Pathophysiology of Heart Failure

Tanai, Edit; Frantz, Stefan

doi:10.1002/cphy.c140055

Cited by 438 publications

(364 citation statements)

References 133 publications

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“…Furthermore, direct microinjection of an AT2R agonist into the IML in normotensive rats produced sympathoinhibition [31]. Central AT2R stimulation by icv infusion was also able to reduce sympathetic outflow in heart failure [25], which is a state of profound sympathoexcitation [38]. …”

Section: At2r and The Regulation Of Sympathetic Outflowmentioning

confidence: 99%

Centrally Mediated Cardiovascular Actions of the Angiotensin II Type 2 Receptor

Steckelings

Kloet

Sumners

2017

Trends in Endocrinology & Metabolism

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Sustained increases in activity of the sympathetic neural pathways that exit the brain and which increase blood pressure are a major underlying factor in resistant hypertension. Recently available information on the occurrence of angiotensin II type 2 receptors (AT2R) within or adjacent to brain cardiovascular control centers is consistent with findings that stimulation of these receptors lowers blood pressure, particularly during hypertension of neurogenic origin. Up until recently, brain AT2R had not been considered by many to play a role in the central control of blood pressure. Demonstration of these powerful anti-hypertensive effects of brain AT2R opens the door to reconsideration of their role in blood pressure regulation, and their consideration as a novel therapeutic avenue for resistant hypertension.

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Section: At2r and The Regulation Of Sympathetic Outflowmentioning

confidence: 99%

Centrally Mediated Cardiovascular Actions of the Angiotensin II Type 2 Receptor

Steckelings

Kloet

Sumners

2017

Trends in Endocrinology & Metabolism

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“…It acts at the level of cell genome like other steroid hormones. According to modern concepts, weak inhibition of aldosterone activity is one of the possible reasons for insufficient efficacy of standard therapy in the treatment of chronic heart failure with post-infarction cardiosclerosis [10].…”

Section: Problem Statement and Analysis Of The Recent Researchmentioning

confidence: 99%

Dynamics of Heart Failure Markers in Patients after Past Myocardial Infarction with the Use of Potassium and Magnesium Salts of Gluconic Acid, Eplerenone and Rivaroxaban

Савчук

Vakaliuk

2017

Arch. clin. med.

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The objective of the research was to increase the efficiency of treatment of patients with chronic heart failure (CHF) and post-infarction cardiosclerosis by adding potassium and magnesium salts of gluconic acid, eplerenone and rivaroxaban to the background therapy taking into account the indices of growth differentiation factor 15 (GDF-15), aldosterone and galectin-3. Materials and methods of the research. Emmunoenzymometric determination of the galectin-3, GDF-15 and aldosterone levels concentration in blood serum was conducted to achieve the stated objective. 42 patients with CHF and post-infarction cardiosclerosis after coronary artery stenting in the acute period of myocardial infarction (MI) were examined. The patients were randomized into four groups according to the peculiarities of treatment. Group I included patients with CHF and post-infarction cardiosclerosis treated with the background therapy (BT). Group II consisted of patients with CHF who were treated with BT and addition of potassium and magnesium salts of gluconic acid. Group III included patients with CHF who were prescribed eplerenone secondary to BT. Group IV consisted of patients who were treated with BT and rivaroxaban. Results. The proposed treatment regimens were proved to be effective in reduction of GDF-15, aldosterone and galectin-3 indices in 12 months of treatment. Conducted therapy with the use of rivaroxaban secondary to BT led to more intensive decrease in GDF-15 concentration in comparison with the use of potassium and magnesium salts of gluconic acid or eplerenone on the background of BT. This index constituted (2110.21±107.4) pg/ml before the treatment in these patients and significantly decreased to (1286.75±109.6) pg/ml being significantly before the therapy. The performed treatment with the use of eplerenone secondary to BT was proved to be more effective for normalization of aldosterone and galectin-3 levels in blood serum compared to other studied treatment regimens. The average value of aldosterone changed in the treatment process by 67.24%. Thus, the average level of this index constituted (139.8±7.63) pg/ml before the treatment and was equal to (45.8±5.52) pg/ml at the end of the treatment course. The average value of galectin-3 in patients with CHF and post-infarction cardiosclerosis was noted to be (34.69±1.67) ng/ml before the treatment. It constituted (22.53±0.98) ng/ml after the end of treatment being significantly lower compared to the value before the treatment. The average value of this index changed in the course of twelve-month treatment by 35.05%. Lower risk of sudden cardiac arrest (SCA), acute coronary syndrome (ACS) and stroke was observed in the patients with CHF and post-infarction cardiosclerosis with the use of rivaroxaban secondary to BT. Conclusions. Thus, the use of rivaroxaban combination therapy secondary to BT led to more intensive decrease in GDF-15 concentration in comparison with the use of potassium and magnesium salts of gluconic acid or eplerenone. Conducted therapy with the use o...

