Sage Journals: Discover world-class research

Abstract

Objectives

To elucidate the clinical significance of differences between home- and clinic-measured systolic blood pressure (SBP) in patients with treated hypertension, and to assess the correlations between SBPs and arterial stiffness.

Methods

Patients with treated hypertension measured their blood pressure (BP) themselves once, at home, in the morning (<1 h after awakening) using an automated oscillometric sphygmomanometer. Clinic BP was measured once, at an outpatient clinic on the same day, using a similar instrument. Arterial stiffness was measured by cardio–ankle vascular index (CAVI). Differences between home and clinic SBPs, and the correlations between CAVI and home SBP, clinic SBP, and the difference between home and clinic SBPs, were analysed.

Results

Seventy-six patients with treated hypertension (mean age, 71 years) were evaluated. There was no statistically significant difference between home and clinic SBP (mean ± SD 132 ± 14 and 133 ± 16 mmHg, respectively). Home SBP showed no correlation with CAVI, whereas clinic SBP showed a weak correlation. The difference between the home and clinic SBP showed a stronger correlation with CAVI, and was statistically significant.

Conclusions

The difference between home- and clinic-measured SBP showed a better correlation with arterial stiffness than did either home or clinic SBP alone.

Keywords

Hypertension home blood pressure clinic blood pressure arterial stiffness systolic blood pressure CAVI

Introduction

It is well known that hypertension is a risk factor for cardiovascular events including stroke, ischaemic heart disease and heart failure.^1–3 The clinical studies producing these results have, however, been performed using clinic blood pressure (BP) as the only measure of BP.⁴ There is increasing evidence regarding the usefulness of BP measurements conducted at home, by patients themselves.^5,6 Average values of home BP measurement are generally stable; therefore, reproducibility of home BP measurements is considered to be good.⁷ Home BP measurement is useful for assessing the effectiveness of antihypertensive drugs.⁸ Patients with hypertension who exhibit a discrepancy between home and clinic BP measurement are described as having either “masked” hypertension, if home BP is higher,⁹ or “white coat” hypertension, if home BP is lower.¹⁰ It is supposed that patients with “masked” or “white coat” hypertension are at heightened risk of cardiovascular events.^11–13 Thus, both clinic and home BP measurements are important markers for BP control, in clinical settings.

Arterial stiffness is an index for assessing atherosclerosis, and is also an independent predictor of cardiovascular events (including fatal and nonfatal coronary events) and fatal strokes in hypertensive patients.^14,15 The cardio–ankle vascular index (CAVI) is an index of arterial stiffness¹⁶ that has been used for assessing such stiffness in the clinical setting.¹⁷

The present study evaluated the differences between single, same-day, home and clinic systolic BP (SBP) measurements in patients with treated hypertension. The study also assessed the correlation between arterial stiffness measured by CAVI and home SBP and clinic SBP, and also assessed the difference between the two SBPs.

Patients and methods

Study population

Consecutive patients who had been diagnosed with hypertension (defined as SBP ≥140 mmHg and/or diastolic BP (DBP) ≥90 mmHg) who attended a regular hypertension clinic at Kagawa University Hospital, Kagawa, Japan, were enrolled into the study. The diagnosis of hypertension was based on one BP reading within 1 year of study entry. This study was conducted between January 2012 and December 2012. All patients were treated with at least one antihypertensive drug. The dose of antihypertensive therapy was stable and changes to therapy were not allowed within 3 months prior to study entry. Patients with a history of heart failure, stroke or obvious heart disease were excluded.The protocol was approved by the Ethics Committee of Kagawa University. Written informed consent was obtained from all participants.

BP measurement

Participants were asked to measure their home BP once, in the morning (<1 h after awakening and before taking any antihypertensive drug) on the same day they were due to visit the outpatient clinic. They measured their BP in the upper right arm, in the sitting position, using their own automated oscillometric sphygmomanometers and without a human observer. Patients were not specifically trained by study staff to use the sphygmomanometers, but they were asked to follow the instruction manuals. Because patients were using their own sphygmomanometers there was no standardization in the equipment used and it was unknown whether their equipment was properly calibrated. The results were recorded manually by the patients. The patients were asked to record systolic and diastolic BP readings in the morning (<1 h after awakening and before taking any antihypertensive drug) every day, in booklets provided by the investigators.

