Abstract
The impact of a nondipping blood pressure (BP) pattern, defined as (awake systolic BP – sleep systolic BP)/awake systolic BP < 0.1, on cardiovascular events in populations with different degrees of carotid atherosclerosis is uncertain. The authors hypothesized that a nondipping BP pattern would show differential predictive power for cardiovascular events, including total cardiovascular death, sudden death, nonfatal cardiovascular events, and nonfatal stroke, between populations with and without carotid atherosclerosis. To test this hypothesis, the authors analyzed 493 patients (mean age 67.9 years, 47.5% men) from the J‐HOP (Japan Morning Surge‐Home Blood Pressure) study for whom ambulatory BP monitoring and carotid intima‐media thickness data were available. Twenty‐nine cardiovascular events occurred during follow‐up (1867 person‐years). A nondipping BP pattern was independently associated with cardiovascular events in the population without carotid atherosclerosis, defined as carotid intima‐media thickness < 1.1 mm after adjustment for other cardiovascular risk factors including age, sex, diabetes mellitus, chronic kidney disease, and 24‐hour systolic BP (hazard ratio, 8.15; 95% confidence interval, 1.76–37.78 [P < .01]). This association was not found in the population with carotid intima‐media thickness ≥ 1.1 mm. Therefore, in the hypertensive population without carotid atherosclerosis, physicians should consider ambulatory BP monitoring to determine the nocturnal BP pattern as an alternative approach to assessing cardiovascular events.
Keywords: ambulatory blood pressure, Asian, atherosclerosis, nondipping
1. INTRODUCTION
The nondipping blood pressure (BP) pattern, as assessed by ambulatory BP monitoring (ABPM), has been well recognized for its association with cardiovascular events independent of 24‐hour BP levels in the general population and untreated hypertensive population.1, 2 Although a few studies have reported an association between the nondipping BP pattern and cardiovascular outcomes in high‐risk populations such as patients with diabetes mellitus (DM) and/or prior cardiovascular events, these reports have generally been limited by the small number of patients3 or the use of different protocols for ABPM based on the meta‐analysis of individual patient data.4
It has been established that populations with progression of surrogate organ damage or prior cardiovascular disease are at high risk for cardiovascular events and their recurrence. Therefore, in these populations, the impact of a nondipping BP pattern on cardiovascular events might be lower compared with that in a population without a high risk for cardiovascular events. In other words, the prognostic impact of a nondipping BP pattern might be more apparent in the population without a high risk for cardiovascular events. Thus, the causal relationship between a nondipping BP pattern and cardiovascular events in populations with versus those without high risk for cardiovascular events still needs to be clarified.
Because of our access to data from the J‐HOP (Japan Morning Surge‐Home Blood Pressure) study, we are uniquely positioned to address this gap in knowledge. The J‐HOP study enrolled patients with a history of or risk factors for cardiovascular disease and prospectively performed follow‐up for cardiovascular events. Part of this study's population performed ABPM. Patients with carotid atherosclerosis are known to have moderate to high risk for cardiovascular events.5, 6 The present study was designed to determine whether the nondipping BP pattern would have a prognostic impact in hypertensive populations with and without carotid atherosclerosis defined by carotid intima‐media thickness (CIMT), and to shed new light on the nondipping BP pattern as a predictor of future cardiovascular events in these populations.
2. METHODS
2.1. Study design
The J‐HOP study was a prospective observational study. Patients in the J‐HOP study were recruited consecutively from January 2005 to May 2012 by doctors at 71 institutions throughout Japan and followed up through March 2015 for cardiovascular events.7 All patients provided written informed consent. The ethics committee of the internal review board of the Jichi Medical University School of Medicine, Tochigi, Japan, approved the protocol.
2.2. Study patients
A total of 4310 ambulatory outpatients who had one or more cardiovascular risks were enrolled in the J‐HOP study during the aforementioned period. Patients who had malignancy or chronic inflammatory disease were excluded. In the present study, the 493 patients for whom ABPM data and CIMT measurements were available were included in the analyses.