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“…Progressive HF with reduced LV ejection fraction (LVEF) is the consequence, and it results in systemic compensatory mechanisms, namely activation of the renin-angiotensin-aldosterone system [3]. These initially beneficial and compensatory effects on haemodynamics nourish, however, in the mid-and long-term negative adaptive remodelling processes of the heart itself, further promoting the progression of LV dysfunction (vicious circle).…”

Section: Introductionmentioning

confidence: 99%

The endothelial nitric oxide synthase cofactor tetrahydrobiopterin shields the remote myocardium from apoptosis after experimental myocardial infarction in vivo

et al. 2017

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A b s t r a c tBackground: Following myocardial infarction (MI), apoptosis occurs early in the remote myocardium and contributes to the processes of myocardial remodelling. Increased nitrosative stress is a well-known and potent inductor of myocardial apoptosis. Excess activation of endothelial nitric oxide synthase (eNOS) increases its uncoupling potential and results in nitrosative stress via formation of peroxynitrite. However, the pathophysiological role of eNOS signalling in the remote myocardium after MI is as yet undefined. Aim:The impact of eNOS activation on pro-and anti-apoptotic signalling in the remote myocardium and the influence of pretreatment with the eNOS cofactor tetrahydrobiopterin (BH4) on eNOS activation, nitrosative stress level, and apoptosis induction and execution were studied in a rat MI model in vivo.Results: Twenty-four hours after anterior MI, eNOS activity in animals treated with left anterior descending coronary artery ligation (LIG) significantly increased in the posterior left ventricular (LV) myocardium as did protein nitrosylation when compared to sham treatment. This was paralleled by induction of apoptosis via the extrinsic and intrinsic pathways. Moreover, anti-apoptotic signalling via protein kinase B/Akt and glycogen synthase-kinase 3 beta was suppressed. Notably, pretreatment with the eNOS cofactor BH4 reduced eNOS activation, prevented excess protein nitrosylation, blunted apoptosis induction, facilitated anti-apoptotic signalling, and eventually prevented apoptosis execution. Conclusions:Here we showed that 24 h after experimental MI in rats in vivo, apoptosis was induced in the posterior non-infarcted LV wall. Evidence is presented that pretreatment with the eNOS cofactor BH4 resulted in less nitrosative stress and weakened apoptotic processes, although the stabilisers contained did participate in this phenomenon. Because apoptosis is a crucial component of myocardial remodelling, influencing eNOS signalling might be an interesting pharmacological target for the development of novel anti-remodelling therapies.

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Pathophysiology of Heart Failure

Cited by 438 publications

References 133 publications

Centrally Mediated Cardiovascular Actions of the Angiotensin II Type 2 Receptor

Centrally Mediated Cardiovascular Actions of the Angiotensin II Type 2 Receptor

Dynamics of Heart Failure Markers in Patients after Past Myocardial Infarction with the Use of Potassium and Magnesium Salts of Gluconic Acid, Eplerenone and Rivaroxaban

The endothelial nitric oxide synthase cofactor tetrahydrobiopterin shields the remote myocardium from apoptosis after experimental myocardial infarction in vivo

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