Biomarkers of Volume Overload and Edema in Heart Failure With Reduced Ejection Fraction

Chiorescu, Roxana Mihaela; Lazar, Roxana-Daiana; Buksa, Sándor-Botond; Mocan, Mihaela; Blendea, Dan

doi:10.3389/fcvm.2022.910100

Cited by 9 publications

(8 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that the plasma levels of vasopressin are elevated during the development of heart failure [251][252][253]. While the activation of the V 1a receptors via vasopressin results in the development of vasoconstriction, hypertension, cardiac hypertrophy and heart failure, the activation of the V 2 receptors is associated with fluid retention, leading to the development of volume overload, venous congestion, edema and lung congestion [254][255][256][257][258][259]. Vasopressin not only causes water retention but also results in kidney dysfunction in heart failure patients.…”

Section: Role Of Vasopressin In Cardiac Hypertrophy and Heart Failurementioning

confidence: 99%

Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure

Dhalla,

Mota,

Elimban

et al. 2024

Cells

View full text Add to dashboard Cite

Heart failure is the common concluding pathway for a majority of cardiovascular diseases and is associated with cardiac dysfunction. Since heart failure is invariably preceded by adaptive or maladaptive cardiac hypertrophy, several biochemical mechanisms have been proposed to explain the development of cardiac hypertrophy and progression to heart failure. One of these includes the activation of different neuroendocrine systems for elevating the circulating levels of different vasoactive hormones such as catecholamines, angiotensin II, vasopressin, serotonin and endothelins. All these hormones are released in the circulation and stimulate different signal transduction systems by acting on their respective receptors on the cell membrane to promote protein synthesis in cardiomyocytes and induce cardiac hypertrophy. The elevated levels of these vasoactive hormones induce hemodynamic overload, increase ventricular wall tension, increase protein synthesis and the occurrence of cardiac remodeling. In addition, there occurs an increase in proinflammatory cytokines and collagen synthesis for the induction of myocardial fibrosis and the transition of adaptive to maladaptive hypertrophy. The prolonged exposure of the hypertrophied heart to these vasoactive hormones has been reported to result in the oxidation of catecholamines and serotonin via monoamine oxidase as well as the activation of NADPH oxidase via angiotensin II and endothelins to promote oxidative stress. The development of oxidative stress produces subcellular defects, Ca2+-handling abnormalities, mitochondrial Ca2+-overload and cardiac dysfunction by activating different proteases and depressing cardiac gene expression, in addition to destabilizing the extracellular matrix upon activating some metalloproteinases. These observations support the view that elevated levels of various vasoactive hormones, by producing hemodynamic overload and activating their respective receptor-mediated signal transduction mechanisms, induce cardiac hypertrophy. Furthermore, the occurrence of oxidative stress due to the prolonged exposure of the hypertrophied heart to these hormones plays a critical role in the progression of heart failure.

show abstract

Section: Role Of Vasopressin In Cardiac Hypertrophy and Heart Failurementioning

confidence: 99%

Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure

Dhalla,

Mota,

Elimban

et al. 2024

Cells

View full text Add to dashboard Cite

show abstract

“…Myocardial remodeling in HFpEF differs from myocardial remodeling in HFrEF, which is caused by the death of cardiomyocytes due to oxidative stress caused by various factors such as ischemia, infection, and toxicity ( Figure 1 ) [ 13 , 14 , 15 ].…”

Section: Main Pathophysiological Mechanisms Involved In the Productio...mentioning

confidence: 99%

“…In HFrEF, decreased cardiac output causes activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system, the arginine-vasopressin system, natriuretic peptides, and endothelin, all of which cause water and salt retention in the body. Thus, activation of the renin-angiotensin-aldosterone system is a primary mechanism in HFrEF, and inhibition of its overexpression is a primary means of treatment in this category of patients [ 15 ].…”

Section: Treatment Of Patients With Hfpefmentioning

confidence: 99%

Current Insights and Future Directions in the Treatment of Heart Failure with Preserved Ejection Fraction

Chiorescu,

Lazar,

Ruda

et al. 2023

IJMS

Self Cite

View full text Add to dashboard Cite

Heart failure is a clinical syndrome associated with poor quality of life, substantial healthcare resource utilization, and premature mortality, in large part related to high rates of hospitalizations. The clinical manifestations of heart failure are similar regardless of the ejection fraction. Unlike heart failure with reduced ejection fraction, there are few therapeutic options for treating heart failure with preserved ejection fraction. Molecular therapies that have shown reduced mortality and morbidity in heart failure with reduced ejection have not been proven to be effective for patients with heart failure and preserved ejection fraction. The study of pathophysiological processes involved in the production of heart failure with preserved ejection fraction is the basis for identifying new therapeutic means. In this narrative review, we intend to synthesize the existing therapeutic means, but also those under research (metabolic and microRNA therapy) for the treatment of heart failure with preserved ejection fraction.

show abstract

“…Acting in this multimodal way to increase the atherosclerotic process, Galectin-3 has a central place and represents a target for prevention therapies. At present, statins have shown their effect on lowering the level of Galectin-3 in various studies [ 192 ], but other therapies, such as Quinapril, mineralocorticoid receptor antagonists, and N-acetyllactosamin, were shown to have a positive effect on the level of Galectin-3 [ 193 , 194 , 195 ]. On the other hand, Doxazosin exacerbates the expression of Galectin-3 in cardiomyocytes [ 196 ].…”

Section: Proteomics Of Vulnerable Plaquesmentioning

confidence: 99%

Vulnerable Atherosclerotic Plaque: Is There a Molecular Signature?

Chiorescu

Mocan

Buda³

et al. 2022

IJMS

Self Cite

View full text Add to dashboard Cite

Atherosclerosis and its clinical manifestations, coronary and cerebral artery diseases, are the most common cause of death worldwide. The main pathophysiological mechanism for these complications is the rupture of vulnerable atherosclerotic plaques and subsequent thrombosis. Pathological studies of the vulnerable lesions showed that more frequently, plaques rich in lipids and with a high level of inflammation, responsible for mild or moderate stenosis, are more prone to rupture, leading to acute events. Identifying the vulnerable plaques helps to stratify patients at risk of developing acute vascular events. Traditional imaging methods based on plaque appearance and size are not reliable in prediction the risk of rupture. Intravascular imaging is a novel technique able to identify vulnerable lesions, but it is invasive and an operator-dependent technique. This review aims to summarize the current data from literature regarding the main biomarkers involved in the attempt to diagnose vulnerable atherosclerotic lesions. These biomarkers could be the base for risk stratification and development of the new therapeutic drugs in the treatment of patients with vulnerable atherosclerotic plaques.

show abstract

Biomarkers of Volume Overload and Edema in Heart Failure With Reduced Ejection Fraction

Cited by 9 publications

References 92 publications

Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure

Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure

Current Insights and Future Directions in the Treatment of Heart Failure with Preserved Ejection Fraction

Vulnerable Atherosclerotic Plaque: Is There a Molecular Signature?

Contact Info

Product

Resources

About