Patients attended the outpatient clinic visit on the morning of the same day as they recorded their home SBP, for measurement of their SBP in a clinical setting. There was no set limit to the time between the home and clinic SBP measurements, and patients were not instructed as to whether or not they could take their hypertension medication before or after the clinic visit.

When participants arrived at the outpatient clinic, they rested for ≥1 min before their SBP was measured. Clinic SBP was measured once, while the patient was in the sitting position, by a physician trained in using the automated oscillometric sphygmomanometer (HEM-1040, Omron, Kyoto, Japan).

Both home and clinic SBP measurements for each patient were based on a single reading. There was no protocol in the case of aberrant readings. Differences between the single home and clinic SBP readings for each patient were calculated. These SBP measurements were performed within 3 months before or after the day when the CAVI measurements or blood examinations (see below) were performed.

Assessment of arterial stiffness by CAVI

The CAVI was measured using an automatic vascular screening system (VaSera™ VS-1000; Fukuda Densi, Tokyo, Japan), with the patient resting in a supine position. Pulse wave velocity (PWV) was obtained by dividing the vascular length by the time it took for the pulse wave to propagate from the aortic valve to the ankle. SBP and DBP were measured at the brachial artery. The formula used to calculate CAVI was as follows: CAVI = a[(2ρ/ΔP) × ln (SBP/DBP) PWV²] + b, where ΔP is SBP – DBP, ρ is blood density, and a and b are scale conversion constants to match aortic PWV. The principle underlying the CAVI has been described previously.¹⁶ The CAVI reflects the stiffness of the aorta, femoral artery and tibial artery as a whole; theoretically, it is not affected by BP. All these measurements and calculations were performed on the VaSera™ VS-1000. For each patient, electrocardiogram electrodes were placed on both wrists, a microphone for detecting heart sounds was placed on the sternum, and cuffs were wrapped around both arms and both ankles. After automatic measurements, the values of right and left CAVI were calculated. The mean values of the right and left CAVI scores were used for analysis.

Blood sample collection

Blood samples were taken in the morning after an 8-h overnight fast. Blood was collected into tubes containing 1.8 mg/ml ethylenediamine tetra-acetic acid and was analysed immediately. Serum total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), glycosylated haemoglobin (HbA_1c), and uric acid concentrations were measured by standard laboratory techniques. Relationships between laboratory data, BP parameters and other clinical characteristics, including CAVI, were analysed.

Statistical analyses

Statistical analyses were performed using the SPSS® statistical software package, version 18.0 (SPSS Inc., Chicago, IL, USA) for Windows®. Data were expressed as the mean ± SD. A paired t-test was used to compare the single home and clinic SBP measurements. Correlations between SBP parameters and other variables were assessed by univariate linear regression analyses. Values of P < 0.05 were considered to be statistically significant.

Results

A total of 76 patients (35 males, 41 females; mean ± SD age 71 ± 8 years [range 53–88 years]) were included in the study. Clinical and demographic characteristics of the patients are presented in Table 1. The high mean value of CAVI indicated the presence of arterial stiffness in the patient group as a whole. The mean values of home and clinic SBP were not particularly high: in all patients, hypertension was being appropriately controlled by medication. Figure 1 shows the differences between same-day home and clinic SBP measurements. Compared with home SBP, the clinic SBP increased in 40 (53%) patients but decreased in 36 (47%) patients, and there was no significant overall difference between the mean home and clinic SBPs. The mean of the individual differences between the two measurements was 15 ± 12 mmHg.

Figure 1.

Difference between same-day home- and clinic-measured systolic blood pressure (SBP) readings in patients with treated hypertension (n = 76). There was no significant overall difference between the mean ± SD SBP measured at home (132 ± 14 mmHg) and in the clinic (133 ± 16 mmHg); one measurement per location. Central black horizontal lines show the mean values for each timepoint; extremities of vertical lines show the SD.

Table 1.

Clinical and demographic characteristics of patients with treated hypertension (n = 76), included in a study examining the clinical significance of differences between single, same-day, home- and clinic-measured systolic blood pressure readings.

