Cardiac Hypertrophy and Fibrosis in the Metabolic Syndrome: A Role for Aldosterone and the Mineralocorticoid Receptor

Essick, Eric E.; Sam, Flora

doi:10.4061/2011/346985

Cited by 33 publications

(26 citation statements)

References 146 publications

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“…As expected, morbid obesity was accompanied in our patients by changes in cardiac function and structure, mainly characterized by the left ventricular hypertrophy and diastolic dysfunction, which confirms the results of previous studies [5,[27][28][29]. Several factors influence the development of cardiac remodelling.…”

Section: Discussionsupporting

confidence: 77%

“…Several factors influence the development of cardiac remodelling. Load conditions, circulating volume and blood pressure hormones such as insulin and leptin, as well as neurohormonal activation with increased sympathetic tone are interrelated and ultimately lead to cardiac hypertrophy and geometric remodelling in an effort to adapt to the overall demands [6,7,28,30]. Bariatric surgery leads to the cessation of stimuli for cardiac remodelling in several ways, beyond the weight loss.…”

Section: Discussionmentioning

confidence: 99%

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The impact of bariatric surgery on renal and cardiac functions in morbidly obese patients

Luaces¹,

Martínez‐Martínez²,

Medina³

et al. 2012

Nephrology Dialysis Transplantation

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Background. Cardiac adaptation to obesity includes both structural and functional alterations in the heart. The kidneys also suffer the consequence of excessive increase of body weight. This study aims to assess the functional, cardiac and renal changes in a cohort of morbidly obese patients, as well as changes after bariatric surgery-the last therapeutic option for these patients. Methods. Patients referred for bariatric surgery were prospectively included. In each case, transthoracic echocardiography and a blood test were performed before the procedure and repeated 1 year after surgery. The estimation of the glomerular filtration rate (GFR) was addressed by the Cockroft-Gault lean body weight formula. Results. Sixty-one patients completed the 1-year followup. Of these, 81.9% were female. The mean age was 41.1 ± 9.8 years and the mean body mass index was 47.4 ± 5 kg/m 2 , decreasing to 30.5 ± 5.07 kg/m 2 after the procedure. Before surgery, the estimated GFR was 92.7 ± 25.4 mL/min, with hyperfiltration being present in 14.8% of patients, whereas an impaired GFR was detected in 8.3%. Patients showed preserved systolic function and cardiac remodelling. Diastolic function was abnormal in 27.9% of patients. At the 1-year follow-up, favourable changes in the left ventricular geometry and related haemodynamic status were observed. There was no significant change in the estimated GFR in the overall group, although hyperfiltration was ameliorated in 9.8% and a poor GFR was improved in 3.3.%. The improvement was not associated with changes in either blood pressure or the BMI. However, in this group of patients the amelioration of the GFR was associated with an increased stroke volume and improvement in diastolic function. Conclusions. In morbidly obese patients, GFR is usually normal and only a small percentage of them show hyperfiltration or a reduced GFR. Bariatric surgery has a favourable impact on renal function in only a reduced group of patients who also experience an improvement in cardiac performance.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

The impact of bariatric surgery on renal and cardiac functions in morbidly obese patients

Luaces¹,

Martínez‐Martínez²,

Medina³

et al. 2012

Nephrology Dialysis Transplantation

View full text Add to dashboard Cite

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“…Neurohumoral activation (sympathoexcitation and excitation of the renin-angiotensin-aldosterone system in resting conditions) and a decrease in baroreflex sensitivity (BRS) play a key role in the genesis and progression of various major diseases such as diabetes [1,2], metabolic syndrome [3,4] and heart failure [5][6][7][8]. The therapeutic spectrum for these diseases is diverse, pharmacotherapy being a cornerstone, but lifestyle changes including regular physical exercise considerably improve prognosis and partly revert the abnormal resting conditions of neurohumoral activation and decreased BRS, for example as in heart failure [9].…”

Section: Introductionmentioning

confidence: 99%

Neurocardiological differences between musicians and control subjects

et al. 2013

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Background Exercise training is beneficial in health and disease. Part of the training effect materialises in the brainstem due to the exercise-associated somatosensory nerve traffic. Because active music making also involves somatosensory nerve traffic, we hypothesised that this will have training effects resembling those of physical exercise. Methods We compared two groups of healthy, young subjects between 18 and 30 years: 25 music students (13/12 male/ female, group M) and 28 controls (12/16 male/female, group C), peers, who were non-musicians. Measurement sessions to determine resting heart rate, resting blood pressure and baroreflex sensitivity (BRS) were held during morning hours.

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“…Mineralocorticoids stimulate vascular [10,23,24,29,30,31], cardiac [8,24,29,32,33,34,35,36,37,38,39,40], renal [24,26,36,41,42,43], peritoneal [14,17] and pancreatic [44] fibrosis.…”

Section: Effect Of Mineralocorticoids On Inflammation and Fibrosismentioning

confidence: 99%

Mineralocorticoid and SGK1-Sensitive Inflammation and Tissue Fibrosis

Artunc¹,

Läng

2014

Nephron Physiol

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Effects of mineralocorticoids are not restricted to regulation of epithelial salt transport, extracellular volume and blood pressure; mineralocorticoids also influence a wide variety of seemingly unrelated functions such as inflammation and fibrosis. The present brief review addresses the role of mineralocorticoids in the orchestration of these latter processes. Mineralocorticoids foster inflammation as well as vascular, cardiac, renal and peritoneal fibrosis. Mechanisms involved in mineralocorticoid-sensitive inflammation and fibrosis include the serum- and glucocorticoid-inducible kinase 1 (SGK1), which is genomically upregulated by mineralocorticoids and transforming growth factor β (TGF-β), and stimulated by mineralocorticoid-sensitive phosphatidylinositide 3-kinase. SGK1 upregulates the inflammatory transcription factor nuclear factor-κB, which in turn stimulates the expression of diverse inflammatory mediators including connective tissue growth factor. Moreover, SGK1 inhibits the degradation of the TGF-β-dependent transcription factors Smad2/3. Mineralocorticoids foster the development of T_H17 cells, which is compromised following SGK1 deletion. Excessive SGK1 expression is observed in a wide variety of fibrosing diseases including lung fibrosis, diabetic nephropathy, glomerulonephritis, obstructive kidney disease, experimental nephrotic syndrome, obstructive nephropathy, liver cirrhosis, fibrosing pancreatitis, peritoneal fibrosis, Crohn's disease and celiac disease. The untoward inflammatory and fibrosing effects of mineralocorticoids could be blunted or even reversed by mineralocorticoid receptor blockers, which may thus be considered in the treatment of inflammatory and/or fibrosing disease.

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Cardiac Hypertrophy and Fibrosis in the Metabolic Syndrome: A Role for Aldosterone and the Mineralocorticoid Receptor

Cited by 33 publications

References 146 publications

The impact of bariatric surgery on renal and cardiac functions in morbidly obese patients

The impact of bariatric surgery on renal and cardiac functions in morbidly obese patients

Neurocardiological differences between musicians and control subjects

Mineralocorticoid and SGK1-Sensitive Inflammation and Tissue Fibrosis

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