Abstract
Paradoxical increase in blood pressure (BP) during sleep, exceeding those of awake BP, is called the “riser” BP pattern, and known as an abnormal circadian BP rhythm, has been reported to be associated with adverse cardiovascular prognoses. However, the significance of ambulatory BP in heart failure patients with preserved ejection fraction (HFpEF) has never been reported. Here, we tested our hypothesis that abnormal circadian BP rhythm is associated with HFpEF. The authors enrolled 508 patients with hospitalized HF (age 68±13 years; 315 men, 193 women). There were 232 cases of HFpEF and 276 cases of heart failure with reduced ejection fraction (HFrEF). The riser BP pattern was significantly more frequent in the HFpEF (28.9%) group compared with the HFrEF group (19.9%). In a multivariable logistic regression analysis, the riser BP pattern was associated with HFpEF (odds ratio, 1.73; 95% confidence interval, 1.02–2.91; P=.041) independent of the other covariates. In conclusion, the riser BP pattern was associated with HFpEF.
Heart failure (HF) with preserved ejection fraction (HFpEF) is observed in approximately one half of patients with HF, and its prognosis is as poor as that of HF with reduced ejection fraction (HFrEF).1 The patient population with HFpEF is associated with older age, female sex, and hypertension compared with patients with HFrEF.2 The underlying pathophysiology of HFpEF is multifactorial, and several cardiac and noncardiac comorbidities are related to the development of HFpEF.3 The myocardial abnormalities in HFpEF are left ventricular (LV) diastolic relaxation impairment and myocardial stiffening.
Previous studies have revealed that hypertension is a frequent comorbid condition in HFpEF patients3 and that it is strongly associated with the development of HFpEF.4 Hypertension leads to LV hypertrophy and results in increased LV stiffness and LV diastolic dysfunction. These myocardial functional and structural changes contribute to the development of HFpEF.
Nocturnal hypertension was observed to be strongly associated with hypertensive target organ damage and prognosis.5 Paradoxical increase in blood pressure (BP) during sleep, exceeding those of awake BP, is called the riser BP pattern, and is known as an abnormal circadian BP rhythm. The riser BP pattern was demonstrated to present a significant risk for hypertensive target organ damage and cardiovascular death.6, 7, 8, 9
In our previous study, the group of HF patients with the riser BP pattern was more likely to be female and to have hypertension and atrial fibrillation compared with the HF patients without the riser BP pattern.10 These characteristics of the HF patients with the riser BP pattern were similar to those of the HFpEF patients in previous reports. HFpEF and the riser BP pattern may thus have a common pathogenesis, such as autonomic dysfunction. Because one of the causes of the riser BP pattern is autonomic dysfunction, we hypothesized that the riser BP pattern, an extreme phenotype of autonomic dysfunction, may contribute to the development of HFpEF. We performed the present study to test this hypothesis in HF patients.
Methods
Study Population
The present study used a cross‐sectional, observational design. We recruited patients who were hospitalized with a diagnosis of HF at one of five institutions (Jichi Medical University Hospital, Shioya General Hospital, Utsunomiya Social Insurance Hospital, Shin‐Oyama Municipal Hospital, and the International University of Health and Welfare Hospital, Tochigi, Japan) from July 2007 to September 2013. The baseline examinations were performed when the symptoms of HF had improved and stabilized, and in most cases just before the patient left the hospital. All of the patients were seen by cardiologists and were diagnosed with HF. Our study included not only first‐ever HF patients but also recurrent HF patients.
The patients who did not agree to undergo ambulatory BP monitoring (ABPM) during hospitalization were not included. We excluded patients with documented dementia, delirium, infections, depression during treatment, renal failure (serum creatinine >3 mg/dL), cancer, other severe noncardiovascular diseases, or a pacemaker or implantable cardioverter defibrillator implantation. Patients lacking any of the required data were excluded. This study was approved by the research ethics committee, Jichi Medical University School of Medicine, and the ethics committees of the other four hospitals. Informed consent was obtained from all patients.