Characteristic	Data
Sex, male/female	35/41
Age, years	71 ± 8
BMI, kg/m²	23.7 ± 3.3
Diabetes mellitus	10 (13)
Dyslipidaemia	47 (62)
Antihypertensive medication used
ARB/ACEI	54 (71)
CCB	60 (79)
ß-blocker	14 (18)
Diuretic	15 (20)
Statin	17 (22)
Total cholesterol, mg/dl	192 ± 31
HDL–C, mg/dl	53 ± 13
Triglycerides, mg/dl	116 ± 53
HbA_1c, %	5.4 ± 0.5
Uric acid, mg/dl	5.4 ± 1.2
CAVI	8.8 ± 1.2
Home SBP, mmHg	132 ± 14
Clinic SBP, mmHg	133 ± 16
Differences between home and clinic SBPs, mmHg	15 ± 12

Data presented as n/n, mean ± SD or n (%) of patients.

BMI: body mass index; ARB: angiotensin II receptor blocker; ACEI: angiotensin converting enzyme inhibitors; CCB: calcium channel blocker; HDL–C: high-density lipoprotein cholesterol; HbA_1c, glycosylated haemoglobin; CAVI: cardio–ankle vascular index; SBP: systolic blood pressure.

Home-measured SBP did not show a significant correlation with age, whereas clinic-measured SBP showed a weak correlation with age (r = 0.297, P = 0.009), and the difference between the home and clinic SBP showed the strongest correlation with age (r = 0.486, P < 0.001) (Table 2). Similarly, home-measured SBP showed no correlation with CAVI, but clinic-measured SBP showed a weak correlation with CAVI (r = 0.316, P = 0.005), and the difference between home and clinic SBP showed the strongest correlation with CAVI (r = 0.600, P < 0.001) (Figure 2; Table 2). There was also a significant correlation between BMI and home-measured SBP (P = 0.010), and between uric acid and the difference between the home and clinic SBPs (P = 0.037) (Table 2).

Figure 2.

Relationships between cardio–ankle vascular index (CAVI) and (a) home systolic blood pressure (SBP), (b) clinic SBP, and (c) the difference between home and clinic SBPs, measured during a single day in patients with treated hypertension (n = 76). The home SBP measurements showed no correlation with CAVI (r = 0.105, P ≥ 0.05), but clinic SBP showed a weak correlation with CAVI (r = 0.316, P = 0.005). The difference between home and clinic SBPs showed the best correlation with CAVI (r = 0.600, P < 0.001).

Table 2.

Linear regression analyses of the relationships between home systolic blood pressure (SBP), clinic SBP and the difference between home and clinic SBP (measured once on a single day), with other clinical characteristics, in patients with treated hypertension (n = 76).

Characteristic	Home SBP		Clinic SBP		Differences between home and clinic SBPs
Characteristic	r	Statistical significance^a	r	Statistical significance^a	r	Statistical significance^a
Age	0.071	NS	0.297	P = 0.009	0.486	P < 0.001
BMI	0.293	P = 0.010	0.037	NS	−0.210	NS
Diabetes mellitus	0.058	NS	0.061	NS	0.128	NS
Dyslipidaemia	0.039	NS	−0.175	NS	−0.182	NS
Antihypertensive medication
ARB/ACEI	0.047	NS	0.041	NS	−0.010	NS
CCB	0.207	NS	−0.085	NS	−0.210	NS
ß-blockers	0.001	NS	0.034	NS	0.019	NS
Diuretics	−0.083	NS	0.014	NS	−0.036	NS
Statins	0.110	NS	−0.103	NS	−0.117	NS
Total cholesterol	−0.195	NS	−0.040	NS	−0.123	NS
HDL–C	−0.061	NS	−0.067	NS	−0.119	NS
Triglycerides	−0.040	NS	0.161	NS	0.165	NS
HbA_1c	0.143	NS	0.137	NS	0.073	NS
Uric acid	−0.023	NS	−0.023	NS	0.239	P = 0.037
CAVI	0.105	NS	0.316	P = 0.005	0.600	P < 0.001

Univariate linear regression analyses.

Discussion

The present study evaluated the clinical significance, in patients being treated for hypertension, of the difference between single home and clinic SBP measurements. These measurements were taken on the same day (by the patient and physician, respectively), and the clinical significance was evaluated by analysing the correlation between differences in BP and arterial stiffness, as assessed by CAVI. The study demonstrated the following: (i) that there was a high degree of variability in home and clinic SBP measurement, with values measured at the outpatient clinic showing an increase in 53% of patients and a decrease in 47% of patients, compared with values taken at home on the same morning; (ii) there was no significant mean difference between individual home and clinic SBP measurements; (iii) same-day home and clinic SBPs showed no or weak correlations with arterial stiffness, assessed by CAVI, while the difference between home and clinic SBPs showed a stronger correlation with arterial stiffness. The finding that, in approximately one half of the patients, the clinic SBP measurements were higher than the home SBP measurements, while in the other half the reverse was true, may indicate that the study included some patients who were prone to the ‘white-coat effect' and some who had ‘masked hypertension'. As the study only took a single home and clinic measurement from each patient, however, the likelihood of natural variability in BP readings cannot be ruled out.