2.3. Cardiovascular risk definition
Cardiovascular risk in this study included DM or glucose intolerance, hyperlipidemia, smoking, and chronic kidney disease (CKD). Glucose intolerance was defined as fasting glucose levels ≥110 mg/dL or glucose levels ≥140 mg/dL at 2 hours after a 75‐g oral glucose tolerance test. DM was defined by self‐report of the use of oral hypoglycemic medication, fasting plasma glucose ≥126 mg/dL, or glycated hemoglobin (National Glycohemoglobin Standardization Program) ≥6.5%.8, 9 Dyslipidemia was defined by self‐report of the use of lipid‐lowering medication, total cholesterol level ≥240 mg/dL, triglycerides ≥150, or high‐density lipoprotein <40 mg/dL,10 and CKD was defined as the presence of proteinuria or serum creatinine levels ≥1.1 mg/dL.
2.4. ABPM and definition of dipping BP pattern
ABPM was performed using a validated device: either TM‐2421 or TM‐2425 (A&D).11 Measurements were taken at 30‐minute intervals for 24 hours on a weekday.12, 13 Awake and sleeping periods were defined according to the records in the patient diaries. Sleep BP was calculated as the average of the BP values from the time that the patient went to bed until the time of awakening, and awake BP was defined as the average BP recorded during the rest of the day. Patients were considered to have adequate ABPM if they had ≥10 awake and five or more sleep systolic BP (SBP) and diastolic BP measurements. A normal dipping BP pattern was defined as (awake SBP – sleep SBP)/awake SBP ≥ 0.1, and a nondipping BP pattern was defined as (awake SBP – sleep SBP)/awake SBP < 0.1. Office BPs were measured using an upper arm cuff oscillometric BP device (HEM‐5001, Omron). The appropriate cuff size for individual arm circumference was used. Three clinic BP readings were taken at 15‐second intervals with the patient in a sitting position after 2 minutes of rest.
2.5. Carotid echography
The CIMT was assessed using a standard B‐mode ultrasound device at each institute and performed by each institute's ultrasonographers, who were not involved in the statistical analyses of the study. CIMT was measured at three points proximal to the bilateral carotid bulb (far wall) in 10‐mm plaque‐free segments at the end‐diastolic phase. If plaque existed at the measuring point, an appropriate adjacent portion was selected. The mean of the right and left maximum CIMT (total of 6 points) was used in the analysis. We defined atherosclerosis using the cutoff value of CIMT ≥ 1.1 mm according to the Japan Atherosclerotic Society statement, which proposed that healthy Japanese individuals with a mean CIMT of 1.14 ± 0.35 mm had >5% 10‐year absolute risk of cardiovascular disease.10
2.6. Follow‐up and events
Patients’ statuses were recorded until March 2015, for a total of 3.8 ± 2.1 years (1867 person‐years). The primary end point was cardiovascular events, including total cardiovascular death, sudden death, nonfatal cardiovascular event, and nonfatal stroke, as ascertained by ongoing reports from physicians at each institute. Details of the outcomes ascertainment were defined in a previous study.7
2.7. Statistical analysis
Baseline characteristic data are shown as means ± standard deviations. Chi‐square test of independence was used for comparisons between groups for categorical variables and the analysis of covariance for continuous variables. Cumulative incidences of primary composite end points in the groups when subdivided according to nocturnal BP pattern were plotted as Kaplan‐Meier curves, and the differences were assessed by the log‐rank test. For the association between nondipping BP pattern and cardiovascular events, the hazard ratios (HRs) and 95% confidence intervals (CIs) of cardiovascular events in the groups with CIMT < 1.1 mm and ≥1.1 mm were calculated using Cox proportional hazards models to examine BP parameters for cardiovascular events. We used conventional cardiovascular risk factors and covariates that showed significant differences between the populations with and without cardiovascular events (Table S1). In model 1, the Cox regression analyses included age, sex, DM, CKD, and 24‐hour SBP as covariates. In model 2, we added a nondipping BP pattern to model 1. The proportionality assumption for the Cox analyses was confirmed graphically. We tested for the interaction to determine the association between nondipping BP pattern and the groups with CIMT < 1.1 mm and ≥1.1 mm by introducing an interaction term in the models. All statistical analyses were performed with IBM SPSS Statistics for Macintosh, version 20.0. A probability value <.05 was considered statistically significant.
