White-coat hypertension and cardiovascular risk

Cerasola, Giovanni; Cottone, Santina; Nardi, Emilio; D??lgnoto, Giovanni; Volpe, Vito; Mul??, Giuseppe; Carollo, Caterina

doi:10.1097/00043798-199512000-00009

Cited by 44 publications

(26 citation statements)

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“…29 Other potential biologic mediators of LV hypertrophy in subjects with MetS may be certain peptide hormones, such as angiotensin II and leptin, which are secreted by white adipose tissue. 20 Our findings also suggest that the clustering of features of MetS, frequently described in WCHs, may be at least in part responsible for the cardiac abnormalities, and probably for the increased cardiovascular risk displayed in some, but not all, series regarding subjects with WCH [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] . On the other hand, the greater values of both LV mass and LV chamber diameter that we observed in WCHs without MetS when compared to those of normotensive controls, seem to indicate that WCH per se, independently of MetS, may not be innocuous for the heart.…”

Section: Discussionmentioning

confidence: 91%

“…1,2 Indeed, the studies that evaluated the effects of WCH on hypertensive target organ damage and on the occurrence of future cardiovascular events yielded conflicting results. [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] It has long been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities, including elevated triglycerides, reduced high-density lipoprotein (HDL) cholesterol, glucose intolerance, abdominal obesity and insulin resistance, which are the main features of the metabolic syndrome (MetS). MetS, which may precede the appearance of sustained hypertension, contributes to the development of hypertensive target organ damage and atherosclerotic diseases.…”

Section: Introductionmentioning

confidence: 99%

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Metabolic syndrome in subjects with white-coat hypertension: impact on left ventricular structure and function

et al. 2007

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Some reports have suggested that white-coat hypertension (WCH) is associated with some features of the metabolic syndrome (MetS). These metabolic disturbances, instead of WCH per se, may potentially explain the greater extent of end-organ damage sometimes observed in WCH subjects (WCHs) when compared to normotensive individuals (NTs). The aim of the present cross-sectional study was to compare left ventricular (LV) structure and function in three groups of subjects: WCHs with MetS, WCHs without MetS and NTs. A total of 145 WCHs, 35% of whom had MetS, were enrolled. As controls, 35 NTs were also studied. In all subjects, routine blood chemistry, echocardiographic examination and 24-h ambulatory blood pressure monitoring were performed. When compared with WCHs without MetS, those with MetS showed higher LV mass indexed by height elevated by a power of 2.7 (LVMH 2.7 ) (49.6714.8 vs 38.979.8 g/m 2.7 ; Po0.0001). The same parameter was greater in WCHs without MetS than in NTs (3278 g/m 2.7 ; P ¼ 0.004). Moreover, the E-wave deceleration time was longer in WCHs with MetS than in those without it (236.2766.4 vs 200.5730.8 ms; Po0.0001). The relationship of MetS with LVMH 2.7 was confirmed in multivariate regression models. Our results seem to suggest that MetS may have a deleterious influence on LV structure and function in WCH. However, WCH, being associated with an increased LV mass, also in subjects without MetS, may not be considered as an innocuous phenomenon.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Metabolic syndrome in subjects with white-coat hypertension: impact on left ventricular structure and function

et al. 2007

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“…11 It is interesting to note that previous comparative studies of WCH vs normotension have shown higher 24-h BPs in the WCH group. 6,7,11 This would at least suggest that within the normal range, WCH patients have a higher 24-h BP load, occupying a higher pressure stratum than normotensives. The subtle changes in left ventricular mass could be accounted for by this BP discrepancy.…”

Section: Discussionmentioning

confidence: 99%

“…1 Variously termed 'white coat hypertension', 'clinical hypertension', or 'isolated clinic hypertension' 2 (we will herein refer to the phenomenon as white coat hypertension (WCH)), it has been assumed that the lack of sustained hypertension in these patients reflects a reactive sympathetic nervous system, and predicts a benign prognosis. A number of studies looking at evidence of target organ damage have given equivocal results; left ventricular hypertrophy and renal dysfunction have both been described as occurring in association with WCH, [3][4][5][6][7][8] while other studies have not documented an association. [9][10][11][12] These studies have largely shown significantly higher mean BP in the WCH group, and it may be that the documented elevation of cardiac and renal indices of end-organ involvement found Conclusion: White coat hypertension is indeed associated with a larger left ventricular muscle mass than normotensives and these changes are independent of the actual 24-h BP load, and may reflect increased BP lability, sympathetic nervous system derangement, or a genetic propensity in people with white coat hypertension to stress-related hypertensive reactions, as part of a pre-hypertensive state.…”

