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(Hypertension. 2008;52:856.)
© 2008 American Heart Association, Inc.
Original Articles |
From the Center for Behavioral Cardiovascular Health, Department of Medicine (J.I., D.J.C., S.K., J.E.S., T.G.P.), Columbia University Medical Center, New York; and the Department of Psychiatry and Behavioral Science (J.E.S.), Stony Brook University, Stony Brook, NY.
Correspondence to Thomas G. Pickering, MD, DPhil, Center for Behavioral Cardiovascular Health, Division of General Medicine, Department of Medicine, Columbia University Medical Center, 622 West 168th St, New York, NY 10032. E-mail tp2114{at}columbia.edu
| Abstract |
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20% less than CBP with antihypertensive treatments. Daytime systolic BP falls 15% less and nighttime systolic BP falls 30% less than home systolic BP.
Key Words: home blood pressure self-measured blood pressure clinic blood pressure meta-analysis
| Introduction |
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Recently, devices for the self-measurement of home BP have become widely available, and their use for the evaluation of the effects of antihypertensive treatment has been endorsed by national and international guidelines,5–7 which recommend that BP should be measured both in the morning and at night. Like 24-hour ambulatory blood pressure, home BPs also have greater predictive value for cardiovascular events than clinic BPs.8,9 Home BP monitoring is less expensive and more suited to long-term repeated use than 24-hour ambulatory BP monitoring,10 and can assess the effectiveness of antihypertensive medication on BP control at different times of the day. Verberk et al11 reported in the meta-analysis of home BP monitoring that the average reductions of clinic BP (20.1/13.6 mm Hg) produced by antihypertensive medications were larger than the reductions of home BP (13.9/9.1 mm Hg), but the number of studies available for this analysis was small (6 articles).
The purpose of this study was to compare, in a meta-analysis, the changes in home and clinic BP produced by different antihypertensive drugs, including the changes in both morning and evening BP levels.
| Methods |
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Article Selection
A flow chart summarizing the article selection process is shown in Figure 1.12–41 The full text of those articles identified as potentially relevant on the basis of their titles and abstracts was reviewed by 2 independent investigators (J.I. and D.J.C.). The criteria for articles to be included in the present meta-analysis were as follows: (1) study evaluated the effect(s) of at least one antihypertensive drug therapy, (2) results published for both home BP and clinic BP, pre- and posttreatment, (3) home BP measured using a semiautomatic or automatic upper-arm cuff oscillometric device, and (4) home BP measured in the morning and/or evening according to the guidelines.5–7 Studies were excluded from our analysis if they included: (1) pregnant women, (2) children, (3) patients on hemodialysis, and (4) patients with severe arrhythmia. We included 2 articles in which home BPs were measured only in the morning31,36 (the morning home BPs were used as the average home BPs in these studies) and one article in which BP was measured in the morning, at noon, and in the evening.16 We included some articles in which the method of clinic BP measurements was not clearly described,15,19,24,30,31,33,35–37 or in which clinic BP was measured only once per clinic visit,31 but we repeated our analyses excluding these articles. Rater differences in the selection of articles were discussed, and the last author (T.G.P.) resolved any remaining discrepancies concerning article eligibility.
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Data Extraction
The averages of age, percentage of males, body mass index, antihypertensive medication use, dose and timing of antihypertensive drugs, and the methods of clinic and home BP measurements for each study were all abstracted as background data. The levels and changes of the clinic and home BPs and their standard deviations (SD) during the antihypertensive treatment periods were also collected. One article40 published data only for mean BP and pulse pressure, but the systolic and diastolic BP could be obtained from the original database, because the first author of this meta-analysis was a coauthor of the article. In 7 articles,18,20,22,25,26,32,39 24-hour ambulatory BP data were also available, which we included in our analysis.