3. RESULTS
3.1. Baseline characteristics
The populations included in this substudy were older, had a higher number of antihypertensive medication used and generally had lower SBP and diastolic BP levels of both office and ABPM than the other populations in the J‐HOP cohort (Table S2).
Among the 493 patients included in the analysis, the percentage of men was lower than the percentage of women (47.5% versus 52.5%). The average age was 67.9 ± 12.1 years. Patients with a nondipping BP pattern were older, had a higher prevalence of DM, and had a lower glomerular filtration rate than those with the normal dipping BP pattern. Mean body mass index was 24.5 ± 3.6 kg/m2. Mean CIMT was 1.13 ± 0.59 mm. Carotid plaques were detected in 18.3% of the patients, but there was no significant difference in the presence of carotid plaque between patients with normal dipping and those with nondipping BP patterns, either in the group with CIMT < 1.1 mm or in that with CIMT ≥ 1.1 mm. The majority of patients were currently on hypertensive medication (89.9%). Baseline BP data are shown in Table 1.
Table 1.
Baseline characteristics
| Measures | All patients (N = 493) | CIMT < 1.1 mm (N = 326) | CIMT ≥ 1.1 mm (N = 167) | ||||
|---|---|---|---|---|---|---|---|
| Normal dipping (n = 208) | Nondipping (n = 118) | P value | Normal dipping (n = 93) | Nondipping (n = 74) | P value | ||
| Age, y | 67.9 ± 12.1 | 65.8 ± 13.3 | 67.0 ± 13.0 | .15 | 68.9 ± 9.3 | 72.7 ± 8.2 | <.01 |
| Men, % | 47.5 | 42.8 | 38.1 | .41 | 60.2 | 59.5 | .92 |
| BMI, kg/m2 | 24.5 ± 3.6 | 25.1 ± 3.7 | 24.4 ± 3.5 | .10 | 24.0 ± 3.2 | 23.7 ± 3.6 | .58 |
| Waist‐hip ratio | 0.90 ± 0.07 | 0.91 ± 0.07 | 0.89 ± 0.06 | <.01 | 0.91 ± 0.07 | 0.90 ± 0.08 | .46 |
| Current smoker, % | 12.2 | 11.1 | 9.3 | .62 | 18.3 | 12.2 | .28 |
| Family history, % | 64.5 | 62.0 | 63.6 | .78 | 68.8 | 67.6 | .86 |
| Diabetes mellitus, % | 21.3 | 20.4 | 28.0 | .01 | 16.3 | 25.7 | .42 |
| Dyslipidemia, % | 37.3 | 37.6 | 33.0 | .22 | 39.9 | 36.5 | .89 |
| Hypertension treatment, % | 89.9 | 89.2 | 91.5 | .46 | 88.9 | 90.5 | .78 |
| Total cholesterol, mg/dL | 202.4 ± 32.9 | 201.3 ± 33.9 | 197.8 ± 34.9 | .38 | 193.3 ± 28.4 | 200.5 ± 33.0 | .13 |
| Glycated hemoglobin, % | 5.5 ± 0.8 | 5.4 ± 0.7 | 5.5 ± 0.9 | .09 | 5.4 ± 0.7 | 5.5 ± 0.8 | .20 |
| GFR, mL/min/1.73m2 | 73.4 ± 17.5 | 72.1 ± 19.4 | 69.1 ± 20.6 | .20 | 73.1 ± 20.6 | 65.2 ± 17.9 | .01 |
| Hypertension medication, % | |||||||
| CCB | 55 | 54.3 | 57.6 | .64 | 51.6 | 56.8 | .54 |
| ACEI | 5.3 | 5.3 | 3.4 | .59 | 4.3 | 9.5 | .22 |
| ARB | 69.8 | 72.1 | 78 | .29 | 55.9 | 67.6 | .15 |
| Diuretics | 40.7 | 41.3 | 44.1 | .56 | 33.4 | 43.3 | .14 |
| α‐Blockers | 5.9 | 3.4 | 8.5 | .07 | 6.5 | 8.1 | .77 |
