Pathophysiology and the cardiorenal connection in heart failure. Circulating hormones:biomarkers or mediators (original) (raw)
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Neurohumoral Activation in Heart Failure
International Journal of Molecular Sciences
In patients with heart failure (HF), the neuroendocrine systems of the sympathetic nervous system (SNS), the renin–angiotensin–aldosterone system (RAAS) and the arginine vasopressin (AVP) system, are activated to various degrees producing often-observed tachycardia and concomitant increased systemic vascular resistance. Furthermore, sustained neurohormonal activation plays a key role in the progression of HF and may be responsible for the pathogenetic mechanisms leading to the perpetuation of the pathophysiology and worsening of the HF signs and symptoms. There are biomarkers of activation of these neurohormonal pathways, such as the natriuretic peptides, catecholamine levels and neprilysin and various newer ones, which may be employed to better understand the mechanisms of HF drugs and also aid in defining the subgroups of patients who might benefit from specific therapies, irrespective of the degree of left ventricular dysfunction. These therapies are directed against these neuroh...
Heart failure and neuroendocrine activation: diagnostic, prognostic and therapeutic perspectives
Clinical Physiology, 2001
The important neuroendocrine systems involved in heart failure are reviewed with special emphasis on their possible role in pathophysiology and their relation to prognostic and diagnostic information. Plasma levels of noradrenaline (NA), renin, vasopressin, endothelin-1, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and tumour necrosis factor-a (TNF-a) are all elevated in heart failure. Activity of the sympathetic nervous system as re¯ected by NA is correlated to mortality and seems to possess independent prognostic information. Several studies have now documented the bene®cial effect of b-blockade in chronic heart failure (CHF). Renin seems to be a poor prognostic marker in CHF possibly because of the interference with diuretic treatment, angiotensin converting enzyme (ACE)-inhibitors and angiotensin II antagonist, and probably also because of the signi®cance of tissue renin-angiotensin system (RAS), poorly re¯ected by plasma renin. On the other hand, several large-scale trials with ACE-inhibitors and angiotensin II antagonists have demonstrated reduced mortality and morbidity in CHF. Plasma vasopressin does not seem to possess prognostic information but testing of non-peptide antagonists is ongoing. Endothelin-1 seems to have independent prognostic information and endothelin receptor antagonists may represent a therapeutic possibility.
Neurohormones and Cytokines in Heart Failure. Correlation With Coronary Flow Reserve
Revista Española de Cardiología (English Edition), 2005
In heart failure, the coronary flow reserve (CFR) measured by positron-emission tomography (PET) is reduced. As neurohormone and cytokine levels are also altered in patients with the condition, our aim was to determine whether there is a correlation between CFR and neurohormone and cytokine levels.
Neurohormones, inflammatory mediators, and cardiovascular injury in the setting of heart failure
Heart Failure Reviews, 2019
Neurohormones and inflammatory mediators have effects in both the heart and the peripheral vasculature. In patients with heart failure (HF), neurohormonal activation and increased levels of inflammatory mediators promote ventricular remodeling and development of HF, as well as vascular dysfunction and arterial stiffness. These processes may lead to a vicious cycle, whereby arterial stiffness perpetuates further ventricular remodeling leading to exacerbation of symptoms. Although significant advances have been made in the treatment of HF, currently available treatment strategies slow, but do not halt, this cycle. The current treatment for HF patients involves the inhibition of neurohormonal activation, which can reduce morbidity and mortality related to this condition. Beyond benefits associated with neurohormonal blockade, other strategies have focused on inhibition of inflammatory pathways implicated in the pathogenesis of HF. Unfortunately, attempts to target inflammation have not yet been successful to improve prognosis of HF. Further work is required to interrupt key maladaptive mechanisms involved in disease progression. Keywords Neurohormones. Inflammatory mediators and cardiovascular injury in the setting of heart failure. Ventricular remodeling. Vascular dysfunction. Arterial stiffness
Hypertension and Heart Failure: Role of Neurohormonal Mechanisms
Clinical and Experimental Hypertension, 2004
Hypertension represents the most common associated cause of heart failure, and it is frequently involved in the pathogenesis of left ventricular dysfunction and its progression towards congestive heart failure. A common pathophysiological link of hypertension to heart failure is represented by the abnormalities of the neurohormonal profile and its impact on cardiac function, systemic hemodynamics and salt/water balance. This article synthetically reviews this aspect together with a specific analysis of the significance of measurements of neurohormones for diagnosis and prognostic stratification in heart failure.