History of hypertension was defined by self‐reports, medical records, and a history of antihypertensive medication use. Diabetes mellitus was defined by a fasting glucose level ≥126 mg/dL, a random nonfasting glucose level ≥200 mg/dL, or the use of antidiabetic drugs or insulin.11 Dyslipidemia was defined as a total cholesterol level >240 mg/dL, a triglyceride level >150 mg/dL,12 or the use of an oral lipid‐lowering drug. Body mass index was calculated as weight/height2 (kg/m2). Estimated glomerular filtration rate (eGFR) was calculated by the Modification of Diet in Renal Disease formula for Japanese patients as: eGFR (mL/min/1.73 m2)=194×(serum creatinine [mg/dL]−1.094×(age[years])−0.287×0.739 (if female).13 Chronic kidney disease (CKD) was defined as eGFR <60 mL/min/1.73 m2, and the severity of proteinuria was not considered for the diagnosis of CKD. CKD stage was classified in accordance with the Kidney Disease: Improving Global Outcomes (KDIGO) classification on the basis of eGFR as: grade 1, eGFR ≥90 mL/min/1.73 m2; grade 2, eGFR=60 to 89 mL/min/1.73 m2; grade 3a, eGFR=45 to 59 mL/min/1.73 m2; grade 3b, eGFR=30 to 44 mL/min/1.73 m2; grade 4, eGFR=15 to 29 mL/min/1.73 m2; and grade 5, eGFR<15 mL/min/1.73 m2.14 The number of each CKD category was as follows: grade 1, 41; grade 2, 172; grade 3a, 121; grade 3b, 102; grade 4, 72; and grade 5, 0. Electrocardiographically verified LV hypertrophy was defined as an abnormally high voltage of QRS complex (R in V5 plus S in V1 >3.5 mV) associated with either flat T waves (<10% of the R wave) or ST‐segment depression and biphasic T waves.15
BP Measurement
When the patient's HF was stabilized, a single session of noninvasive ABPM was performed by an automatic system using electric cuff inflation (TM‐2430; A&D Co., Tokyo, Japan), which recorded both BP (by the oscillometric method) and pulse rate every 30 minutes for 24 hours. The accuracy of this device was validated.16 A minimum of 20 valid awake readings and six valid sleep readings was used to define the awake and sleep BP, but all patients had many more valid readings.
Sleep BP was defined as the average of BP measurements during the time the patient was in bed, and awake BP was defined as the average of BP measurements recorded during the rest of the day. The nocturnal BP fall (%) was calculated as (awake systolic BP [SBP]−sleep SBP)/awake SBP.
We classified the patients’ nocturnal BP fall into the following three patterns: riser pattern if the nocturnal BP fall was <0%, nondipper pattern if it was between 0% and 10%, and dipper pattern if it was >10%.9 The number of each BP category was as follows: dippers, 138; nondippers, 248; and risers, 122. Because the number of extreme dippers (nocturnal BP fall >20%) was very small (n=22), extreme dippers were combined with dippers and classified as “dippers” in the present study.
A well‐trained technician measured casual BP by ABPM device before the ABPM was hooked up. A casual BP reading was taken twice after the patient rested for 5 minutes in the sitting position. The average of two BP readings was used in the analysis.
Echocardiography
Transthoracic two‐dimensional echocardiography (Sonos 5500 and iE 33; Philips, Andover, MA, USA) was performed in all patients. End‐diastolic dimensions of the left ventricle (LVDd), interventricular septum (IVS), and posterior wall thickness (PWT) were measured in the M‐mode and occasionally in the B‐mode parasternal long‐axis view. LV mass (LVM) was calculated from LVDd, IVS, and PWT according to Devereux's formula17 and normalized to the body surface area to obtain the LVM index. LV ejection fraction (LVEF) was calculated by the Teichholz method.18 The relative wall thickness (RWT) was calculated as 2* PWT/LVDd. HFpEF was defined as LVEF >45%, and HFrEF was defined as LVEF ≤45%.19
Other Examinations
Blood was drawn in patients after 10 minutes of rest in the supine position. Brain‐type natriuretic peptide (BNP) was measured from extracted plasma using highly sensitive noncompetitive immunoradiometric assays (Shiono‐RIA; Shionogi, Osaka, Japan).20 Briefly, this assay system uses two monoclonal antibodies against human BNP, one recognizing a carboxy‐terminal sequence and the other the ring structure of human BNP, and the assay measures BNP by sandwiching it between the two antibodies. The cross‐reactivity with human ANP was <0.001% on a molar basis, and the minimal detection limit of this assay kit is 4 pg/mL of human BNP.