Data Synthesis
The changes in clinic and home BPs were extracted for each of the eligible studies, excluding data for the placebo and control groups,14,40 and also excluding 9 articles in which the method of clinic BP measurements were not described.15,19,24,30,31,33,35–37 The exclusion criteria of the 9 articles were as follows: (1) the technique or device of clinic BP measurements were not written, (2) the clinic BP was measured only once, and (3) the clinic BP was not measured by physicians or nurses. There were 13 articles in which home BP data were described separately for the morning and evening BP.12–15,18,20,23,25,30,37,38,40,41 We also evaluated the changes in clinic, morning, and evening BP depending on whether the antihypertensive medication was taken in the morning12–15,18,20,23,25,30,41 or in the evening.12,37,38,40 The effects of different antihypertensive drug classes on the changes in clinic and home BP (using morning dosing) were evaluated for calcium channel blockers (6 studies),12,16,17,25,35,37 angiotensin converting enzyme inhibitors (5 studies),13,14,18,21,22 and angiotensin II receptor blockers (7 studies).18,20–22,24,33,41 Finally, we were able to compare the reductions of home BP with those of 24-hour BP in 7 articles,18,20,22,25,26,32,39 and with daytime BP and nighttime BP in 5 articles.22,25,26,32,39
Statistical Analysis
The changes in BP measured before and after antihypertensive treatment periods are shown as mean±SE, and the BPs measured at baseline are shown as mean±SD. In the data sets in which standard deviations after the treatment periods were unavailable, it was assumed that the SDs of the BP before and after treatment were the same. As most of the accepted articles did not show SDs of the changes in clinic and home BP, the SDs were calculated using the formula42: [(SD at baseline)2+(SD at follow-up)2–2 r (SD at baseline) (SD at follow-up)](0.5). The r values of changes in clinic and home BPs were estimated from a study in which all variables were available (ie, clinic systolic BP 0.50, clinic diastolic BP 0.32, home systolic BP 0.56, home diastolic BP 0.75, morning systolic BP 0.61, morning diastolic BP 0.78, evening systolic BP 0.54, evening diastolic BP 0.72).40 Before we evaluated the changes in clinic and home BP, we performed a heterogeneity test. The estimates of change in clinic and home BP exhibited significant heterogeneity across articles, and data synthesis was therefore performed using an unstandardized random effects model. Simple correlations between the reductions of BP were evaluated using Pearsons test weighted by the number of subjects enrolled in the studies. The differences in the change in clinic and home BP were calculated in all data sets, and meta-analyzed using a random effects model, except for the differences between home and 24-hour or daytime diastolic BP. These differences were analyzed using a fixed effects model because there was no significant heterogeneity. Additionally, the treatment induced BP changes corrected for the level of BP were calculated using the Oldham correction43 (corrected BP change=actual change divided by the average of pre- and posttreatment BPs). The mean pre- and posttreatment BPs were meta-analyzed using a random effects model. All statistical analyses were performed using Excel-based (Microsoft Corp) meta-analysis worksheets (developed by J.E.S. and J.I.) and SPSS (version 14.0, SPSS Inc).
| Results |
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In the 7 articles in which 24-hour average BPs were available (n=1246),18,20,22,25,26,32,39 the changes in clinic, home, and 24-hour ambulatory BPs were –15.2±0.07/–10.2±0.10 mm Hg, –12.6±0.06/–8.2±0.07 mm Hg, –11.9±0.04/–8.5±0.02 mm Hg, respectively, and the differences between home and 24-hour ambulatory systolic BP was significant (1.2 mm Hg, 95% CI 0.8 to 1.5 mm Hg, P<0.001). Home systolic BP decreased 6% more than the 24-hour average systolic BP. The reductions of home diastolic BP and 24-hour diastolic BP (8.2 and 8.5 mm Hg) were similar, although the difference was statistically significant (0.4 mm Hg, 95% CI 0.2 to 0.7 mm Hg, P<0.001).