Section: Introductionmentioning

confidence: 99%

Is elevation of clinic blood pressure in patients with white coat hypertension who have normal ambulatory blood pressure associated with target organ changes?

et al. 1998

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Background:The issue as to whether white coat hypertension is a pathologically significant entity, with associated target organ changes, or that the condition carries the same risk for target organ involvement as normotension, is undecided. Previous studies which have shown pathological correlates between white coat hypertension and target organ damage have not controlled for the most obvious confounder, mean 24 h blood pressure (BP). Methods and results: In this study we retrospectively identified 33 age and sex-matched pairs, one group with normal BP, the other with white coat hypertension. The white coat hypertensive group showed significantly greater left ventricular mass indexed for body surface area than normal controls (99.0 g/m 2 vs 78.3 g/m 2 , P Ͻ

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“…3 The question whether the white coat and masking phenomena are linked with increased BP variability remains to be answered; 4 considerable data links increased BP variability to worse prognosis in patients with elevated BP or controlled hypertension, [5][6][7][8][9][10] whereas several studies suggest that prognosis of patients with WCH and MH is worse than that of subjects with 'truly' normal BP. [11][12][13] Recently, both WCH and MH have been shown to predict sustained hypertension in subsequent ambulatory monitoring. 14 Our hypothesis in this study was that large differences between clinic and ambulatory BP, found among patients with both MH and WCH, can be associated with increased ambulatory BP variability.…”

Section: Introductionmentioning

confidence: 99%

The role of blood pressure variability in misdiagnosed clinic hypertension

et al. 2010

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Blood pressure (BP) assessment may be vulnerable to bias by increased BP variability. Uncertainty in determining BP control is inherent to the clinic setting. We analyzed a registry of 3949 patients referred for ambulatory BP monitoring. The difference between clinic and ambulatory readings was plotted against ambulatory BP variability, assessed by standard deviation. In addition, BP variability of patients with clinic and awake ambulatory hypertension was compared with that of patients with controlled BP and sustained hypertension, respectively. The average clinic-ambulatory systolic BP difference was 5 ± 17/3 ± 9 mm Hg. Patients with 410-mm Hg systolic difference had higher systolic ambulatory BP standard deviation (14.9 ± 4.2 mm Hg) compared to patients with a difference of 0 to 10-mm Hg (standard deviation 12.5 ± 3.7 mm Hg). Patients with masking (negative clinic-ambulatory BP difference) also had comparatively higher standard deviation (14.4±4.9 mm Hg Po0.0001). Greater ambulatory BP variability carried increased risk for both false diagnosis of hypertension (odds ratio (OR): 2.09, 95% confidence interval (CI): 1.58-2.76), and missed clinic diagnosis of hypertension (OR: 1.86, 95% confidence interval: 1.48-2.33). The former was more striking in women, in whom high variability carried greater odds for false diagnosis of hypertension (OR: 2.76, 95% confidence interval: 1.96-3.89). Thus, clinic misjudgment of BP control may stem in part from high BP variability. Women with high BP variability are more susceptible to hypertension misdiagnosis. It is possible that high BP variability contributes to the increased cardiovascular risk related to both masked hypertension and white coat hypertension.

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White-coat hypertension and cardiovascular risk

Cited by 44 publications

References 0 publications

Metabolic syndrome in subjects with white-coat hypertension: impact on left ventricular structure and function

Metabolic syndrome in subjects with white-coat hypertension: impact on left ventricular structure and function

Is elevation of clinic blood pressure in patients with white coat hypertension who have normal ambulatory blood pressure associated with target organ changes?

The role of blood pressure variability in misdiagnosed clinic hypertension

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