Abstract
Arterial stiffness, assessed through pulse wave velocity (PWV), independently predicts cardiovascular outcomes. In untreated persons, white‐coat hypertension (WCH) has been related to arterial stiffness, but data in treated patients with WCH are scarce. The authors aimed to determine a possible association between WCH and arterial stiffness in this population. Adult treated hypertensive patients underwent home blood pressure monitoring and PWV assessment. Variables associated with PWV in univariable analyses were entered into a multivariable linear regression model. The study included 121 patients, 33.9% men, median age 67.9 (interquartile range 18.4) years, 5.8% with diabetes, and 3.3% with a history of cardiovascular or cerebrovascular disease. In multivariable analysis, WCH in treated hypertensive patients remained a determinant of PWV: β=1.1 (95% confidence interval, 0.1–2.1 [P=.037]; adjusted R 2 0.49). In conclusion, WCH is independently associated with arterial stiffness in treated hypertensive patients. Whether this high‐risk association is offset by antihypertensive treatment should be further investigated.
Arterial stiffness, assessed through carotid‐femoral pulse wave velocity (PWV), has shown an independent predictive value for cardiovascular outcomes and mortality in longitudinal studies.1, 2, 3, 4, 5 PWV is currently recommended as a screening test for subclinical target organ damage in hypertensive patients.6, 7, 8
On the other hand, white‐coat hypertension (WCH) is usually considered an “innocent” phenomenon, which entails the same cardiovascular risk as that of normotensive persons, both in treated and untreated populations.9, 10 The term WCH is usually reserved for untreated individuals. In treated hypertensive patients, WCH is not considered a correct term, but there is no universal consensus on how to name the phenomenon in this population. For this study, we decided to use the term isolated office uncontrolled hypertension (IOUH) for treated patients with high office blood pressure (BP) and normal out‐of‐office BP. The risk in these patients is higher than in normotensive persons. However, the risk is the same as that in patients with treated sustained normotension.9 As a consequence, no changes are usually made in the treatment strategy when a treated hypertensive patient is diagnosed with IOUH.
Although in untreated persons WCH has been related to target organ damage, including arterial stiffness,11, 12, 13 data in treated patients with IOUH are scarce. The purpose of the present study was to determine a possible association between IOUH and arterial stiffness in treated hypertensive patients.
Methods
Study Population
This cross‐sectional study included hypertensive patients 18 years or older treated in the Hypertension Section of Hospital Italiano de Buenos Aires. All of them were under antihypertensive treatment. Patients unable to understand the indications to perform home BP monitoring (HBPM), patients with arrhythmias that precluded the use of the oscillometric method, significant stenosis of the femoral or carotid arteries or a history of stent or surgery, or carotid sinus hypersensitivity as well as patients in whom the carotid or femoral pulse was not palpable were excluded from the study.
Medical records of all patients were reviewed to extract data regarding risk factors (diabetes, smoking status), history of cardiovascular disease (coronary heart disease and cerebrovascular disease), and the use of antihypertensive drugs. Laboratory data from 6 months prior to HBPM were also collected from medical records.
The study protocol was approved by the local ethics committee and all patients who accepted to participate gave informed consent.
Anthropometric and BP Measurements
Weight and height were assessed in all patients and body mass index (BMI) was calculated as weight/height2 (kg/m2). Office BP was subsequently measured thrice in the nondominant arm, 1 minute apart (the average of the three readings was used for analysis), after a 5‐minute rest with the patient in a sitting position, arm supported at the heart level, using an appropriate cuff size according to the patient's arm circumference. For this purpose, a validated automatic oscillometric device (Omron HEM‐7200; Omron Corp., Tokyo, Japan) was used.14
Home BP Monitoring
A validated automated oscillometric device (Omron HEM‐705CP‐II, Omron Corp.) was used for HBPM.15 Patients were instructed to register duplicate sitting BP readings (2 minutes apart) in the nondominant arm for 4 days:16 in the morning (before breakfast and medication), afternoon, and evening. The BP readings stored in the devices’ memory were used for analysis. First‐day measurements were discarded. Patients with fewer than 16 home BP readings were excluded from the analysis.