| β‐Blockers | 12.6 | 11.5 | 12.7 | .86 | 12.9 | 14.9 | .82 |
| No. of hypertension medication, % | |||||||
| None | 10.1 | 11.1 | 8.5 | ‐ | 10.8 | 9.5 | ‐ |
| 1 | 31.1 | 29.3 | 26.3 | ‐ | 44.1 | 27 | ‐ |
| 2 | 27.2 | 28.8 | 28 | ‐ | 22.6 | 27 | ‐ |
| ≥3 | 31.6 | 30.8 | 37.2 | ‐ | 22.5 | 36.5 | ‐ |
| Evening dose of hypertension medication, % | 33.5 | 34.6 | 39 | .47 | 26.9 | 29.7 | .73 |
| SBP, mmHg | |||||||
| Office | 140 ± 16 | 139 ± 16 | 137 ± 17 | .22 | 143 ± 12 | 142 ± 16 | .50 |
| 24‐h | 128 ± 12 | 127 ± 12 | 127 ± 13 | .93 | 131 ± 10 | 131 ± 13 | .69 |
| Awake | 134 ± 13 | 135 ± 13 | 128 ± 13 | <.01 | 139 ± 12 | 132 ± 14 | <.01 |
| Sleep | 117 ± 14 | 110 ± 12 | 123 ± 13 | <.01 | 115 ± 11 | 128 ± 15 | <.01 |
| DBP, mmHg | |||||||
| Office | 78 ± 11 | 79 ± 11 | 76 ± 11 | <.01 | 80 ± 10 | 76 ± 10 | <.01 |
| 24‐h | 75 ± 9 | 76 ± 9 | 74 ± 9 | .04 | 77 ± 8 | 75 ± 9 | .05 |
| Awake | 79 ± 9 | 80 ± 9 | 75 ± 9 | <.01 | 82 ± 9 | 76 ± 8 | <.01 |
| Sleep | 68 ± 9 | 65 ± 8 | 70 ± 8 | <.01 | 68 ± 8 | 72 ± 9 | <.01 |
| CIMT, mm | 1.13 ± 0.59 | 0.86 ± 0.13 | 0.87 ± 0.12 | .28 | 1.75 ± 0.91 | 1.55 ± 0.49 | .09 |
| Presence of carotid plaque, % | 18.3 | 19.2 | 18.6 | .51 | 16.1 | 17.6 | .48 |
| Cardiovascular event, No. | 29 | 2 | 11 | <.01 | 9 | 7 | .9 |
Abbreviations: ACEI, angiotensin‐converting enzyme inhibitor; ARB, angiotensin receptor blocker; BMI, body mass index; CIMT, carotid intima‐media thickness; CCB, calcium channel blocker; DBP, diastolic blood pressure; GFR, glomerular filtration rate; SBP, systolic blood pressure.
3.2. Cardiovascular events
During the mean follow up of 3.8 ± 2.1 years (1867 person‐years), 29 cardiovascular events occurred. The incidence of cardiovascular events was lowest in the population with a normal dipping BP pattern and CIMT < 1.1 mm (Table 1). In comparison with patients with CIMT < 1.1 mm and a normal dipping BP pattern, patients with CIMT < 1.1 mm and a nondipping BP pattern had significantly higher incidence of cardiovascular events (log‐rank = 13.39, P < .01) (Figure), while there was no prognostic impact of the nondipping BP pattern in the group with CIMT ≥ 1.1 mm (Figure S1).
Figure 1.
Long‐term cumulative incidence of cardiovascular events according to nocturnal blood pressure pattern. Kaplan‐Meier curves of patients with carotid intima‐media thickness < 1.1 mm stratified according to nondipping blood pressure (BP) pattern (gray line) and normal dipping BP pattern (black line). The hazard ratio (HR) and 95% confidence interval (CI) of cardiovascular events in nondipping BP pattern were calculated using Cox regression analysis, after adjustments for age, sex, diabetes mellitus, chronic kidney disease, and 24‐hour systolic BP.
