Complementary and Incremental Mortality Risk Prediction by Cortisol and Aldosterone in Chronic Heart Failure

Güder, Gülmisal; Bauersachs, Johann; Frantz, Stefan; Weismann, Dirk; Allolio, Bruno; Ertl, Georg; Angermann, Christiane E.; Störk, Stefan

doi:10.1161/circulationaha.106.653964

Cited by 269 publications

(187 citation statements)

References 48 publications

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“…In the Caerphilly Heart Study, Davey-Smith et al (113) reported a positive association between the plasma cortisol/testosterone ratio and incident vascular disease; cortisol alone was not an independent predictor. In smaller studies, higher plasma cortisol has also been associated with the extent of atheromatous disease quantified by coronary angiography (114), and predicted mortality in patients with heart failure (115). Polymorphisms in the GR gene have recently been associated with cardiovascular event rate in populationbased studies in Rotterdam (SWJ Lamberts, personal communication) and Sydney (116) ( Table 1).…”

Section: Endogenous Glucocorticoidsmentioning

confidence: 98%

Glucocorticoids and Cardiovascular Disease

Walker¹

2007

European Journal of Endocrinology

467

386

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Chronic excessive activation of glucocorticoid receptors induces obesity, insulin resistance, glucose intolerance, dyslipidaemia and hypertension. Subtle abnormalities of the hypothalamic-pituitaryadrenal axis and/or of tissue sensitivity to glucocorticoids are also associated with these cardiovascular risk factors in patients with the metabolic syndrome. Furthermore, glucocorticoids have direct effects on the heart and blood vessels, mediated by both glucocorticoid and mineralocorticoid receptors and modified by local metabolism of glucocorticoids by the 11b-hydroxysteroid dehydrogenase enzymes. These effects influence vascular function, atherogenesis and vascular remodelling following intravascular injury or ischaemia. This article reviews the systemic and cardiovascular effects of glucocorticoids, and the evidence that glucocorticoids not only promote the incidence and progression of atherogenesis but also modify the recovery from occlusive vascular events and intravascular injury. The conclusion is that manipulation of glucocorticoid action within metabolic and cardiovascular tissues may provide novel therapeutic avenues to combat cardiovascular disease.European Journal of Endocrinology 157 545-559

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Section: Endogenous Glucocorticoidsmentioning

confidence: 98%

Glucocorticoids and Cardiovascular Disease

Walker¹

2007

European Journal of Endocrinology

467

386

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“…Aldosterone is also produced within the heart and works directly on heart tissue at the sites where the hormone is produced. 66 Increased levels of aldosterone in the circulation or in heart tissue stimulate excessive production of collagen, which leads to cardiac fibrosis and cardiac remodeling. 66 Further, cortisol may mimic the effects of aldosterone in patients with heart failure because of changes caused by damage to myocardial tissue.…”

Section: Activation Of the Hpa Axismentioning

confidence: 99%

“…66 Increased levels of aldosterone in the circulation or in heart tissue stimulate excessive production of collagen, which leads to cardiac fibrosis and cardiac remodeling. 66 Further, cortisol may mimic the effects of aldosterone in patients with heart failure because of changes caused by damage to myocardial tissue. 66 Elevated serum levels of cortisol and aldosterone are independent predictors of mortality in patients with heart failure.…”

Section: Activation Of the Hpa Axismentioning

confidence: 99%

“…66 Further, cortisol may mimic the effects of aldosterone in patients with heart failure because of changes caused by damage to myocardial tissue. 66 Elevated serum levels of cortisol and aldosterone are independent predictors of mortality in patients with heart failure. 67 Aldosterone level is also elevated in patients with depression and may precipitate depression.…”

Section: Activation Of the Hpa Axismentioning

confidence: 99%

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Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