A pulse oximetry device (PULSOX‐M24; Konica Minolta, Osaka, Japan) was used to evaluate the nocturnal oxygen saturation change, which is a frequent comorbid condition in HF patients. We performed the nocturnal pulse oximetry and ABPM simultaneously. The device was attached to the arm opposite that of the ABPM‐attached arm before the patient went to bed and was removed after he or she woke up.
We used the value of oxygen desaturation per hour (oxygen desaturation index [ODI]) as an indicator of nocturnal intermittent hypoxia. A 3% ODI was selected as an index of oxygen desaturation, representing the number of events per hour of recording time in which the blood oxygen fell by >3%. We adopted the cutoff value as 3% ODI ≥5 because it was reported that the sensitivity and specificity were 80% and 95%, respectively, for detecting the apnea‐hypopnea index of ≥5 by polysomnography using a cutoff threshold of 3% ODI ≥5.21
The Mini‐Mental State Examination (MMSE),22 a test of cognitive function, and the Center for Epidemiologic Studies Depression Scale (CES‐D),23 a test of depressive symptoms, were performed just before the patient left the hospital, when his or her conditions had improved and stabilized.
Statistical Analyses
All statistical analyses were carried out with SPSS software, version 21.0 (IBM, Armonk, NY, USA). The unpaired t test was performed to test mean differences between the HFpEF and HFrEF groups (Tables 1 and 2). The chi‐square test was used to compare proportions (Tables 1 and 2).
Table 1.
Baseline Characteristics of Patients
| HFpEF Group (n=232) | HFrEF Group (n=276) | P Value | |
|---|---|---|---|
| Age, y | 72±11 | 65±14 | <.01 |
| Male, No. (%) | 118 (50.9) | 197 (71.4) | <.01 |
| Body mass index, kg/m2 | 23.3±4.8 | 22.6±4.6 | .10 |
| NYHA III or IV, % | 53 (23.0) | 71 (25.9) | .26 |
| Underlying heart disease | |||
| IHD, No. (%) | 49 (21.1) | 112 (40.6) | <.01 |
| Non‐IHD, No. (%) | 183 (78.9) | 164 (59.4) | <.01 |
| History of hypertension, No. (%) | 119 (75.3) | 148 (72.5) | .32 |
| Diabetes, No. (%) | 84 (36.2) | 103 (37.3) | .43 |
| Atrial fibrillation, No. (%) | 80 (34.6) | 64 (23.2) | <.01 |
| Cardiovascular drugs | |||
| Calcium channel blockers, No. (%) | 105 (45.3) | 61 (22.1) | <.01 |
| ACE inhibitors, No. (%) | 89 (38.4) | 159 (57.6) | <.01 |
| ARB, No. (%) | 101 (43.5) | 87 (31.5) | <.01 |
| β‐Blockers, No. (%) | 141 (60.8) | 212 (76.8) | <.01 |
| α‐Blockers, No. (%) | 17 (7.3) | 6 (2.2) | <.01 |
| Diuretics, No. (%) | 201 (86.6) | 353 (91.7) | .046 |
| Antiplatelet drugs, No. (%) | 93 (40.1) | 148 (53.6) | <.01 |
| Warfarin, No. (%) | 98 (42.2) | 149 (54.0) | <.01 |
| Creatinine, mg/dL | 1.2±0.9 | 1.1±0.6 | .88 |
| Hematocrit, % | 37.0±6.5 | 39.8±6.9 | <.01 |
| Fasting glucose, mg/dL | 127±47 | 127±51 | .99 |
| Hemoglobin A1c, % | 5.8±1.7 | 6.1±1.7 | .042 |
| eGFR, mL/min | 57±37 | 58±26 | .77 |
| BNP, pg/mLa | 158±3 | 287±3 | <.01 |
| Adrenaline, pg/mLa | 25.0±2.2 | 22.4±2.3 | .49 |
| Noradrenaline, pg/mLa | 311±2 | 330±2 | .59 |
| Aldosterone, pg/mLa | 56.8±2.1 | 75.9±2.4 | .08 |
| PRA,a pg/mL | 1.7±4.9 | 2.4±3.6 | .25 |
| ECG‐LVH, No. (%) | 63 (27.2) | 88 (32.1) | .13 |
| LVDd, mm | 50±8 | 60±9 | <.01 |
| RWT | 0.48±0.14 | 0.37±0.12 | <.01 |
