Seasonal Variation of Home Blood Pressure and Its Association With Target Organ Damage: The J-HOP Study (Japan Morning Surge-Home Blood Pressure).

BACKGROUND: Although seasonal variation of home blood pressure (BP) has been reported to be higher in winter, seasonal difference in home BP (HBP) and its association with target organ damage (TOD) remains unclear. METHODS: This is a cross-sectional study using the dataset from the Japan Morning Surge-Home Blood Pressure (J-HOP) study to assess seasonal differences in HBP, prevalence of masked hypertension, and association of HBP with TOD. The J-HOP study is a nationwide, multicenter prospective study whose participants with cardiovascular risks underwent morning and evening HBP measurements for a 14-day period in 71 institutions throughout Japan. Urine albumin-creatinine ratio (UACR) and serum-B-type natriuretic peptide (BNP) were obtained at enrollment. RESULTS: Among 4,267 participants (mean age, 64.9 ± 10.9 years; 46.9% male; 91.4% hypertensives), 1,060, 979, 1,224, and 1,004 participants were enrolled in spring, summer, autumn, and winter, respectively. Morning and evening home systolic/diastolic BP levels, and prevalence of masked hypertension (office BP <140/90 mm Hg and HBP ≥135/85 mm Hg) were significantly lower in summer than other seasons after adjustment for covariates. When we assessed the interaction between BP parameters and each season for an association with TOD, we found the association between morning home diastolic BP and each of UACR and BNP was stronger in winter than other seasons (both P for interaction <0.05). CONCLUSIONS: In this study, we revealed that the prevalence of masked hypertension was higher in other seasons than in summer and found a notable association between morning home diastolic BP and TOD in winter.

Vascular α1-Adrenergic Receptor Responsiveness in Masked Hypertension.

BACKGROUND: Masked hypertension (nonhypertensive in the clinic setting but hypertensive outside the clinic during wakefulness) is characterized by increased blood pressure in response to physical and emotional stressors that activate the sympathetic nervous system (SNS). However, no studies have assessed vascular reactivity to a pharmacological SNS challenge in individuals with masked hypertension. METHODS: We analyzed data from 161 adults aged 25 to 45 years (mean ± standard deviation age 33 ± 6 years; 48% were African American and 43% were female). Participants completed ambulatory blood pressure monitoring, and a standardized α 1-adrenergic agonist phenylephrine test that determines the dose of phenylephrine required to increase a participant's mean arterial pressure by 25 mm Hg (PD25). RESULTS: Twenty-one participants were considered to have masked hypertension (clinic systolic blood pressure (SBP) <140 and diastolic blood pressure (DBP) <90 mm Hg but awake SBP ≥135 or DBP ≥85 mm Hg), 28 had sustained hypertension (clinic SBP ≥140 or DBP ≥90 mm Hg and awake SBP ≥135 or DBP ≥85 mm Hg), and 106 had sustained normotension (clinic SBP <140 and DBP <90 mm Hg and awake SBP <135 and DBP <85 mm Hg). After multivariable adjustment, the mean (±SE) PD25 was less in participants with masked hypertension compared with their counterparts with sustained normotension (222.1 ± 33.2 vs. 328.7 ± 15.0; P = 0.012), but similar to that observed in subjects with sustained hypertension (254.8 ± 31.0; P =0.12). CONCLUSIONS: Among young and middle-aged adults, masked hypertension is associated with increased vascular reactivity to a SNS challenge, which may contribute to elevated awake BPs as well as to increased cardiovascular disease risk.

The impact of apelin and relaxin plasma levels in masked hypertension and white coat hypertension.

Masked hypertension (HTN) and white coat hypertension represent two reverse forms of clinical HTN with questionable prognostic significance. Recent evidence supports that low apelin and relaxin plasma levels contribute to vascular damage accelerating atherogenesis and predisposing to HTN and cardiovascular (CV) events. The aim of this study was to compare apelin and relaxin plasma levels between patients with masked hypertension (MH) and those with white coat HTN (WCH). Overall, 130 patients not receiving antihypertensive therapy were studied. All patients underwent 24-hour ambulatory BP monitoring (ABPM) and office BP measurements. Plasma apelin and relaxin levels were measured by ELISA method. According to BP recordings, 24 subjects had MH (group A) and 32 had WCH (group B). Apelin (200 ± 111 pg/mL vs 305 ± 127 pg/mL, P < 0.01) and relaxin (35.2 ± 6.7 pg/mL vs 46.8 ± 23.6 pg/mL, P < 0.01) plasma levels were significantly lower in patients with MH compared to those with WCH, respectively. In conclusion, our findings showed that patients with MH had significantly lower apelin and relaxin levels compared to those with WCH. This observation implies an additional prognostic role for adipokines supporting the concept that MH is closer to essential HTN whereas WCH is a more benign condition.

Out-of-Clinic Sympathetic Activity Is Increased in Patients With Masked Uncontrolled Hypertension.

