scholarly journals The apelin-APJ system in the evolution of heart failure

2015 ◽  
Vol 88 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Cerasela Mihaela Goidescu ◽  
Luminița Animarie Vida-Simiti

Heart failure is a chronic, progressive disease in which the overexpression of biologically active molecules and neurohomonal activation are the key factors of the evolution and natural history. The apelin-APJ system is a newly discovered molecular pathway and the RAAS counterbalance is its principal effect. The apelin is a potent inotrope, vasodilator and diuretic with crucial cardioprotective effects against angiotensin and aldosterone injuries. Intense and prolonged RAAS induces the downregulation of the apelin and its receptor at myocardial level and cancels their protection. Compared to the vasoactive agents used in the treatment of acute heart failure, exogen apelin has unique intropic and vasodilatory effects without deleterious consequences, being a promising therapeutic option.

2020 ◽  
Vol 98 (3) ◽  
pp. 178-184
Author(s):  
T. V. Chernyakova ◽  
A. Yu. Brezhnev ◽  
I. R. Gazizova ◽  
A. V. Kuroyedov ◽  
A. V. Seleznev

In the review we have integrated all up-to-date knowledge concerning clinical course and treatment of glaucoma among pregnant women to help specialists choose a proper policy of treatment for such a complicated group of patients. Glaucoma is a chronic progressive disease. It rarely occurs among childbearing aged women. Nevertheless the probability to manage pregnant patients having glaucoma has been recently increasing. The situation is complicated by the fact that there are no recommendations on how to treat glaucoma among pregnant women. As we know, eye pressure is progressively going down from the first to the third trimester, so we often have to correct hypotensive therapy. Besides, it is necessary to take into account the effect of applied medicines on mother health and evaluate possible teratogenic complications for a fetus. The only medicine against glaucoma which belongs to category B according to FDA classification is brimonidine. Medicines of the other groups should be prescribed with care. Laser treatment or surgery may also be a relevant decision when monitoring patients who are planning pregnancy or just bearing a child. Such treatment should be also accompanied by medicines.


The prevalence of heart failure is markedly increased in individuals with diabetes mellitus. Numerous observational studies suggest that this increased risk for heart failure can be attributed to exacerbated vascular complications and the presence of increased risk factors in diabetic subjects. In addition, experimental studies revealed the presence of a number of distinct molecular alterations in the myocardium that occur independently of vascular disease and hypertension. Many of these molecular alterations are similarly observed in failing hearts of nondiabetic patients and have thus been proposed to contribute to the increased risk for heart failure in diabetes. The interest in understanding the underlying mechanisms of impaired cardio- vascular outcomes in diabetic individuals has much increased since the demonstration of cardioprotective effects of SGLT-2 inhibitors and GLP-1 receptor agonists in recent clinical trials. The current review therefore summarizes the distinct mechanisms that have been proposed to increase the risk for heart failure in diabetes mellitus.


Author(s):  
Mitsuo Sobajima ◽  
Nobuyuki Fukuda ◽  
Hiroshi Ueno ◽  
Koichiro Kinugawa

Abstract Background  The safety and efficacy of MitraClip for advanced heart failure (HF) patients who are inotrope-dependent or mechanically supported are unknown. Case summary  The patient was a 71-year-old man diagnosed as dilated cardiomyopathy in 2003. He was admitted due to worsening HF in January 2019 and became dependent upon intravenous infusion of inotropes. During the 8-month hospitalization, his haemodynamics were relatively static with bed rest and continuous inotropes, but he was definitely dependent on them. Our multidisciplinary team decided to perform both cardiac resynchronization therapy (CRT) and MitraClip under Impella support. First, Impella was inserted from left subclavian artery. After a week, CRT was implanted from right subclavian vein, and the QRS duration of electrocardiogram became remarkably narrow. MitraClip was performed 2 weeks after Impella, and functional mitral regurgitation improved from severe to mild, and Impella was removed on the same day. Inotropes could be ceased, and he was discharged 2 months after MitraClip. Discussion  During inotrope-dependent status, there was a risk that HF would worsen with haemodynamic collapse when performing CRT implantation, and we firstly supported his haemodynamics by Impella. Cardiac resynchronization therapy implantation before MitraClip seemed to be crucial. In fact, the mitral valve morphology before Impella insertion had very poor coaptation of the anterior and posterior leaflets that was not optimal for MitraClip procedure. But the Impella support and correction of dyssynchrony by CRT markedly improved the coaptation of those leaflets. The combination therapy of CRT and MitraClip unloading with Impella maybe a new therapeutic option for advanced HF.


Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3322 ◽  
Author(s):  
Xuguang Li ◽  
Tianyi Yuan ◽  
Di Chen ◽  
Yucai Chen ◽  
Shuchan Sun ◽  
...  