| LVM index, g/m2 | 150±54 | 166±47 | <.01 |
| LVH on echo, No. (%) | 165 (73.0) | 223 (82.6) | <.01 |
| LVEF, % | 59±10 | 31±8 | <.01 |
| 3% ODI | 12±12 | 13±12 | .30 |
| 3% ODI ≥5, No. (%) | 137 (65) | 173 (68) | .31 |
| CES‐D score | 10.2±7.3 | 10.1±8.0 | .88 |
| MMSE score | 23.9±5.2 | 25.3±4.4 | <.01 |
Abbreviations: ACE, angiotensin‐converting enzyme; ARB, angiotensin receptor blocker; BNP, brain‐type natriuretic peptide; CES‐D, Center for Epidemiologic Studies Depression Scale; echo, echocardiography; eGFR, estimated glomerular filtration rate; ECG‐LVH, left ventricular hypertrophy verified by electrocardiography; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; IHD, ischemic heart disease; LVDd, left ventricular diastolic diameter; LVM, left ventricular mass; LVH, left ventricular hypertrophy; LVEF, left ventricular ejection fraction; MMSE, Mini‐Mental State Examination; NYHA, New York Heart Association; ODI, oxygen desaturation index; PRA, plasma renin activity; RWT, relative wall thickness. aGeometric mean.
Table 2.
BP and PR at Baseline
| HFpEF Group (n=232) | HFrEF Group (n=276) | P Value | |
|---|---|---|---|
| Casual SBP, mm Hg | 126±22 | 116±22 | <.01 |
| Casual DBP, mm Hg | 70±14 | 71±14 | .63 |
| Casual PP, mm Hg | 58±24 | 48±23 | <.01 |
| Casual PR, beats per min | 71±14 | 73±15 | .28 |
| 24‐h SBP, mm Hg | 123±19 | 116±18 | <.01 |
| 24‐h DBP, mm Hg | 69±10 | 69±10 | .76 |
| 24‐h PP, mm Hg | 54±14 | 46±13 | <.01 |
| 24‐h PR, beats per min | 67±11 | 69±11 | .042 |
| Awake SBP, mm Hg | 125±17 | 118±18 | <.01 |
| Awake DBP, mm Hg | 71±10 | 71±10 | .95 |
| Awake PP, mm Hg | 55±13 | 47±13 | <.01 |
| Awake PR, beats per min | 69±11 | 71±12 | .06 |
| Sleep SBP, mm Hg | 120±20 | 112±20 | <.01 |
| Sleep DBP, mm Hg | 67±12 | 67±12 | .42 |
| Sleep PP, mm Hg | 53±15 | 45±14 | <.01 |
| Sleep PR, beats per min | 64±11 | 67±12 | .02 |
| Dipper, No. (%) | 71 (30.6) | 67 (24.3) | .07 |
| Nondipper, No. (%) | 94 (40.5) | 154 (55.8) | <.01 |
| Riser, No. (%) | 67 (28.9) | 55 (19.9) | .01 |
Abbreviations: DBP, diastolic blood pressure; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; PP, pulse pressure; PR, pulse rate; SBP, systolic blood pressure.
We performed a two‐step process to determine the covariates. In the first step, in order to investigate factors associated with HFpEF, we performed a multivariable logistic regression analysis with the stepwise method using all potential variables except the riser BP pattern. We included age; sex; hematocrit level; logBNP; use of calcium channel blockers, angiotensin‐converting enzyme inhibitors, angiotensin receptor blockers, β‐blockers, α‐blockers, antiplatelet drugs, or warfarin; ischemic heart disease; nonischemic heart disease; LVDd; RWT; LVM index; MMSE; casual SBP; 24‐hour SBP; awake SBP; and sleep SBP. The variables with P<.01 in the first‐step analysis were included as covariates in the second‐step analysis. As a result, age, logBNP, β‐blocker use, and LVDd were significant, and these variables were entered into the second‐step multivariate model with riser BP pattern (Figure). The data are expressed as means±standard deviation or number (percentages). Two‐tailed P values <.05 were considered significant.