Masked uncontrolled hypertension (MUCH) is defined as controlled automated office blood pressure (BP; AOBP <135/85 mm Hg) in-clinic in patients receiving antihypertensive medication(s) but uncontrolled BP out-of-clinic by 24-hour ambulatory BP monitoring (ABPM; awake ≥135/85 mm Hg). We hypothesized that MUCH patients have greater out-of-clinic sympathetic activity compared with true controlled hypertensives. Patients being treated for hypertension were prospectively recruited after 3 or more consecutive clinic visits. All patients were evaluated by in-clinic automated office BP, plasma catecholamines, and spot-urine/plasma metanephrines. In addition, out-of-clinic 24-hour ABPM, 24-hour urinary for catecholamines and metanephrines was done. Out of 237 patients recruited, 169 patients had controlled in-clinic BP of which 156 patients had completed ABPM. Seventy-four were true controlled hypertensives, that is controlled by clinic automated office BP and by out-of-clinic ABPM. The remaining 82 were controlled by clinic automated office BP, but uncontrolled during out-of-clinic ABPM, indicative of MUCH. After exclusion of 4 patients because of inadequate or lack of 24-hour urinary collections, 72 true controlled hypertensive and 80 MUCH patients were analyzed. MUCH patients had significantly higher out-of-clinic BP variability and lower heart rate variability compared with true controlled hypertensives, as well as higher levels of out-of-clinic urinary catecholamines and metanephrines levels consistent with higher out-of-clinic sympathetic activity. In contrast, there was no difference in in-clinic plasma catecholamines and spot-urine/plasma levels of metanephrines between the 2 groups, consistent with similar levels of sympathetic activity while in clinic. MUCH patients have evidence of heightened out-of-clinic sympathetic activity compared with true controlled hypertensives, which may contribute to the development of MUCH.

Asymmetric dimethylarginine levels are associated with augmentation index across naïve untreated patients with different hypertension phenotypes.

Asymmetric dimethylarginine (ADMA) is a robust marker of endothelial dysfunction in patients with essential hypertension. We investigated ADMA levels and their association with vascular damage in untreated hypertension. We enrolled consecutive patients with untreated, recently diagnosed hypertension and age-matched normotensive individuals. 24-hour blood pressure, central hemodynamics, and arterial stiffness were recorded. A total of 311 individuals were studied: 165 with essential hypertension, 50 with masked hypertension, 25 with white-coat hypertension, and 71 normotensive individuals. ADMA levels significantly correlated with aortic augmentation index (AIx75) (r = .156, P = .006), aortic pulse pressure (r = .153, P = .007) and marginally with carotid-femoral pulse wave velocity (r = .110, P = .051), as well as with diastolic office BP. In the multivariate model, aortic AIx75 and age were the only statistically significant predictors of ADMA. This is the largest study to document an independent association between ADMA and aortic AIx75 but not with other indices of arterial stiffness.

Association of ambulatory blood pressure variability with coronary artery calcium.

Blood pressure (BP) variability is associated with progression to clinical atherosclerosis. The evidence is inconclusive if BP variability predicts cardiovascular outcomes in low-risk populations. The aim of this study was to analyze the association of 24-hour BP variability with coronary artery calcium (CAC) among a group of individuals without coronary artery disease. The Masked Hypertension Study targeted patients with borderline high BP (120-149 mm Hg systolic and/or 80-95 mm Hg diastolic). Ambulatory blood pressure monitoring (ABPM) was performed at two time-points, 8 days apart. CAC was measured at exit visit via cardiac CT and reported as Agatston Score. Weighted standard deviations and average real variability were calculated from ABPM. Of the 322 participants who underwent cardiac CT, 26% (84) had CAC present, 52% (168) were female, and 21% (64) were black. BP variability did not differ by CAC group. In this low cardiovascular risk group, CAC was not associated with 24-hour ambulatory BP variability.

Are increased oxidative stress and asymmetric dimethylarginine levels associated with masked hypertension?

OBJECTIVE: In this study, our aim was to determine total oxidative stress and asymmetric dimethylarginine (ADMA) levels in patients with masked hypertension (MHT) and to examine their association with blood pressure. METHODS: Fifty patients diagnosed with MHT and 48 healthy volunteers without any known chronic diseases have been included in this study. RESULTS: When compared to the control group, patients with MHT had higher levels of mean ADMA (p < 0.001), total oxidant status (TOS) (p < 0.001), and oxidative stress index (OSI) (p < 0.001), and a lower mean total antioxidant status (TAS) (p < 0.001) level. While a positive correlation was determined between the systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels with ADMA, TOS, and OSI levels, a negative correlation was determined with the TAS level. During the stepwise multivariable logistic regression analysis, age (OR = 1.221; p = 0.003), body mass index (OR = 1.512; p = 0.005), low density lipoprotein (OR = 0.925; p = 0.016), ADMA (OR = 1.200; p = 0.002), and OSI (OR = 3.750; p = 0.002) levels were determined to be the predictors of MHT. During the linear regression analysis, it was determined that the independent risk factors of SBP and DBP are ADMA and OSI, and the independent risk factor of TOS, OSI, and ADMA is SBP. Our study found out that oxidative stress and ADMA levels of patients with MHT are higher than those of the control group. ADMA and OSI were determined to be predictors of MHT. CONCLUSION: Based on these results, it could be said that oxidative stress, and therefore the ADMA level, could have an effect on the etiopathogenesis of MHT.