Chapa

Akintade

Son

et al. 2014

Critical Care Nurse

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H eart failure is an epidemic with national and global implications. Compared with the situation in other cardiac diseases, the incidence and prevalence of heart failure continue to increase despite recent advancements in understanding and treatment. Increased survival after myocardial infarction, aging of the population, and increased incidence of diabetes are contributing factors. This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:1. Describe the biopsychosocial holistic model for cardiovascular health 2. Identify 2 neurohormonal pathways and their impact in heart failure 3. Identify nursing implications for heart failure, depression, and anxiety CNE Continuing Nursing EducationCover Depression and anxiety are common comorbid conditions in patients with heart failure. Patients with heart failure and depression have increased mortality. The association of anxiety with increased mortality in patients with heart failure is not established. The purpose of this article is to illustrate the similarities of the underlying pathophysiology of heart failure, depression, and anxiety by using the Biopsychosocial Holistic Model of Cardiovascular Health. Depression and anxiety affect biological processes of cardiovascular function in patients with heart failure by altering neurohormonal function via activation of the hypothalamic-pituitary-adrenal axis, autonomic dysregulation, and activation of cytokine cascades and platelets. Patients with heart failure and depression or anxiety may exhibit a continued cycle of heart failure progression, increased depression, and increased anxiety. Understanding the underlying pathophysiological relationships in patients with heart failure who experience comorbid depression and/or anxiety is critical in order to implement appropriate treatments, educate patients and caregivers, and educate other health professionals. (Critical Care Nurse. 2014;34[2]:14-25)

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“…Serum levels of the hormone aldosterone are increased in patients with HF with both reduced and preserved ejection fraction (HFrEF and HFpEF, respectively), and predict mortality risk (Guder et al. 2007; Girerd et al. 2013).…”

Section: Introductionmentioning

confidence: 99%

Endothelial mineralocorticoid receptor contributes to systolic dysfunction induced by pressure overload without modulating cardiac hypertrophy or inflammation

et al. 2017

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Heart Failure (HF) is associated with increased circulating levels of aldosterone and systemic inflammation. Mineralocorticoid receptor (MR) antagonists block aldosterone action and decrease mortality in patients with congestive HF. However, the molecular mechanisms underlying the therapeutic benefits of MR antagonists remain unclear. MR is expressed in all cell types in the heart, including the endothelial cells (EC), in which aldosterone induces the expression of intercellular adhesion molecule 1 (ICAM‐1). Recently, we reported that ICAM‐1 regulates cardiac inflammation and cardiac function in mice subjected to transverse aortic constriction (TAC). Whether MR specifically in endothelial cells (EC) contributes to the several mechanisms of pathological cardiac remodeling and cardiac dysfunction remains unclear. Basal cardiac function and LV dimensions were comparable in mice with MR selectively deleted from ECs (EC‐MR −/−) and wild‐type littermate controls (EC‐MR +/+). MR was specifically deleted in heart EC, and in EC‐containing tissues, but not in leukocytes of TAC EC‐MR −/− mice. While EC‐MR −/− TAC mice showed preserved systolic function and some alterations in the expression of fetal genes, the proinflammatory cytokine TNF α and the endothelin receptors in the LV as compared to EC‐MR +/+ TAC mice, no difference was observed between both TAC groups in overall cardiac hypertrophy, ICAM‐1 LV expression and leukocyte infiltration, cardiac fibrosis or capillary rarefaction, all hallmarks of pathological cardiac remodeling. Our data indicate that EC‐MR contributes to the transition of cardiac hypertrophy to systolic dysfunction independently of other maladaptive changes induced by LV pressure overload.

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Complementary and Incremental Mortality Risk Prediction by Cortisol and Aldosterone in Chronic Heart Failure

Cited by 269 publications

References 48 publications

Glucocorticoids and Cardiovascular Disease

Glucocorticoids and Cardiovascular Disease

Pathophysiological Relationships Between Heart Failure and Depression and Anxiety

Endothelial mineralocorticoid receptor contributes to systolic dysfunction induced by pressure overload without modulating cardiac hypertrophy or inflammation

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