Figure 1.
Predicting heart failure with preserved ejection fraction (HFpEF) or heart failure with reduced ejection fraction (HFrEF): multivariable logistic regression analysis results. Odds ratios indicate the HFpEF associated with the condition present in dichotomous variables and the increase in age, brain‐type natriuretic peptide (BNP), and left ventricular diastolic diameter (LVDd) for continuous variables. *Geometric mean.
Results
We enrolled 508 patients (315 men, 193 women), and all patients were analyzed in the present study. The mean age of the patients was 68±13 years. When HFpEF was defined as LVEF >45%, there were 232 cases of HFpEF and 276 cases of HFrEF.
As shown in Table 1, the baseline characteristics of the HFpEF and HFrEF groups differed. The ages and the percentage of women were both significantly higher in the HFpEF group than in the HFrEF group. The prevalence of ischemic heart disease (IHD) was lower and the prevalence of non‐IHD was higher in the HFpEF group than in the HFrEF group. The prevalence of atrial fibrillation was significantly higher in the HFpEF group. In echocardiographic parameters, the HFpEF group showed smaller LVDd values and lower LVM indices than the HFrEF group. With regard to BP, the HFpEF group showed higher casual and ambulatory SBP levels (Table 2). The nondipper BP pattern was significantly more frequent in the HFrEF group (55.8%) than in the HFpEF group (40.5%; P<.01). The riser BP pattern was significantly more frequent in the HFpEF group (28.9%) than in the HFrEF group (19.9%; P=.01).
We performed a multivariable logistic regression analysis to investigate factors associated with HFpEF. When nonriser BP pattern was set as the reference, a riser BP pattern was significantly associated with HFpEF (odds ratio [OR], 1.73; 95% confidence interval [CI], 1.02–2.91; P=.041) independent of other covariates (Figure).
In addition, we performed univariate analysis to investigate the association between CKD and HFpEF. According to the CKD stage, there were no significant associations between CKD stages and HFpEF (Table S1). When we added eGFR to the multivariable logistic regression analysis, eGFR was not significantly associated with HFpEF (Table S2).
By contrast, we performed multivariable logistic regression analysis to investigate the association between HFrEF and nondipping, which included nondipper and riser BP pattern. Nondipping was not associated with HFrEF (OR, 0.89; 95% CI, 0.52–1.51; P=.66) (Table S3).
Discussion
The results of the present study demonstrated that the abnormal circadian BP rhythm known as the riser BP pattern was associated with HFpEF. Abnormal circadian BP rhythm has been previously reported in HF patients24; however, that study did not separate HFpEF patients from HFrEF patients. The present study is thus the first to show an association between the riser BP pattern and HFpEF.
The association between riser BP pattern and HFpEF could be explained by the following mechanisms. In patients with the riser BP pattern, a pressure overload at night could facilitate the cardiac load, especially LV hypertrophy and increased LV stiffness. Hypertensive target organ damage is advanced in hypertensive patients with the riser BP pattern.6, 9 These cardiac damages observed in patients with the riser BP pattern may contribute to HFpEF.
It was reported that patients with advanced age, obesity, diabetes, dyslipidemia, a history of stroke or coronary heart disease, and CKD show an association with the riser BP pattern.25 Sleep apnea syndrome and poor sleep quality are additional causes of the riser BP pattern. In the present study, the prevalence of sleep apnea syndrome evaluated by nocturnal pulse oximetry was similar between the HFpEF and HFrEF groups. However, sleep quality was not evaluated.
With regard to CKD, kidney function could be one of the independent risk factors for autonomic dysfunction,26 such as riser BP pattern. However, CKD itself and eGFR were not associated with HFpEF in the present study.