In the 5 articles in which both daytime BP and nighttime BP were separately available (n=801; excluding 2 articles in which only 24-hour average BP data were available),22,25,26,32,39 the treatment-induced changes are shown in Figure 5. Thus home systolic BP decreased 15% more than daytime ambulatory systolic BP, and 30% more than nighttime ambulatory systolic BP. The differences in home and daytime BP reductions were 1.6 mm Hg (95% CI 1.1 to 2.2 mm Hg, P<0.001) for systolic and 0.2 mm Hg (95% CI –0.4 to 0.8 mm Hg, P=0.55) for diastolic, and that in home and nighttime BP reductions were 3.8 mm Hg (95% CI 3.3 to 4.4 mm Hg, P<0.001) for systolic and 1.2 mm Hg (95% CI 0.6 to 1.8 mm Hg, P<0.001) for diastolic. Additionally, the treatment-induced BP changes corrected for the level of BPs by using the Oldham correction were 10.3% for clinic systolic BP, 10.9% for clinic diastolic BP, 10.1% for home systolic BP, 10.4% for home diastolic BP, 8.5% for daytime systolic BP, 9.0% for daytime diastolic BP, 8.1% for nighttime systolic BP, and 9.0% for nighttime diastolic BP.
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In the 10 articles in which antihypertensive drugs were taken in the morning (n=1809),12–15,18,20,23,25,30,41 the changes in clinic, morning, and evening BP were –13.0±0.04/–11.2±0.04 mm Hg, –10.8±0.08/–6.1±0.09 mm Hg, –11.7±0.06/–7.4±0.06 mm Hg. The evening BP was reduced marginally more than morning BP (the difference: 1.1 mm Hg [95% CI 0.9 to 1.2 mm Hg, P<0.001] for systolic and 1.5 mm Hg [95% CI 1.3 to 1.6 mm Hg, P<0.001] for diastolic). In the 4 articles in which antihypertensive drugs were taken in the evening (n=399),12,37,38,40 the changes in clinic, morning, and evening BP were –8.2±0.07/–5.0± 0.10 mm Hg, –12.5±0.17/–7.5±0.20 mm Hg, –5.6±0.12/–3.8±0.15 mm Hg. The morning BP reduced more than evening BP (the difference: 6.8 mm Hg [95% CI 6.57 to 6.95 mm Hg, P<0.001] for systolic and 3.6 mm Hg [95% CI 3.4 to 3.9 mm Hg, P<0.001] for diastolic).
In 6 articles12,16,17,25,35,41 the effects of calcium channel blockers (taken in the morning) on the reduction of CBP and HBP were 17.5±0.10/12.4±0.13 mm Hg and 14.1±0.07/9.1±0.08 mm Hg, and the differences between clinic and home BP were 3.3 mm Hg (95% CI 3.1 to 3.5 mm Hg, P<0.001) for systolic and 3.0 mm Hg (95% CI 2.8 to 3.3 mm Hg). The BP reductions corrected for the level of BPs by using the Oldham correction were 11.4% for clinic systolic BP, 13.5% for clinic diastolic BP, 9.5% for home systolic BP, and 10.2% for home diastolic BP. In 5 articles,13,14,18,21,22 the effects of angiotensin converting enzyme inhibitors on the reduction of clinic BP and home BP were 15.1±0.07/10.9±0.08 mm Hg and 11.9±0.15/6.8±0.14 mm Hg, and the difference between clinic and home BP were 3.2 mm Hg (95% CI 3.0 to 3.4 mm Hg) for systolic and 4.3 mm Hg (95% CI 3.7 to 4.9 mm Hg) for diastolic. The BP reductions corrected for the level of BPs by using the Oldham correction were 9.9% for clinic systolic BP, 11.4% for clinic diastolic BP, 8.4% for home systolic BP, and 7.6% for home diastolic BP. In 7 articles,18,20,22,24,33,41 the effect of angiotensin II receptor blockers on reduction of CBP and HBP were 17.6±0.07/10.5±0.11 mm Hg and 9.9±0.23/6.5±0.14 mm Hg, and the difference between clinic and home BP were 8.0 mm Hg (95% CI 7.8 to 8.2 mm Hg) for systolic and 3.2 mm Hg (95% CI 2.7 to 3.8 mm Hg) for diastolic. The BP reductions corrected for the level of BPs by using the Oldham correction were 14.3% for clinic systolic BP, 11.2% for clinic diastolic BP, 6.9% for home systolic BP, and 7.3% for home diastolic BP. In 2 articles in which there were placebo or control subjects,14,40 the changes in clinic and home BP were –4.5±0.89/–4.8±0.17 mm Hg and –2.1±0.32/–1.9±0.37 mm Hg, respectively (the difference; both P<0.001).