PWV Measurements
PWV was measured after a 5‐minute rest with the patient in a supine position, using either a SphygmoCor (AtCor Medical, Sydney, Australia) or Aortic (Exxer, Buenos Aires, Argentina) device, previously validated against the former, with an excellent level of agreement.17 Details of both methods have been described elsewhere. Briefly, SphygmoCor uses a tonometric Millar transducer, allowing carotid‐femoral PWV measurements in two steps: the first step is used to simultaneously record carotid pulse wave and ECG, whereas the second step is the recording of femoral pulse wave and ECG. The foot‐to‐foot method is applied in order to determine transit time between carotid and femoral pressure waves. In turn, intersecting tangent algorithms are used to identify such wave foots. In order to calculate the traveled distance, two distances on the body surface are measured: from the sternal notch to the femoral location and from the sternal notch to the carotid location of the respective pulse wave recording. The traveled distance is automatically calculated as the difference between the femoral location‐sternal notch minus the sternal notch‐carotid location.18 The Aortic uses simultaneous pressure signals sampled at 1 KHz on 24 bits, allowing PWV determination in one step, given that two piezo‐electronic transducers simultaneously register PWV at the neck and the groin. Transit time between both wave foots are then calculated in milliseconds, using the foot‐to‐foot method, similar to SphygmoCor.17 When these two devices were compared applying the Bland‐Altman method in our institution, we found a mean difference of 0.02 (±0.84) m/s, which is considered an excellent level of agreement, according to the Artery Society recommendations for PWV measurement.17
Definition of Clinical Variables
Patients were classified into four groups according to the accepted limit of 140/90 mm Hg for office BP measurements and 135/85 mm Hg for HBPM: sustained normotension, when BP was below the limit for each of the methods; sustained hypertension, when BP was greater than or equal to the limit for each of the methods; isolated office uncontrolled hypertension (IOUH), when BP was greater than or equal to the limit for office measurement and below the limit for HBPM; and masked uncontrolled hypertension (MUCH), when BP was below the limit for office measurement and greater than or equal to the limit for HBPM.
Finally, the white‐coat effect (WCE) was calculated as the difference between mean office BP and mean home BP.
Statistical Analysis
Characteristics of patients with and without IOUH among those with home‐controlled hypertension were compared using t test or Mann‐Whitney test for continuous variables and chi‐square test or Fisher test for categorical variables, as appropriate. A two‐sided P value <.05 was considered statistically significant.
We explored the variables associated with PWV through univariable linear regression analyses and then a multivariable linear regression analysis was performed to evaluate independent determinants of PWV. The model was constructed based on clinical criteria, introducing variables associated with PWV from univariable analyses, along with variables that were not statistically significant in our analyses but which were identified as relevant predictors of PWV in previous studies. Variables with non‐normal distribution were log‐transformed.
Results
The study included 121 patients, 33.9% men, median age 67.9 (interquartile range [IQR] 18.4) years, 5.8% had diabetes, 4.1% were smokers, and 3.3% had a history of cardiovascular or cerebrovascular disease. On average, patients were treated with 2.1 (±1.1) antihypertensive drugs, office BP was 140.8 (±16.9)/78.5 (±9.3) mm Hg, and home BP was 131.3 (±12.7)/73.7 (±9) mm Hg.
The prevalence of sustained normotension, IOUH, MUCH, and sustained hypertension were 39.6%, 19%, 11.6%, and 29.8%, respectively.
Comparing patients with IOUH with those with sustained normotension, the former were older (71.6 [IQR 9.4] vs 60 [IQR 15.7] years, P=.004), had a higher office BP (147.7 [IQR 16]/81.7 [IQR 15] vs 129.7 [IQR 12.7]/77.7 [IQR 9.2] mm Hg, P<.001/.02), a lower home diastolic BP (67 [IQR 8] vs 75.5 [IQR 8.75] mm Hg, P=.002), and a higher PWV (9.2 [IQR 3.4] vs 8 [IQR 2.3] m/s, P<.001). No other characteristics—including cardiovascular risk factors, history of cardiovascular disease, or laboratory data—were significantly different among these groups. Of note, BP measured during PWV assessment was not different between groups. Home BP and PWV profiles of these two groups are depicted in Table 1, and antihypertensive treatment is shown in Table 2.
Table 1.
