Modulation of RAAS-natriuretic peptides in the treatment of HF: Old guys and newcomers

Mollace, Vincenzo; Gliozzi, Micaela; Capuano, Annalisa; Rossi, Francesco

doi:10.1016/j.ijcard.2016.03.085

Cited by 15 publications

(9 citation statements)

References 38 publications

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“…The present study clarified the correlation between EI and HF severity in patients with CHD. Decompensated HF generally leads to fluid retention caused by increased ventricular filling pressure and neurohormonal activation . In the present study, EI was significantly correlated with NYHA FC or log BNP level.…”

Section: Discussionsupporting

confidence: 57%

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Bioelectrical impedance analysis in the management of heart failure in adult patients with congenital heart disease

Satō

Inai

Shimizu

et al. 2018

Congenital Heart Disease

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| INTRODUC TI ONFluid retention with dyspnea is the most often encountered cause of rehospitalization after acute heart failure (HF). Decompensated HF generally leads to fluid overload caused by elevated ventricular filling pressure or neurohormonal activation. Thus, the ability to recognize and quantify fluid retention is critical for the treatment of HF; however, optimal markers for the presence of fluid retention have yet to be identified. Brain natriuretic peptide (BNP) testing, chest radiography, cardiac ultrasonography, and blood sampling are insufficient for assessing fluid retention.Bioelectrical impedance analysis (BIA) was recently introduced in many clinical fields, such as cardiology, nephrology, hepatology, nutrition, and rehabilitation. 1-9 BIA is a safe, rapid, and noninvasive assessment method that involves the application of alternating currents to the body to achieve 8-polar tactile-electrode impedance. These impedances are obtained using differences in cell membrane permeability based on variable frequencies. AbstractObjective: The recognition of fluid retention is critical in treating heart failure (HF).Bioelectrical impedance analysis (BIA) is a well-known noninvasive method; however, data on its role in managing patients with congenital heart disease (CHD) are limited.Here, we aimed to clarify the correlation between BIA and HF severity as well as the prognostic value of BIA in adult patients with CHD.Design: This prospective single-center study included 170 patients with CHD admitted between 2013 and 2015. We evaluated BIA parameters (intra-and extracellular water, protein, and mineral levels, edema index [EI, extracellular water-to-total body water ratio]), laboratory values, and HF-related admission prevalence. Results: Patients with New York Heart Association (NYHA) functional classes III-IVhad a higher EI than those with NYHA classes I-II (mean ± SD, 0.398 ± 0.011 vs 0.384 ± 0.017, P < .001). EI was significantly correlated with brain natriuretic peptide level (r = 0.51, P < .001). During the mean follow-up period of 7.1 months, Kaplan-Meier analysis showed that a discharge EI > 0.386, the median value in the present study, was significantly associated with a future increased risk of HF-related admission (HR = 4.15, 95% CI = 1.70-11.58, P < .001). A body weight reduction during hospitalization was also related to EI reduction.Conclusions: EI determined using BIA could be a useful marker for HF severity that could predict future HF-related admissions in adult patients with CHD.

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Section: Discussionsupporting

confidence: 57%

“…Decompensated HF generally leads to fluid retention caused by increased ventricular filling pressure and neurohormonal activation. [19][20][21][22][23][24][25] In the present study, EI was significantly correlated with NYHA FC or log BNP…”

Section: Correlation Between Bia and Hf Severitysupporting

confidence: 61%

Bioelectrical impedance analysis in the management of heart failure in adult patients with congenital heart disease

Satō

Inai

Shimizu

et al. 2018

Congenital Heart Disease

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“…While the activation of these systems during the early phase of HF may normalize cardiac output and perfusion, chronic activation has a deleterious impact on the outcome of this condition, promoting structural and functional changes in the myocardium and the vasculature that eventually contribute to decompensated HF (100-103). Thus, in order to prevent the progression of HF and to improve morbidity and mortality, several treatments targeting this axis and modulate their activity have been developed (104,105). HF is also a risk factor for neurodegenerative disorders, possibly because impaired blood flow and neurohormonal activation favor accumulation of Aβ plaques and neurofibrillary tangles (106), indicating the strict link between aging and chronic disorders.…”

Section: Neurohormonal Factorsmentioning

confidence: 99%

“…Furthermore, treatment with ACE-I and ARBs represent a valid therapeutic option for aged people (105,135,136), improving cerebral blood flow and reducing the 1-year risk of fall in elderly people (137), even though in hypertensive patients it is associated with worse gait performance (138) and appears to have no effect on walking distance or on agerelated decline of muscle strength (139).…”