| Discussion |
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The changes in clinic and home BP (systolic/diastolic) produced by antihypertensive drug treatments were –15.2/–10.3 mm Hg and –12.2/–8.0 mm Hg, respectively, and these reductions of BP were smaller than the values shown in the Verberks previous meta-analysis.11 The changes in home and clinic BPs were linearly related to each other in the present meta-analysis, such that the effect on home BP was typically about 80% of the effect on clinic BP. Mancia and Parati4 reported that the reductions of clinic BP and 24-hour BP with antihypertensive treatments were –24.9/–14.5 mm Hg and –14.6/–9.2 mm Hg, respectively, and that the effect on 24-hour ambulatory BP was about 60% of the effect on clinic BP. Taken together, these results indicate that the reduction of home BP is about 20% smaller, and that of 24-hour BP 40% smaller than the reduction of clinic BP produced by antihypertensive drugs. The greater reductions of clinic BP than home BP with antihypertensive treatment were attributable to the difference in BP levels at baseline (usually clinic BP>home BP). This indicated that the lower the baseline BP levels are, the smaller the difference in the BP reduction between clinic BP and home BP will be.
In our meta-analysis of 7 studies which included 24-hour BP data as well as home BP,18,20,22,25,26,32,39 the reduction of 24-hour systolic BP was indeed less than the reduction of home SBP by 6%. When we analyzed the data in 5 studies in which both daytime and nighttime SBP were available,22,25,26,32,39 the reductions of 24-hour systolic BP, daytime systolic BP, and nighttime systolic BP were about 15%, 15%, and 30% smaller than that of home systolic BP. In the meta-analysis of Mancia and Parati,4 it was also reported that nighttime BP was reduced less than daytime BP by antihypertensive drugs taken in the morning. Our meta-analysis indicated that the reduction of daytime BP was smaller than that of home BP. The difficulties in reducing nighttime BP might derive from morning dosing of antihypertensive drugs. To obtain nighttime BP control, Kario et al44 previously reported that nighttime dosing of doxazosin, an
-adrenergic blocker, is effective. Additionally, Hermida et al45–47 have reported that angiotensin II receptor blockers taken at bedtime reduced nighttime BP significantly more than when taken in the morning.
It is not clear why home BP exhibits a smaller reduction than clinic BP and a greater reduction than 24-hour BP after antihypertensive drug treatment. The baseline levels of clinic BP were higher than home BP, and there might be a regression-to-the-mean effect. The regression line of baseline BP levels and the BP reduction were similar between clinic BP and home BP. Even in placebo or control groups, the reductions of clinic BP were larger than home BP. Additionally, there might be a white coat effect (transient BP elevation in the physicians office) which is generally recognized to be reduced by both active and placebo treatment.48 Another factor affecting the differences in the reductions of clinic and home BP seems to be the timing of the administration of antihypertensive medications. Antihypertensive drugs taken in the evening reduced morning BP greater than clinic BP.
In some trials the BP decline was larger at home than in the office; in other trials this difference was negligible, and in some the office BP decline was 3 times larger. These differences in the reductions of CBP and HBP might be explained by inaccuracy of CBP measurements, because some studies did not describe the technique of CBP measurements (ie, the BP devices and number of measurements). Therefore, we analyzed the reductions of CBP and HBP after excluding data sets in which the methods of clinic BP measurement were not clearly described; however, the reductions of CBP and HBP were similar to the results of the whole data set.
Perspectives
The reduction of home BP produced by antihypertensive drug treatment is about 80% of the magnitude of the reduction of clinic BP.
| Acknowledgments |
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Sources of Funding
This work was supported in part by grants from NHLBI (R24 HL76857 and PO1-HL 47540). J.I. is supported in part by a grant from Mitsubishi Pharma Research Foundation.
Disclosures
None.
Received April 28, 2008; first decision May 13, 2008; accepted August 24, 2008.
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