The main purpose of the present study was to evaluate whether there was any clinical significance in the calculated difference between home and clinic SBPs. Compared with either measurement alone, the difference between home and clinic SBPs showed a stronger correlation with arterial stiffness, as estimated by CAVI. In addition, correlations between atherosclerosis-related factors (namely, BMI and uric acid levels) and the home SBP measurement, and the difference between home and clinic SBPs, respectively, were observed. Studies have demonstrated associations between systemic atherosclerotic change and 24-h^18,19 or visit-to-visit²⁰ BP variability. There are, however, few data about the relationship between atherosclerosis and same-day SBP differences between home and clinic SBPs. It is possible that patients with a large variation between home and clinic SBP measurement are at heightened risk of developing atherosclerosis. Recently, visit-to-visit variability in SBP has been shown to be a predictor of stroke.^21,22 Thus, we consider that clinical examination and care for atherosclerosis-related diseases may be needed in patients who show a large variation between home and clinic SBPs. In addition, and perhaps a greater level of attention should be paid to the magnitude of differences between home and clinic SBPs, rather than the absolute values of each measurement.

Age is an important risk factor in atherosclerosis,^23,24 and CAVI is a parameter of arterial stiffness that reflects one important factor of atherosclerosis. It is well known that the CAVI increases with advancing age,^16,17 and that increased BP variability is a characteristic of elderly patients with hypertension.^25,26 This may explain the correlation we observed between the difference between the home and clinic SBP, and both age and CAVI.

There were several limitations to the present study. First, participants measured their home BP using their own equipment, which was different compared with the equipment used in to measure the clinic BP. In addition, there was very likely to be a high degree of inter-individual variability in the make and model of equipment used for home BP measurements. Also, there was no way of knowing if the patient’s own equipment had been properly calibrated. Therefore, potential variations between home and clinic SBP measurements due to lack of standardization cannot be ruled out. Secondly, only one BP measurement was taken in each setting (home and clinic) for each patient. Consequently, the calculated difference between the home and clinic values could be due to natural daily variations in BP rather than any clinically significant effect. Thirdly, neither atherosclerosis nor its progression was actively assessed in the present study. Finally, there was no specification to the patient as to whether they could take their prescribed hypertension medicine before or after the clinic visit. Thus, the timing of antihypertensive drug administration in the morning may have influenced the clinic BP reading. These limitations regarding the methodology may have affected the results of this study. Larger studies that take an average of multiple measurements of patients’ SBP both at home and in the clinic, on a single day and over time, should be carried out to verify the clinical significance of the findings of this study.

In conclusion, the difference between single home and clinic SBP measurements, in patients with treated hypertension, showed better correlation with arterial stiffness than did either the specific home or clinic SBP measurement itself.

Footnotes

Declaration of conflicting interest

The authors declare that there are no conflicts of interest.

Funding

This study was supported in part by a Grant-in-Aid (Scientific Research [B]) No. 23300190 to S.S.) for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan and Japan Society for the Promotion of Science (JSPS).

References

Lawes

Rodgers

Bennett

. Blood pressure and cardiovascular disease in the Asia Pacific region. J Hypertens 2003; 21: 707–716.

Moser

Hebert

Hennekens

. An overview of the meta-analyses of the hypertension treatment trials. Arch Intern Med 1991; 151: 1277–1279.

Tsutsui

Tsuchihashi-Makaya

Kinugawa

. Characteristics and outcomes of patients with heart failure in general practices and hospitals. Circ J 2007; 71: 449–454.

Nasothimiou

Tzamouranis

Rarra

. Diagnostic accuracy of home vs. ambulatory blood pressure monitoring in untreated and treated hypertension. Hypertens Res 2012; 35: 750–755.

Mancia

Facchetti

Bombelli

. Long-term risk of mortality associated with selective and combined elevation in office, home, and ambulatory blood pressure. Hypertension 2006; 47: 846–853.

Ohkubo

Imai

Tsuji

. Home blood pressure measurement has a stronger predictive power for mortality than does screening blood pressure measurement: a population-based observation in Ohasama, Japan. J Hypertens 1998; 16: 971–975.