Current Concepts of Neurohormonal Activation in Heart Failure
AACN Advanced Critical Care, 2008
Neurohormonal activation is a commonly cited array of phenomena in the body's physiologic response to heart failure. Although various neurohormones and pharmacologic agents that moderate their pathophysiologic effects have been reviewed in the nursing literature, both the mechanisms of neurohormonal system activation and cellular and organ system effects have been described only in brief. Accordingly, this article reviews mechanisms of neurohormonal activation and describes cellular and cardiovascular effects of the (1) sympathetic nervous system, (2) renin-angiotensin-aldosterone system, (3) kallikrein-kininogen-kinin system, (4) vasopressinergic system, (5) natriuretic peptide systems, and (6) endothelin in the context of heart failure. This article implicitly details the physiologic basis for numerous current and potential future pharmacologic agents used in the management of heart failure. It is intended that this article be used as a reference for advanced clinical nursing practice, research, and education.
Neurohumoral Pathway in Heart Failure
ACI (Acta Cardiologia Indonesiana)
Heart Failure is now considered as one of the leading cause for mortality and morbidity. It is affecting several organs and cause organ damages due to the myocardial failure to pump inadequate oxygenated blood to the body including metabolites, to end organs and peripheral tissues. Heart failure results from multifactorial mechanism including neurohumoral activations including increased activity of the sympathetic nervous system, renin-angiotensin aldosteron system, vasopression and the atrial natriuretic peptide. This neurohumoral pathway has significant contribution to the development of myocardial dysfunction that lead to clinical manifestation of heart failure. Some of the markers in these pathways have now been considered as an independent predictors of prognosis in heart failure patient.
International journal of …, 2005
Patients with chronic congestive heart failure have a sequential and incessant activation of those neurohormonal systems, which control body fluids, cardiac output and systemic blood pressure. Neurohormonal activation is initially selective and regional. Generalized activation is a late event in the natural history of congestive heart failure. Although the ultimate stimulus responsible for the activation of these neurohormonal systems is unknown, a decreased cardiac output and diminished effective blood volume have been proposed as the responsible mechanisms. However, extensive clinical and experimental research suggest that cardiac remodeling and loading of low-pressure cardiac receptors with sympathetic afferents could be the triggering events followed by unloading of high-pressure carotid receptors by decreased cardiac output and diminished effective blood volume.
The American Journal of the Medical Sciences, 2001
Background: In chronic heart failure (CHF), cardiac dysfunction is considered the major determinant of neurohumoral activation but the role of renal impairment has not been defined. We investigated the relationship between both cardiac and renal dysfunction and neurohumoral activation, and their possible influence on prognosis. Methods: Hemodynamics, renal function, plasma neurohormones, and long-term follow-up were evaluated in 148 CHF patients, grouped according to systolic volume index (SVI) and serum creatinine (CRE) values: SVI Ͼ 28 mL/m 2 and CRE Ͻ 1.5 mg/dL (group I, n ϭ 55), SVI Ͻ 28 mL/m 2 and CRE Ͻ 1.5 mg/dL (group II, n ϭ 37), SVI Ͼ 28 mL/m 2 and CRE Ͼ 1.5 mg/dL (group III, n ϭ 25), SVI Ͻ 28 mL/m 2 and CRE Ͼ 1.5 mg/dL (group IV, n ϭ 31). Results: Neurohormones progressively increased from Group I through IV and correlated with both cardiac and renal function. The hemodynamic pattern was similar in patients with normal or abnormal renal function, whereas neurohormones were only moderately increased in the former group and markedly increased in the latter group. Longterm survival progressively decreased from Group I through IV and was significantly poorer in patients with renal dysfunction. Conclusions: Our study confirms that, in CHF, neurohumoral activation is strictly related to long-term survival and that many factors contribute to its development and progression; among these, cardiac and renal dysfunction seem to play a major role. KEY