Conversely, HFpEF could result in the riser BP pattern. One of the possible explanations is the activation of the sympathetic nervous system. In the present study, the HFpEF group showed significantly higher RWT and pulse pressure (PP) values compared with the HFrEF group. Our present findings may be the result of the activation of the sympathetic nervous system. The riser BP pattern is caused by autonomic nervous system dysfunction,27 and activation of the sympathetic nervous system has been observed in HFpEF.28 Therefore, sympathetic nervous system activation in HFpEF is one of the causes of the riser BP pattern. The other mechanism is increased circulating blood volume in HFpEF. Increased circulating blood volume has been reported as another cause of the riser BP pattern.29 In addition, a body fluid shift during the night was observed in HF patients with central sleep apnea.30 Although the participants in that study were HFrEF patients, the movement of body fluid from the legs to the body's center during the night could elevate the nocturnal BP in HFpEF patients. In consideration of these findings, sympathetic nervous system activation, increased circulating blood volume, and fluid shift during the night in HFpEF patients could result in the riser BP pattern.
Study Limitations
This study has some limitations. First, because of the cross‐sectional nature of the study, a cause‐effect relationship could not be inferred. Second, ABPM was performed during hospitalization in this study, even though ABPM in a hospital setting may not represent the patients’ usual daily life and sleep. However, some studies have shown that ABPM has prognostic significance even during hospitalization.31, 32 Third, the dose of antihypertensive medication and the timing of the drug administration could influence the diurnal BP pattern. However, multiple drugs are usually prescribed in HF patients. In the present study, the majority of drugs were taken once in the morning, but some drugs were taken both in the morning and in the evening based on the individualized treatment. Although the timing of drug administration between risers and nonrisers was not completely investigated, some drugs for HF are less likely to affect circadian BP rhythm in this population. Fourth, we did not enter BP parameters into the multivariable logistic regression analysis because all BP parameters were not selected in the first‐step analysis to determine the parameters using the second‐step multivariable analysis. When we entered 24‐hour SBP, awake SBP, and sleep SBP one by one into the multivariable model with the stepwise method in the first‐step analysis, the results of the second‐step analysis were unchanged. This may be because LVM index was used in the first‐step analysis. Fifth, patients with atrial fibrillation were included among the study patients; however, the use of ABPM in patients with atrial fibrillation has been reported and found not to affect 24‐hour BP rhythm.33 Finally, ORs could overestimate the association between the riser BP pattern and HFpEF. We performed additional analysis of estimating prevalence ratios of riser BP pattern between HFpEF and HFrEF groups. As a result, the riser/nonriser ratio was significantly higher in the HFpEF group, and the association between riser BP pattern and HFpEF was observed to be similar to that in the present analysis.
Conclusions
In the present study, the abnormal pattern of circadian BP rhythm, known as the riser BP pattern, was associated with HFpEF. Uncontrolled nocturnal hypertension, which is called the riser BP pattern, may correlate with HFpEF. The evaluation of circadian BP rhythm by ABPM could help physicians stratify patients who are at risk for developing HFpEF.
Disclosure
The authors have no conflicts of interest to disclose.
Supporting information
Table S1. Univariate logistic regression analysis between the CKD stage and HFpEF or HFrEF.
Table S2. Factors associated with HFpEF (multivariable logistic regression analysis).
Table S3. Multivariable logistic regression analysis to predict HFrEF.
Acknowledgments
We gratefully acknowledge Ms Kimiyo Saito, Chisato Mikogai, Hideko Taguchi, Kaori Kobayashi, Mika Kunimatsu, and Miki Sato for the coordination and data management of this study, and Ms Ayako Okura for editorial assistance. The first author (T.K.) and the second author (K.E.) contributed equally to the writing process.
J Clin Hypertens (Greenwich). 2016;18:994–999. DOI: 10.1111/jch.12818. ©2016 Wiley Periodicals, Inc.
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Associated Data
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Supplementary Materials
Table S1. Univariate logistic regression analysis between the CKD stage and HFpEF or HFrEF.
Table S2. Factors associated with HFpEF (multivariable logistic regression analysis).
Table S3. Multivariable logistic regression analysis to predict HFrEF.