Ragot

Genès

Vaur

. Comparison of three blood pressure measurement methods for the evaluation of two antihypertensive drugs: feasibility, agreement, and reproducibility of blood pressure response. Am J Hypertens 2000; 13: 632–639.

Vaur

Dubroca

Dutrey-Dupagne

. Superiority of home blood pressure measurements over office measurements for testing antihypertensive drugs. Blood Press Monit 1998; 3: 107–114.

Pickering

Eguchi

Kario

. Masked hypertension: a review. Hypertens Res 2007; 30: 479–488.

10.

Pickering

Shimbo

Haas

. Ambulatory blood-pressure monitoring. N Engl J Med 2006; 354: 2368–2374.

11.

Bobrie

Chatellier

Genes

. Cardiovascular prognosis of “masked hypertension” detected by blood pressure self-measurement in elderly treated hypertensive patients. JAMA 2004; 291: 1342–1349.

12.

Ohkubo

Kikuya

Metoki

. Prognosis of “masked” hypertension and “white-coat” hypertension detected by 24-h ambulatory blood pressure monitoring 10-year follow-up from the Ohasama study. J Am Coll Cardiol 2005; 46: 508–515.

13.

Ugajin

Hozawa

Ohkubo

. White-coat hypertension as a risk factor for the development of home hypertension: the Ohasama study. Arch Intern Med 2005; 165: 1541–1546.

14.

Montalcini

Gorgone

Pujia

. Association between pulse pressure and subclinical carotid atherosclerosis in normotensive and hypertensive post-menopausal women. Clin Exp Hypertens 2009; 31: 64–70.

15.

Feldstein

Akopian

Olivieri

. Association between nondipper behavior and serum calcium in hypertensive patients with mild-to-moderate chronic renal dysfunction. Clin Exp Hypertens 2012; 34: 417–423.

16.

Shirai

Utino

Otsuka

. A novel blood pressure-independent arterial wall stiffness parameter; cardio-ankle vascular index (CAVI). J Atheroscler Thromb 2006; 13: 101–107.

17.

Shirai

. Analysis of vascular function using the cardio-ankle vascular index (CAVI). Hypertens Res 2011; 34: 684–685.

18.

Kawai

Ohishi

Kamide

. Differences between daytime and nighttime blood pressure variability regarding systemic atherosclerotic change and renal function. Hypertens Res 2013; 36: 232–239.

19.

Iwata

Jin

Schwartz

. Relationship between ambulatory blood pressure and aortic arch atherosclerosis. Atherosclerosis 2012; 221: 427–431.

20.

Okada

Fukui

Tanaka

. Visit-to-visit variability in systolic blood pressure is correlated with diabetic nephropathy and atherosclerosis in patients with type 2 diabetes. Atherosclerosis 2012; 220: 155–159.

21.

Rothwell

Howard

Dolan

. Prognostic significance of visit-to-visit variability, maximum systolic blood pressure, and episodic hypertension. Lancet 2010; 375: 895–905.

22.

Rothwell

. Limitations of the usual blood-pressure hypothesis and importance of variability, instability, and episodic hypertension. Lancet 2010; 375: 938–948.

23.

Marigliano

Scuteri

Cacciafesta

. Hypertension and atherosclerosis in the elderly: pathogenetic common mechanism and intervention strategies. Clin Exp Hypertens 1993; 15: 9–29.

24.

London

Marchais

Guerin

. Arterial stiffness: pathophysiology and clinical impact. Clin Exp Hypertens 2004; 26: 689–699.

25.

Kario

Pickering

Umeda

. Morning surge in blood pressure as a predictor of silent and clinical cerebrovascular disease in elderly hypertensives: a prospective study. Circulation 2003; 107: 1401–1406.

26.

Shimada

Kawamoto

Matsubayashi

. Diurnal blood pressure variations and silent cerebrovascular damage in elderly patients with hypertension. J Hypertens 1992; 10: 875–878.

Clinical significance of differences between home and clinic systolic blood pressure readings in patients with hypertension

Abstract

Objectives

Methods

Results

Conclusions

Keywords

Introduction

Patients and methods

Study population

BP measurement

Assessment of arterial stiffness by CAVI

Blood sample collection

Statistical analyses

Results

Discussion

Footnotes

Declaration of conflicting interest

Funding

References