Home Blood Pressure and PWV Profile in Patients With IOUH and SN
| IOUH | SN | P Value | |
|---|---|---|---|
| SBPa (IQR), mm Hg | 123 (5) | 122.5 (9.75) | ns |
| DBPa (IQR), mm Hg | 67 (8) | 75.5 (8.75) | .002 |
| Mean HR (SD), bpm | 70.1 (±8.6) | 68.7 (±8.6) | ns |
| Morning SBP (IQR), mm Hg | 126 (10) | 124 (9.5) | ns |
| Morning DBP (IQR), mm Hg | 70 (12) | 76 (10.75) | .04 |
| Afternoon SBP (IQR), mm Hg | 119.5 (6.5) | 121.5 (12.5) | ns |
| Afternoon DBP (IQR), mm Hg | 65.5 (9.25) | 72 (11.75) | .004 |
| Evening SBP (IQR), mm Hg | 122 (9) | 124.5 (12.75) | ns |
| Evening DBP (IQR), mm Hg | 67 (10) | 75 (12.5) | <.001 |
| PWV (IQR), m/s | 9.2 (3.4) | 8 (2.3) | <.001 |
| SBP during PWV assessment (IQR), mm Hg | 130 (25) | 121 (19) | ns |
| DBP during PWV assessment (IQR), mm Hg | 70 (12) | 70 (12.7) | ns |
Abbreviations: bpm, beats per minute; DBP, diastolic blood pressure; HR, heart rate; IOUH, isolated office uncontrolled hypertension; IQR, interquartile range; ns, nonsignificant; PWV, pulse wave velocity; SBP, systolic blood pressure; SD, standard deviation; SN, sustained normotension.
Average of all readings, discarding first‐day measurements.
Table 2.
Antihypertensive Treatment in Patients With IOUH and SN
| IOUH | SN | P Value | |
|---|---|---|---|
| No. of antihypertensive drugs (±SD) | 1.9 (±1.3) | 2.1 (±1) | ns |
| ACE inhibitors, % | 43.5 | 45.8 | ns |
| ARBs | 39.1 | 39.6 | ns |
| Diuretics | 30.4 | 20.8 | ns |
| BBs | 17.4 | 39.6 | .06 |
| CCBs | 43.5 | 50 | ns |
| Other | 0 | 6.2 | ns |
Abbreviations: ACE, angiotensin‐converting enzyme; ARBs, angiotensin receptor blockers; BBs, β‐blockers; CCBs, calcium channel blockers; IOUH, isolated office uncontrolled hypertension; SD, standard deviation; SN, sustained normotension.
The WCE showed a significant correlation with PWV both for systolic (r=0.29, P=.01) and diastolic BP (r=0.33, P=.005) (Figure).
Figure 1.
Correlation between white‐coat effect (WCE) and pulse wave velocity (PWV) for systolic (left) and diastolic (right) blood pressure.
In univariable analyses, IOUH, age, number of antihypertensive drugs, office systolic BP, home systolic BP, diabetes, smoking habits, calcium channel blocker use, history of cardiovascular/cerebrovascular disease, fasting plasma glucose, and serum creatinine showed a significant association with PWV. After adjustments in multivariable analysis not only for these variables but also for sex, BMI, and total cholesterol, which have previously been described as relevant predictors of PWV,19, 20 IOUH remained an independent determinant of PWV: β=1.1 (95% CI, 0.1–2.1 [P=.037], adjusted R 2 0.49) (Table 3).
Table 3.
Multivariable Analysis
| Variable | β Coefficient | 95% CI | P Value |
|---|---|---|---|
| IOUH | 1.1 | 0.1–2.1 | .037 |
| Age | 2.8 | 1.1–4.3 | .001 |
| No. of antihypertensive drugs | −0.8 | −1.7 to 0.04 | ns |
| Office SBP | 1.03 | −2.6 to 4.7 | ns |
| Home SBP | 4.9 | 0.2–9.6 | .04 |
| Diabetes | 2.3 | 0.9–3.7 | .002 |
| Smoking habits | −0.6 | −2.2 to 0.9 | ns |
| CCBs | 1.1 | 0.3–1.9 | .01 |
| History of cardiovascular disease | 2.3 | 0.5–4 | .02 |
| FPG | 0.9 | −0.3 to 2.1 | ns |
| Serum creatinine | 1.6 | 0.2–3 | .03 |
| Sex | −0.7 | −1.5 to 0.1 | ns |
| BMI | 1.3 | −0.7 to 3.2 | ns |
| Total cholesterol | 0.001 | −0.01 to 0.01 | ns |
Abbreviations: BMI, body mass index; CCBs, calcium channel blockers; CI, confidence interval; FPG, fasting plasma glucose; IOUH, isolated office uncontrolled hypertension; ns, nonsignificant; SBP, systolic blood pressure.
