mass
index induced by 12 months of treatment was significantly related to
the treatment-induced change in daytime SBP and DBP (r=0.37
and 0.36, respectively; P<0.001 for both), but not to the
treatment-induced modification of the clinic-daytime BP differences
(multiple regression analysis, ß=-0.10 and -0.14 for the
clinic-daytime difference in SBP and DBP, respectively; P=NS
for both). The treatment-induced change in left ventricular
mass index was also weakly related to the concomitant change in home BP
(r=0.23 for SBP and 0.19 for DBP; P<0.05 for
both) but, again, not to the change in the clinic-home BP differences
(multiple regression analysis, ß=-0.10 and -0.20 for the
clinic-home difference in SBP and DBP, respectively; P=NS
for both). The results are shown in a tridimensional fashion
in Figure 4.
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-LVMI), average daytime BP
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Discussion |
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Our study provides data on all 3 questions mentioned in the introduction. These data will be discussed separately.
Does Antihypertensive Treatment Attenuate the Clinic-Daytime
BP Difference?
In our study, the clinic-daytime SBP and DBP differences observed
in the initial pretreatment period showed marked between-patient
variability. The average differences, however, were reduced after 3
months (-47% and -61%, respectively, for SBP and DBP;
P<0.01), and a slight further reduction was observed after
12 months of treatment (-58% and -77%, respectively, for SBP and
DBP; P<0.01 versus baseline). A clear-cut, although
incomplete, return toward the initial average differences occurred at
the end of the final off-treatment period. This extends previous
reports of an attenuation of these surrogate measures of the
"white-coat effect" after short-term
treatment.21 22 It further shows, however, that this
attenuation tends to progress with the duration of the treatment period
and that active treatment is presumably involved. This, of course,
pertains to the type of treatment used in the present study.
Whether antihypertensive drugs or drug combinations other than
angiotensin-converting enzyme inhibitors and
diuretics perform similarly or differently remains to be
assessed.
Two further points should be mentioned. First, in the final off-treatment period, the clinic-daytime BP differences remained somewhat smaller than in the initial pretreatment period. This may be interpreted as indicating that these surrogate measures of the white-coat effect can indeed be attenuated by time. However, in the final off-treatment period, patients were given a placebo, which may have reduced clinic BP and, thus, the clinic-daytime BP differences when compared with the values seen in the initial pretreatment period in which a placebo was not used. Furthermore, for ethical reasons, the duration of the final placebo period was kept short (4 weeks), which probably prevented full restoration of the initial high BP values. Thus, although the participation of a time factor in the alteration of the clinic-daytime and clinic-home BP differences during treatment cannot be precisely established by our study, its importance is unlikely to be a major one.
Second, the clinic-daytime BP differences observed at various times during the study were almost invariably correlated, although not to a close degree, with the initial ones. This implies that these surrogate measures of the white-coat effect have an individual sign that survives, to some extent, the effect of several modifying influences. Namely, this suggests that a hypertensive patient who was originally in the upper range of this phenomenon tends to remain in this range over time, regardless of whether active treatment is administered.
Is There a Relationship Between the Surrogate Measures of the
White-Coat Effect Derived From Clinic-Daytime and Clinic-Home BP
Differences?
Our study shows that the clinic-home BP difference displays
similarities to but an important discrepancy with the other method of
indirectly quantifying the white-coat effect, the clinic-daytime BP
difference. The similarities consist in the fact that both differences
are characterized by the following: limited reproducibility, both
during and in the absence of antihypertensive treatment; an attenuation
after 3 and 12 months of treatment; and a tendency to return toward
baseline values during placebo administration, although the latter
occurred to a lesser extent in the clinic-home differences than in the
clinic-daytime differences. The discrepancy is that the clinic-home SBP
and DBP differences are no more than half of the corresponding
clinic-daytime differences, both during and in the absence of
treatment. Thus, the white-coat effect is subjected to a highly
discordant quantification, depending on which of the 2 surrogate
methods is used to determine it.
The reasons why the white-coat effect is so markedly greater when indirectly quantified by the clinic-daytime BP differences instead of the clinic-home BP differences are not clarified by our study. We speculate that, in this respect, the former difference is more relevant than the latter, because in hypertensive patients, self-measurements of BP at home may elicit an emotionally induced BP rise,14 15 which is not elicited when BP is measured automatically or semiautomatically by an ambulatory device.23 Evidence is available, however, that neither difference accurately reflects the actual pressor effect of BP measurements in a clinical environment, ie, the "true" white-coat effect.24 25 26 Thus, we can also speculate that the clinic-daytime BP difference is greater than the clinic-home one because daytime BP, which is the average of a large number of readings, undergoes an instantaneous regression to the mean, which makes it lower than the average of a few clinic and a few home readings.
Treatment-Induced Attenuation of the Clinic-Daytime and Clinic-Home
BP Differences Versus Regression of Left Ventricular
Hypertrophy
In the hypertensive patients in the SAMPLE study, the regression
of left ventricular hypertrophy induced by 1
year of antihypertensive treatment correlated with the
treatment-induced reduction of daytime and (less so) home BP but not
with the treatment-induced reduction in clinic BP.14 The
additional important finding of the present study, however, is that
neither the attenuation of the clinic-daytime BP difference nor the
attenuation of the clinic-home BP difference induced by
antihypertensive drug treatment had any relationship with the
treatment-induced regression of left ventricular
hypertrophy. This provides the first longitudinal evidence
that these commonly used surrogate methods of quantifying the
white-coat effect25 do not predict the treatment-induced
improvement of structural cardiac alterations, which is predicted to a
significant degree only by the effect of treatment on a BP obtained
outside the clinic environment.14 This supports the
hypothesis that surrogate measures of the white-coat effect, such as
the clinic-daytime or clinic-home BP differences, are of marginal
clinical significance.4 5 6 25
It should be emphasized that this conclusion is based on echocardiographic left ventricular hypertrophy, ie, on end-organ damage of prognostic significance. This has been demonstrated in observational studies27 28 in which subjects with left ventricular hypertrophy showed an incidence of cardiovascular disease that was greater than that in those without left ventricular hypertrophy. It has also been shown, although less conclusively, in longitudinal studies in which the regression of left ventricular hypertrophy by antihypertensive treatment was accompanied by the reduction of arrhythmias; improvement of cardiac function, coronary reserve, and cardiogenic reflexes; and, in the context of uncontrolled studies, a reduction in cardiovascular mortality.29 30 31 32 33 34 35 36 37 38 It should also be emphasized, however, that the lack of clinical relevance of the surrogate measures of the white-coat effect may apply to the type of patients involved in our study and that whether these measures have any additional clinical value over ambulatory or home BP values in patients with milder hypertension and no end-organ damage remains to be assessed. Further insight on these issues might benefit from additional longitudinal, controlled studies on both uncomplicated and complicated hypertensive individuals to determine the relevance of treatment-induced modifications of clinic-home or clinic-ambulatory BP differences on other organ damage and on cardiovascular morbid events. It also remains to be assessed whether the direct quantification of the "true" white coat effect (ie, the actual increase in BP during a visit by a physician26 ) might have a better clinical value than the surrogate measures of this phenomenon considered in our study.
Received March 29, 1999; accepted September 27, 1999.
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G. Mancia and G. Parati Ambulatory Blood Pressure Monitoring and Organ Damage Hypertension, November 1, 2000; 36(5): 894 - 900. [Abstract] [Full Text] [PDF]
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