Puerarin is a well-known traditional Chinese medicine which has been used for the treatment of cardiovascular diseases. Recently, a new advantageous crystal form of puerarin, puerarin-V, has been developed. However, the cardioprotective effects of puerarin-V on myocardial infarction (MI) heart failure are still unclear. In this research, we aim to evaluate the cardioprotective effects of puerarin-V on the isoproterenol (ISO)-induced MI mice and elucidate the underlying mechanisms. To induce MI in C57BL/6 mice, ISO was administered at 40 mg/kg subcutaneously every 12 h for three times in total. The mice were randomly divided into nine groups: (1) control; (2) ISO; (3) ISO + puerarin injection; (4–9) ISO + puerarin-V at different doses and timings. After treatment, cardiac function was evaluated by electrocardiogram (ECG), biochemical and histochemical analysis. In vitro inflammatory responses and apoptosis were evaluated in human coronary artery endothelial cells (HCAECs) challenged by lipopolysaccharide (LPS). LPS-induced PPAR-Υ/NF-κB and subsequently activation of cytokines were assessed by the western blot and real-time polymerase chain reaction (PCR). Administration of puerarin-V significantly inhibits the typical ST segment depression compared with that in MI mice. Further, puerarin-V treatment significantly improves ventricular wall infarction, decreases the incidence of mortality, and inhibits the levels of myocardial injury markers. Moreover, puerarin-V treatment reduces the inflammatory milieu in the heart of MI mice, thereby blocking the upregulation of proinflammatory cytokines (TNF-α, IL-1β and IL-6). The beneficial effects of puerarin-V might be associated with the normalization in gene expression of PPAR-Υ and PPAR-Υ/NF-κB /ΙκB-α/ΙΚΚα/β phosphorylation. In the in vitro experiment, treatment with puerarin-V (0.3, 1 and 3 μM) significantly reduces cell death and suppresses the inflammation cytokines expression. Likewise, puerarin-V exhibits similar mechanisms. The cardioprotective effects of puerarin-V treatment on MI mice in the pre + post-ISO group seem to be more prominent compared to those in the post-ISO group. Puerarin-V exerts cardioprotective effects against ISO-induced MI in mice, which may be related to the activation of PPAR-γ and the inhibition of NF-κB signaling in vivo and in vitro. Taken together, our research provides a new therapeutic option for the treatment of MI in clinic.


2013 ◽  
Vol 125 (9) ◽  
pp. 409-421 ◽  
Author(s):  
Laura A. Bienvenu ◽  
Melissa E. Reichelt ◽  
Lea M. D. Delbridge ◽  
Morag J. Young

MR (mineralocorticoid receptor) activation in the heart plays a central role in the development of cardiovascular disease, including heart failure. The MR is present in many cell types within the myocardium, including cardiomyocytes, macrophages and the coronary vasculature. The specific role of the MR in each of these cell types in the initiation and progression of cardiac pathophysiology is not fully understood. Cardiomyocyte MRs are increasingly recognized to play a role in regulating cardiac function, electrical conduction and fibrosis, through direct signal mediation and through paracrine MR-dependent activity. Although MR blockade in the heart is an attractive therapeutic option for the treatment of heart failure and other forms of heart disease, current antagonists are limited by side effects owing to MR inactivation in other tissues (including renal targets). This has led to increased efforts to develop therapeutics that are more selective for cardiac MRs and which may have reduced the occurrence of side effects in non-cardiac tissues. A major clinical consideration in the treatment of cardiovascular disease is of the differences between males and females in the incidence and outcomes of cardiac events. There is clinical evidence that female sensitivity to endogenous MRs is more pronounced, and experimentally that MR-targeted interventions may be more efficacious in females. Given that sex differences have been described in MR signalling in a range of experimental settings and that the MR and oestrogen receptor pathways share some common signalling intermediates, it is becoming increasingly apparent that the mechanisms of MRs need to be evaluated in a sex-selective manner. Further research targeted to identify sex differences in cardiomyocyte MR activation and signalling processes has the potential to provide the basis for the development of cardiac-specific MR therapies that may also be sex-specific.


2020 ◽  
Vol 2020 (1) ◽  
Author(s):  
Ghazwan Butrous

[No abstract. Showing first paragraph of article]Pulmonary hypertension is a progressive disease characterized by an elevation of pulmonary artery pressure and pulmonary vascular resistance, leading to right ventricular failure and death. It remains a challenging chronic progressive disease, but the current interest and advent of medical therapy in the last 20 years has significantly changed the perception of medical community in this disease. Pulmonary hypertension is not a specific disease; the majority of cases present with other diseases and various pathological processes that affect the pulmonary vasculature, and consequently increase pulmonary pressure and vascular resistance.


2021 ◽  
Vol 8 (3) ◽  
pp. 20-24
Author(s):  
Nishanam Gururaj ◽  
Nithin Voruganti

Background: Effect of thyroid hormone on cardiac functions is mediated by biologically active T3 which binds to nuclear TR. There is increasing evidence that patients with mild thyroid dysfunctions are presenting with adverse cardiovascular manifestations which includes heart failure. Aim: The present study aimed to determine the existence of low T3 syndrome in patients with chronic heart failure. Material and Methods: This prospective study was conducted in the Department of General Medicine and Cardiology, KMC, and MGM Hospital, Warangal. patients with heart failure were included in the study. A total of n=100 patients were included in the study detailed physical examination was conducted to assess the patient's volume status (rales, edema, jugular venous distension), weight, height, body mass index, and orthostatic blood pressure changes. Complete blood count, blood glucose (fasting and 2 hours postprandial), Fasting serum lipid profile, blood urea, serum creatinine, and serum electrolytes were measured in all patients. Two-dimensional echocardiography was done in patients. Results:Analysis of Echocardiography parametersCompared to patients who were alive (n=90),left ventricular end-diastolic diameter was higher in those whodied (n=10). The mean ejection fraction in died and alive groups were27.19% and 35.12% respectively. Persons who died had asignificantly lower ejection fraction than those alive.When the mean ejection fraction was compared betweenpatients with low total T3 (T3<80 ng/dl) and normal T3 , patients with low T3 had a mean ejection fraction of 29.2% and those with normal T3 levels had a mean ejection fraction of 34.78%. This indicates the mean ejection fraction is lower in patients with low total T3 levels. Conclusion:Within the limitations of the present study it can be concluded that the prevalence of low T3 syndrome in patients with chronic heart failure is common. It was found that patients with lower T3 levels were having a lower ejection fraction.The LVEDD diameterwas negatively correlated with total T3. Therefore, Total T3 levels can be used as an adjunct to other parameters for risk stratification and survival estimation in chronic heart failure.


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