In patients with CIMT < 1.1 mm, 24‐hour SBP level was associated with cardiovascular events (HR, 1.08; 95% CI, 1.02–1.14 [P = .01]) (model 1 in Table 2), and those who showed a nondipping BP pattern had an HR for cardiovascular events of 8.15 (95% CI, 1.76–37.78; P < .01) after adjustment for other conventional cardiovascular risk factors including age, sex, DM, CKD, and 24‐hour SBP (model 2 in Table 2). In patients with CIMT ≥ 1.1 mm, factors that increased the risk of cardiovascular events were age (HR, 1.10; 95% CI, 1.02–1.19 [P = .01]) and CKD (HR, 3.91; 95% CI, 1.29–11.88 [P = .02]), but not a nondipping BP pattern (model 2 in Table 2). We conducted an analysis to assess the heterogeneity of the effect between dipping BP pattern and cardiovascular events by CIMT (<1.1 mm versus ≥ 1.1 mm) with inclusion of interaction terms. Interactions were found between nondipping BP pattern and CIMT in association with cardiovascular events (P < .01).
Table 2.
Cox regression analyses for cardiovascular outcome in groups subdivided according to CIMT
| Covariates | CIMT < 1.1 mm | CIMT ≥ 1.1 mm | ||||||
|---|---|---|---|---|---|---|---|---|
| Model 1 | Model 2 | Model 1 | Model 2 | |||||
| Hazard ratio (95% CI) | P value | Hazard ratio (95% CI) | P value | Hazard ratio (95% CI) | P value | Hazard ratio (95% CI) | P value | |
| Age | 1.08 (1.02–1.14) | .01 | 1.07 (1.01–1.14) | .03 | 1.09 (1.01–1.16) | .02 | 1.10 (1.02–1.19) | .01 |
| Male sex | 2.58 (0.84–7.93) | .10 | 2.11 (0.69–6.41) | .19 | 2.86 (0.87–9.40) | .08 | 3.34 (0.97–11.53) | .06 |
| DM | 1.84 (0.47–7.21) | .38 | 1.25 (0.32–4.87) | .75 | 1.71 (0.58–5.08) | .33 | 1.85 (0.62–5.53) | .27 |
| CKD | 2.79 (0.77–10.08) | .12 | 2.04 (0.56–7.46) | .28 | 3.44 (1.15–10.32) | .03 | 3.91 (1.29–11.88) | .02 |
| 24‐h SBP | 1.05 (1.01–1.09) | .03 | 1.05 (1.01–1.09) | .02 | 1.02 (0.98–1.06) | .27 | 1.02 (0.98–1.06) | .31 |
| Nondipping | – | – | 8.15 (1.76–37.78) | <.01 | – | – | 0.53 (0.17–1.59) | .26 |
Abbreviation: CIMT, carotid intima‐media thickness.
Model 1: hazard ratio and 95% confidence intervals (CIs) were adjusted for age, sex, diabetes mellitus (DM), chronic kidney disease (CKD), and 24‐hour systolic blood pressure (SBP).
Model 2: hazard ratio and 95% CIs were adjusted for age, sex, DM, CKD, 24‐hour SBP, and nondipping blood pressure pattern.
4. DISCUSSION
This study of a clinical Japanese population with a history of or risk factors for cardiovascular diseases demonstrated that a nondipping BP pattern was independently associated with cardiovascular events in the population with CIMT < 1.1 mm after adjustment by age, sex, DM, CKD, and 24‐hour SBP, while this association was not found in the population with CIMT ≥ 1.1 mm. The population with CIMT < 1.1 mm who had a normal dipping BP pattern was found to have the lowest number of cardiovascular events.