Discussion
In our study, we found that IOUH was independently associated with arterial stiffness, assessed through PWV. Although some studies have shown a similar association, they were conducted in untreated populations.11, 12, 13 Aznaouridis and colleagues13 found office systolic BP to be an independent predictor of aortic elastic properties, as opposed to ambulatory BP, in a study conducted in nondiabetic untreated individuals with WCH. In another study conducted by Wimmer and colleagues,11 the authors found that untreated individuals with WCH had increased central aortic pressures compared with normotensive individuals. In turn, de Simone and colleagues12 showed that an estimate of the WCE, ie, the difference between office and ambulatory BP, was associated with increased arterial stiffness in untreated hypertensive individuals. There is almost no information in treated hypertensive patients. Some of these aforementioned studies investigated other parameters of arterial stiffness such as central aortic BP and augmentation index. We did not perform such analysis because the Aortic device we used in some patients has not yet been validated against the SphygmoCor for these parameters.
In a meta‐analysis based on the International Database on Ambulatory Blood Pressure Monitoring in Relation to Cardiovascular Outcomes (IDACO) database, treated patients with IOUH had the same risk as patients with sustained normotension regarding cardiovascular events.9 In fact, IOUH is usually considered an “innocent” phenomenon that does not lead to therapeutic modifications when detected. This is especially true in low‐risk populations, such as ours (only 5.8% of patients were diabetic and only 3.3% had a history of cardiovascular or cerebrovascular disease). It must be noted, however, that the follow‐up in this meta‐analysis was 10.6 years, and that arterial stiffness may take a longer time to translate into clinical outcomes.
On the other hand, certain drug classes have been shown to be superior in reducing aortic stiffness. In the Preterax in Regression of Arterial Stiffness in a Controlled Double‐Blind (REASON) study,21 for instance, a combination of indapamide and perindopril were superior to atenolol in reducing central BP. In the Blood Pressure Lowering of Aliskiren Hydrochlorothiazide (HCTZ) Versus Amlodipine in Stage 2 Hypertension in African Americans (ATLAAST) trial, Ferdinand and colleagues22 showed that a renin inhibitor/diuretic‐based therapy achieved a substantial reduction in central BP as compared with amlodipine monotherapy. In turn, the Conduit Artery Function Evaluation (CAFE) study found perindopril and amlodipine to be superior to the combination of atenolol and bendroflumethiazide in lowering central BP and pulse pressure.23 Of note, brachial pressure reduction was similar in both groups. Moreover, a meta‐analysis conducted by Ong and colleagues24 found that angiotensin‐converting enzyme inhibitors were superior to calcium channel blockers and placebo in reducing aortic stiffness. These results are in line with our study findings, where the use of calcium channel blockers was independently and positively associated with arterial stiffness (Table 3), suggesting a worst performance compared with other antihypertensive drugs. Therefore, hypertensive populations more prone to arterial stiffness, such as patients with IOUH, might benefit from a drug‐class effect.
Given the cross‐sectional nature of this study, no causal relationship can be established. In that sense, a maladaptive cardiovascular response during office visits could be either the cause or the consequence of the higher degree of arterial stiffness found in patients with IOUH. Interestingly, the office BP level used to define IOUH or sustained normotension was measured on a different day than PWV assessment. During PWV measurements, BP levels were not different between groups and thus do not explain the difference in PWV values.
In the context of our results, it could be hypothesized that, like in untreated individuals,25 both office and out‐of‐office BP measurements have prognostic value in treated patients, and those with abnormal BP levels in either of these measurements—even if it is only office BP—are at higher risk than those with sustained normal BP levels.
Study Limitations
Our findings must be interpreted within the context of the study limitations. First, office BP was measured on only one occasion; second, the limited sample size might have precluded the finding of significant associations, described in previous studies, such as the relation between PWV and BMI; third, other variables not investigated in this study, such as a significant inter‐arm difference in BP,26 could have had an influence on the determination of arterial stiffness; and fourth, given that the agreement to classify patients as having IOUH through ambulatory BP monitoring (ABPM) and HBPM is only moderate,27, 28, 29 some patients considered to have IOUH in our study might have been classified as having sustained hypertension if ABPM had been performed. It must be noted, however, that HBPM is the preferred method to follow‐up hypertensive patients under treatment, given better patient tolerance, lower cost, and greater availability in contrast to ABPM.30, 31, 32, 33
Conclusions
IOUH is independently associated with arterial stiffness in treated hypertensive patients. Whether this high‐risk association is offset by antihypertensive treatment regarding cardiovascular outcomes should be investigated in longitudinal studies. In the meantime, it might be advisable to use drugs with a proven favorable profile for aortic stiffness in these patients.
Grant Support
None.
Conflict of Interest
The authors declare that they have no competing interests.
J Clin Hypertens (Greenwich). 2017;19:6–10. DOI: 10.1111/jch.12913. © 2016 Wiley Periodicals, Inc.
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