Serum cholesterol levels, blood pressure response to stress and incidence of stable hypertension in young subjects with high normal blood pressure

Borghi, Claudio; Veronesi, Maddalena; Bacchelli, Stefano; Esposti, Daniela Degli; Cosentino, Eugenio Roberto; Амбросиони, Е.

doi:10.1097/00004872-200402000-00009

Cited by 33 publications

(23 citation statements)

References 38 publications

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“…It is reported that elevated serum cholesterol levels, which were common in hyperlipidemic patients, might have an exaggerated cardiovascular response to stress (Borghi et al, 2004). It suggests that plasma cholesterol might be involved in blood pressure control and regulation In addition, the overwhelming evidence of both the cardioprotective and vasculoprotective profits of statin therapy and the continued discovery of actions of these agents independent of lipid lowering suggested that the modulation of blood pressure by statins may play a role in the hyperlipidemic-hypertensive patient (Chopra, Choksi, & Cavusoglu, 2007).…”

Section: Resultsmentioning

confidence: 99%

Contents of lovastatin, γ-aminobutyric acid and ergothioneine in mushroom fruiting bodies and mycelia

Chen

Hsieh

et al. 2012

LWT

174

133

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Section: Resultsmentioning

confidence: 99%

Contents of lovastatin, γ-aminobutyric acid and ergothioneine in mushroom fruiting bodies and mycelia

Chen

Hsieh

et al. 2012

LWT

174

133

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“…In this study, heterogeneity was mostly due to differences in study populations, measures of exposure and outcome, losses and follow-up time. The effect of heterogeneity was partially overcome by the use of random effects models, subgroup analysis, a combination of effect by study and analysis of the impact of Menkes et al a 22 Markovitz et al d 26 Markovitz et al c 26 Markovitz et al b 26 Markovitz et al a 26 Carroll et al b 44 Carroll et al a 44 Matthews et al f 21 Matthews et al e 21 Matthews et al d 21 Matthews et al c 21 Matthews et al b 21 Matthews et al a 21 Borghi et al 43 Steptoe et al h 25 Steptoe et al g 25 Steptoe et al f 25 Steptoe et al e 25 Steptoe et al d 25 Steptoe et al c 25 Steptoe et al b 25 Steptoe Figure 3 Random effects model, odds ratio and 95% confi dence interval for the combined effect by study and the impact of the exclusion of each study.…”

Section: Discussionmentioning

confidence: 99%

“…Steptoe et al 25 Borghi et al 43 Matthews et al 21 Carroll et al 44 Markovitz et al 26 Menkes et al 22 Meta-analysis random-effects estimates (exponential form) Study ommited Table 3 Combined effect of psychological stress on the increase of the blood pressure in sub-groups of cohorts according to participants and study design. …”

Section: Discussionmentioning

confidence: 99%

Effect of psychological stress on blood pressure increase: a meta-analysis of cohort studies

et al. 2009

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Studies have suggested that chronic exposure to stress may have an influence on increased blood pressure. A systematic review followed by a meta-analysis was conducted aiming to assess the effect of psychological stress on blood pressure increase. Research was mainly conducted in Ingenta, Psycinfo, PubMed, Scopus and Web of Science. Inclusion criteria were: published in any language; from January 1970 to December 2006; prospective cohort design; adults; main exposure psychological/emotional stress; outcome arterial hypertension or blood pressure increase > 3.5mmHg. A total of 2,043 studies were found, of which 110 were cohort studies. Of these, six were eligible and yielded 23 comparison groups and 34,556 subjects. Median follow-up time and loss to follow-up were 11.5 years and 21%. Results showed individuals who had stronger responses to stressor tasks were 21% more likely to develop blood pressure increase when compared to those with less strong responses (OR: 1.21; 95%CI: 1.14-1.28; p < 0.001). Although the magnitude of effect was relatively small, results suggest the relevance of the control of psychological stress to the non-therapeutic management of high blood pressure.

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“…The significant associations between MAP, NE levels, and their interactions in determining lipid levels are correlational and do not prove a causal link. For instance, some investigators suggest that having high normal BP and concomitant elevated serum cholesterol may lead to exaggerated cardiovascular responses to stress, due to endothelial dysfunction resulting from abnormalities of lipid metabolism [48]. Because of the sample size, conclusions pertaining to relationships observed between MAP and NE and specific lipids must be drawn with caution.…”

Section: Discussionmentioning

confidence: 99%

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

et al. 2009

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Hypertension is a known risk factor for cardiovascular disease. Hypertensive individuals show exaggerated norepinephrine (NE) reactivity to stress. Norepinephrine is a known lipolytic factor. It is unclear if, in hypertensive individuals, stress-induced increases in NE are linked with the elevations in stress-induced circulating lipid levels. Such a mechanism could have implications for atherosclerotic plaque formation. In a cross-sectional, quasi-experimentally controlled study, 22 hypertensive and 23 normotensive men (mean +/-SEM, 45 +/-3 years) underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma NE and the plasma lipid profile (total cholesterol [TC], low-density-lipoprotein cholesterol [LDL-C], high-density-lipoprotein cholesterol, and triglycerides) immediately before and after stress and at 20 and 60 minutes of recovery. All lipid levels were corrected for stress hemoconcentration. Compared with normotensives, hypertensives had greater TC (P = .030) and LDL-C (P = .037) stress responses. Independent of each other, mean arterial pressure (MAP) upon screening and immediate increase in NE predicted immediate stress change in TC (MAP: beta = .41, P = .003; NE: beta = .35, P = .010) and LDL-C (MAP: beta = .32, P = .024; NE: beta = .38, P = .008). Mean arterial pressure alone predicted triglycerides stress change (beta = .32, P = .043) independent of NE stress change, age, and BMI. The MAP-by-NE interaction independently predicted immediate stress change of high-density-lipoprotein cholesterol (beta = -.58, P < .001) and of LDL-C (beta = -.25, P < .08). We conclude that MAP and NE stress reactivity may elicit proatherogenic changes of plasma lipids in response to acute psychosocial stress, providing one mechanism by which stress might increase cardiovascular risk in hypertension.

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Serum cholesterol levels, blood pressure response to stress and incidence of stable hypertension in young subjects with high normal blood pressure

Abstract: These data suggest that subjects with high normal BP and elevated serum cholesterol might have an exaggerated cardiovascular response to stress and have an increased risk for stable hypertension that can be detected at young age.

Cited by 33 publications

References 38 publications

Contents of lovastatin, γ-aminobutyric acid and ergothioneine in mushroom fruiting bodies and mycelia

Contents of lovastatin, γ-aminobutyric acid and ergothioneine in mushroom fruiting bodies and mycelia

Effect of psychological stress on blood pressure increase: a meta-analysis of cohort studies

Changes in plasma lipids with psychosocial stress are related to hypertension status and the norepinephrine stress response

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