Section: Neurohormonal Factorsmentioning

confidence: 99%

Role of circulating factors in cardiac aging

Cannatà¹,

Marcon²,

Cimmino³

et al. 2017

J. Thorac. Dis.

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Worldwide increase in life expectancy is a major contributor to the epidemic of chronic degenerative diseases. Aging, indeed, simultaneously affects multiple organ systems, and it has been hypothesized that systemic alterations in regulators of tissue physiology may regulate this process. Cardiac aging itself is a major risk factor for cardiovascular diseases and, because of the intimate relationship with the brain, may contribute to increase the risk of neurodegenerative disorders. Blood-borne factors may play a major role in this complex and still elusive process. A number of studies, mainly based on the revival of parabiosis, a surgical technique very popular during the 70s of the 20 th century to study the effect of a shared circulation in two animals, have indeed shown the potential that humoral factors can control the aging process in different tissues. In this article we review the role of circulating factors in cardiovascular aging. A better understanding of these mechanisms may provide new insights in the aging process and provide novel therapeutic opportunities for chronic age-related disorders.

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“…Furthermore, EP stimulates the β1 receptor of glomerular parietal cells, promotes renin secretion and induces the upregulation of serum renin and Ang II levels ( 5 ). The binding of Ang II to Ang II receptor type 1 (AT1R) causes myocardial cell damage and heart failure ( 6 ). However, Ang II receptor type 2 (AT2R) counteracts the canonical signaling of RAS that is mediated by AT1R.…”

Section: Introductionmentioning

confidence: 99%

Erythropoietin alleviates post-resuscitation myocardial dysfunction in rats potentially through increasing the expression of angiotensin II receptor type 2 in myocardial tissues

et al. 2018

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Activation of renin-angiotensin system (RAS) is one of the pathological mechanisms associated with myocardial ischemia-reperfusion injury following resuscitation. The present study aimed to determine whether erythropoietin (EPO) improves post-resuscitation myocardial dysfunction and how it affects the renin-angiotensin system. Sprague-Dawley rats were randomly divided into sham, vehicle, epinephrine (EP), EPO and EP + EPO groups. Excluding the sham group, all groups underwent cardiopulmonary resuscitation (CPR) 4 min after asphyxia-induced cardiac arrest (CA). EP and/or EPO was administrated by intravenous injection when CPR began. The results demonstrated that the vehicle group exhibited lower mean arterial pressure, left ventricular systolic pressure, maximal ascending rate of left ventricular pressure during left ventricular isovolumic contraction and maximal descending rate of left ventricular pressure during left ventricular isovolumic relaxation (+LVdP/dt max and -LVdP/dt max, respectively), and higher left ventricular end-diastolic pressure, compared with the sham group following return of spontaneous circulation (ROSC). Few significant differences were observed concerning the myocardial function between the vehicle and EP groups; however, compared with the vehicle group, EPO reversed myocardial function indices following ROSC, excluding-LVdP/dt max. Serum renin and angiotensin (Ang) II levels were measured by ELISA. The serum levels of renin and Ang II were significantly increased in the vehicle group compared with the sham group, which was also observed for the myocardial expression of renin and Ang II receptor type 1 (AT1R), as determined by reverse transcription-quantitative polymerase chain reaction and western blotting. EPO alone did not significantly reduce the high serum levels of renin and Ang II post-resuscitation, but changed the protein levels of renin and AT1R expression in myocardial tissues. However, EPO enhanced the myocardial expression of Ang II receptor type 2 (AT2R) following ROSC. In conclusion, the present study confirmed that CA resuscitation activated the renin-Ang II-AT1R signaling pathway, which may contribute to myocardial dysfunction in rats. The present study confirmed that EPO treatment is beneficial for protecting cardiac function post-resuscitation, and the roles of EPO in alleviating post-resuscitation myocardial dysfunction may potentially be associated with enhanced myocardial expression of AT2R.

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Modulation of RAAS-natriuretic peptides in the treatment of HF: Old guys and newcomers

Cited by 15 publications

References 38 publications

Bioelectrical impedance analysis in the management of heart failure in adult patients with congenital heart disease

Bioelectrical impedance analysis in the management of heart failure in adult patients with congenital heart disease

Role of circulating factors in cardiac aging

Erythropoietin alleviates post-resuscitation myocardial dysfunction in rats potentially through increasing the expression of angiotensin II receptor type 2 in myocardial tissues

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