White coat effect, blood pressure and mortality in men: prospective cohort study

Te, Strandberg; Salomaa,

doi:10.1053/euhj.1999.2042

Cited by 79 publications

(62 citation statements)

References 18 publications

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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: 93%

“…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: 93%

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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“…However, it is notable that those which found an increased cardiovascular risk studied high-risk patients and predominantly male subjects. [18][19][20] Studies reporting no increase in risk examined patients who were drawn from the general population 6,7 or which followed up for periods of time less than 10 years. 21,23,24,26 In our own study, 11 years was insufficient for cardiovascular effects to be demonstrable with statistical significance.…”

Section: Discussionmentioning

confidence: 99%

“…Cross-sectional studies have reported an increased incidence of precursors of cardiovascular disease such as left ventricular hypertrophy. [12][13][14][15][16][17] However, prospective studies appear to offer the best opportunity in which to detect an effect and reported studies are divided into those who find that the white-coat effect has adverse consequences for cardiovascular disease [18][19][20] and those that find that it does not. 6,[21][22][23][24][25][26] We have previously reported 11-year mortality data in the General Practice Hypertension Study Group (GPHSG) in subjects with transiently raised clinic DBP, and found the relative risk of cardiovascular death compared with controls was 1.5 in men and 0.7 in women compared to normotensive controls 27 but these results were not statistically significant.…”

Section: Introductionmentioning

confidence: 99%

Transiently elevated diastolic blood pressure is associated with a gender-dependent effect on cardiovascular risk

Wingfield¹,

Grodzicki

Palmer

et al. 2005

J Hum Hypertens

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We assessed the morbidity and mortality of subjects with transiently elevated diastolic pressure in the General Practice Hypertension Study Group (GPHSG) population. A total of 23 578 patients (aged 18-65 years) from seven UK general practices were screened in 1974 for a diastolic blood pressure (DBP4) of X90 mmHg. Two further readings of DBP4 determined hypertensive (either DBP4X90 mmHg) or transient hypertensive (both DBP4o90 mmHg) status. Transients (n ¼ 850) were matched with normotensive controls (n ¼ 824) and risk ratios calculated over a mean follow-up of 18.7 years. Rescreening was conducted in six of the practices (n ¼ 20 942) after 7.7 years. Male transients had a higher relative hazard for cardiovascular mortality than controls (11.8%, 8.6%, adjusted relative hazard 1.59, P ¼ 0.056). Female transients had a lower relative hazard for cardiovascular mortality than controls (3.6%, 5.4%, adjusted relative hazard 0.39, P ¼ 0.018). In all, 422 patients with transient hypertension were rescreened along with 367 matched controls. Significantly more transients were on antihypertensive treatment compared with their controls (odds ratio (OR) [95% CI]) for both male (4.2 [1.6-11.1]) and female patients (2.4 [1.0-5.56]) and more untreated female transients developed hypertension. Male transients had a higher rates of diabetes mellitus (adj OR ¼ 5.1, P ¼ 0.04) and stroke (adj OR 15.9, P ¼ 0.03). This study has shown that transiently elevated DBP in GPHSG is associated with a significantly higher risk of later hypertension in men and women and of diabetes, stroke and cardiovascular mortality in men. Women with this condition have a significantly lower cardiovascular mortality.

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“…Cardiovascular reactivity has several detrimental consequences for human health: high BP reactivity has been linked to hypertension, 12 increased left ventricular mass, 13 carotid atherosclerosis 14 and all-cause mortality. 15 Data from experimental rat models have shown that prenatal malnutrition 16 and prenatal stress, 17 potential determinants of smaller body size at birth and shorter length of gestation, are associated with exaggerated cardiovascular reactivity to restraint stress. In humans, we are aware of only two studies that have examined whether BP reactivity in adult life is predicted by body size or gestational age at birth.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular reactivity to psychological stressors in late adulthood is predicted by gestational age at birth

Feldt

Räikkönen

Eriksson³

et al. 2007

J Hum Hypertens

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The relationships of body size and gestational age at birth with adult blood pressure (BP) are relatively modest compared to their stronger associations with cardiovascular disease. BP reactivity is a strong predictor of cardiovascular morbidity, and it is possible that reactivity, rather than resting level, is determined in utero. We investigated whether body size and gestational age at birth predict BP reactivity during experimentally induced psychosocial stress in late adulthood. A total of 73 men and 80 women born after 36 weeks' gestation in Helsinki, Finland, during 1934-1944 underwent the Trier Social Stress Test (TSST); a standardized psychosocial stress test consisting of a public speech and an arithmetic task. Changes in BP were monitored continuously by a non-invasive finger photoplethysmography (Finometer, FMS, Amsterdam, The Netherlands). The results showed that the most robust early determinant of BP reactivity was gestational age; however, with opposite relationships between the sexes (P for interaction o0.001). A 1-week increase in gestational age was associated with a 3.1 mm Hg (95% confidence interval (CI), 0.2 to 6.0) and 1.2 mm Hg (95% CI, À0.1 to 2.6) decreases in systolic and diastolic BP reactivity in women, but with 5.2 mm Hg (95% CI, 1.9 to 8.4) and 2.3 mm Hg (95% CI, 0.9 to 3.8) increases in men. In conclusion, normal variation in gestational age at birth predicts cardiovascular stress reactivity in later adulthood. Given that hypothalamic-pituitary-adrenal axis contributes to the regulation of autonomic nervous system function and the timing of parturition, and shows well-established sex differences, we speculate a role for early programming of this axis in explaining the findings.

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White coat effect, blood pressure and mortality in men: prospective cohort study

Abstract: The results suggest that white coat hypertension or a large white coat effect is not an innocent phenomenon. It tends to co-exist with metabolic risk factors and predicts total and cardiovascular mortality during long-term follow-up.

Cited by 79 publications

References 18 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

Transiently elevated diastolic blood pressure is associated with a gender-dependent effect on cardiovascular risk

Cardiovascular reactivity to psychological stressors in late adulthood is predicted by gestational age at birth

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