In the present study, a nondipping BP pattern was clearly more predictive of cardiovascular events than a normal dipping BP pattern in the population without carotid atherosclerosis. Previous research has reported that a nondipping BP pattern indicated a worse cardiovascular prognosis than a normal dipping BP pattern in both the general population and a hypertensive population.1, 2 Those results support our findings that a nondipping BP pattern has prognostic impact for cardiovascular events. However, the association between a nondipping BP pattern and cardiovascular events is still controversial in higher‐risk populations such as those with a history of cardiovascular diseases or those with cardiovascular risk factors.3, 4 One of the most important reasons might be that a nondipping BP pattern cannot be explained solely by a simple mechanism. Among the pathophysiological characteristics associated with a nondipping BP pattern, advanced sympathetic nervous system disturbance is one of the most widely reported. This autonomic derangement ultimately leads to target organ damage and cardiovascular diseases.14, 15 In addition, experimental studies have demonstrated that increased sympathetic tone was also associated with insulin resistance, leading to target organ damage or cardiovascular diseases in the long term.16, 17 In addition, a nocturnal BP pattern has been reported to be affected by various factors, such as senility, DM, obesity, and the presence of cardiovascular disease.18, 19 Thus, a nondipping BP pattern and target organ damage overlap. The discrepancy we found for the impact of nondipping BP pattern on cardiovascular outcome may depend on the differential characteristics between the low‐risk and high‐risk populations. Our findings clarified the discrimination of the clinical impact of the nondipping BP pattern for cardiovascular outcome stratified by CIMT.
Our other analyses provided further findings in support of the thesis that the prognostic impact of a nondipping BP pattern depends on the characteristics of the population. In this study, the nondipping BP pattern was not associated with cardiovascular events in the population with CIMT ≥ 1.1 mm. Although the reason for this result could not be clarified in the present investigation, we speculate that it may be as follows. A nondipping BP pattern has been acknowledged with both organ damage20, 21 and cardiovascular events.22, 23 Organ damages, per se, have been established as an intermediate end point associated with cardiovascular events.24, 25 In regard to CIMT, a previous study in a large cohort of older adults (≥65 years) showed that the subpopulation with a CIMT of 1.11 to 1.39 mm showed an HR of 2.30 (95% CI, 1.34–3.88) for MI and 1.69 (95% CI, 1.09–2.62) for stroke after adjustment for conventional cardiovascular risk factors.5 Similar results were reported in a prospective study of a younger population6 and also in meta‐analyses and systematic reviews.26 Thus, organ damage may be an intermediate step linking nondipping BP pattern and cardiovascular outcome. In individuals with organ damage, who already have a high risk for cardiovascular events, the impact of a nondipping BP pattern for cardiovascular events may be diluted. Combined with our present finding that a nondipping BP pattern was associated with cardiovascular events in the population with CIMT < 1.1 mm, these results suggest that physicians should manage patients at risk for cardiovascular events by taking into consideration the dipping BP pattern before the development of organ damage.
STUDY LIMITATIONS
The limitations of our study derive from its relatively small number of patients and cardiovascular events. This study was one of the prespecified analyses. Although interactions were found between a nondipping BP pattern and CIMT in association with cardiovascular events, our findings should be interpreted with caution, and further studies will be required to validate them. Another limitation is that CIMT was measured using different ultrasound devices at each institute. The sonographers measured CIMT according to the standard J‐HOP guidelines and used standard devices for measurement of CIMT. Therefore, the intracoefficient/intercoefficients of variation for CIMT were not assessed. Because we used CIMT as the index of surrogate organ damage, the other indices of organ damages, such as left ventricular hypertrophy and proteinuria, were not evaluated. Finally, the study was limited to an Asian population, therefore it cannot be extrapolated to other ethnic groups.
CONCLUSIONS
In an Asian population with either a history of or risk factors for cardiovascular disease, but without carotid atherosclerosis, a nondipping BP pattern was found to be an independent risk factor for cardiovascular events. Therefore, physicians should not only consider CIMT measurement but also ABPM for nocturnal BP pattern as a prognostic indicator in these populations.
CONFLICT OF INTEREST
K. Kario has received research grants from Teijin Pharma Ltd., Novartis Pharma K.K., Takeda Pharmaceutical Co., Ltd., Omron Healthcare Co., Ltd., and Fukuda Denshi, and honoraria from Mochida Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., Daiichi Sankyo Co., Ltd., and Sumitomo Dainippon Pharma Co., Ltd. The other authors have no conflicts of interest to report.
Supporting information
ACKNOWLEDGMENTS
We gratefully acknowledge the investigators, healthcare workers, study coordinators, and patients who participated in the J‐HOP study.
Kotruchin P, Hoshide S, Kario K. Carotid atherosclerosis and the association between nocturnal blood pressure dipping and cardiovascular events. J Clin Hypertens. 2018;20:450–455. 10.1111/jch.13218
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