Acute heart failure

Author(s):  
Kazem Rahimi

Heart failure is a clinical syndrome characterized by an inadequate cardiac output for the needs of the body in the absence of low filling pressures, and reflects abnormal cardiac structure or function. Although various definitions for acute heart failure (AHF) exist, here AHF is defined as new-onset heart failure or an acute exacerbation of chronic heart failure, requiring urgent therapy. Patients with AHF typically have clinical features of organ hypoperfusion, with or without pulmonary and peripheral oedema.

Author(s):  
Barry L. Karon ◽  
Naveen L. Pereira

Heart failure is a clinical syndrome characterized by the inability of the heart to maintain adequate cardiac output to meet the metabolic demands of the body while still maintaining normal or near-normal ventricular filling pressures. Heart failure may be present at rest, but often it is present only during exertion as a result of the dynamic nature of cardiac demands. For correct treatment of heart failure, the mechanism, underlying cause, and any reversible precipitating factors must be identified. Typical manifestations of heart failure are dyspnea and fatigue that limit activity tolerance and fluid retention leading to pulmonary or peripheral edema. The most recent proposed categorization divided the cardiomyopathies into primary and secondary cardiomyopathies, and the primary disorders are further subdivided as genetic, acquired, or mixed. Although this proposal takes into account our progressive understanding of this heterogeneous group of disorders, the previous phenotypic classification of dilated, hypertrophic, and restrictive diseases still provides utility in day-to-day understanding and management of these disorders.


2019 ◽  
Vol 61 (6) ◽  
Author(s):  
J. A. Ker ◽  
K. Outhoff

In general, heart failure is the end-stage manifestation of cardiovascular disease and is an important and increasing cause of morbidity worldwide. Acute heart failure, whether of new onset or an exacerbation of chronic heart failure, causes sudden congestion, typically presenting as pulmonary oedema. The mortality associated with acute heart failure is extremely high. Potentially life-saving treatments and other burning issues are highlighted in this review.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Wang Juan ◽  
Luo Liangtao ◽  
Li Zhongfeng ◽  
Chen Jianxin ◽  
Chen Chan ◽  
...  

Chronic heart failure (CHF) is a progressive clinical syndrome characterized by inability of the heart to adequately pump blood to meet metabolic demands of the body, and assessment of heart function in chronic heart failure patients is needed to make therapeutic decisions. New York Heart Association( NYHA) classification is usually performed to evaluate heart-function of CHF patients. Nevertheless, this does not take into account metabolic perturbations produced by heart-function impairment. In contrast, metabolomics can investigate many metabolic perturbations within biological systems.The purpose of this study was to assess whether metabolomic profiles of plasma, obtained by proton NMR spectroscopy from CHF patients, are affected by the severity of heart-function impairment. An orthogonal projection to latent-structure analysis was performed to compare NMR spectra of 49 chronic heart failure patients according to NYHA classification.The statistical model obtained showed a good explained variance (R 2 X = 0.13 and R 2 Y = 0.92) and a good predictability (Q 2 Y = 0.68). Metabolomic profiles showed significant differences regarding various metabolites depending of severity of heart-function impairment: levels of high-density lipoprotein, glycol-protein, glutamine, glutamate, were significantly higher in patients with mild CHF compared to severe CHF. Other metabolites such as lactate and amino acids were significantly higher in patients with severe CHF than mild CHF. Our conclusion is that metabolomic NMR analysis provides new insights into metabolic processes related to the severity of heart function impairment in chronic heart failure.


Author(s):  
Farris K. Timimi

Heart failure is a clinical syndrome characterized by inability of the heart to maintain adequate cardiac output to meet the metabolic demands of the body while still maintaining normal or near-normal ventricular filling pressures. Heart failure may be present at rest, but often it is symptomatic only during exertion due to the dynamic nature of cardiac demands. For the optimal treatment of heart failure, the mechanism, underlying cause, and any reversible precipitating factors must be identified. Typical manifestations of heart failure are dyspnea and fatigue limiting activity tolerance and fluid retention leading to pulmonary or peripheral edema.


Author(s):  
Garrick C. Stewart

Heart failure is a complex clinical syndrome occurring in patients with an abnormality of cardiac structure or function that impairs the ability of the heart to fill with or eject blood. Patients with heart failure develop a constellation of symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, poor quality of life, and a shortened life expectancy. Heart failure has also been defined as the failure of the heart to pump enough blood to meet the metabolic demands of the body, or the ability to do so only at elevated filling pressures. Congestive heart failure is the end stage for many cardiac diseases. Cardiomyopathy refers to any condition in which there is a structural abnormality of the myocardium itself.


2019 ◽  
Vol 124 (4) ◽  
pp. 554-559 ◽  
Author(s):  
Anan Younis ◽  
Wesam Mulla ◽  
Ronen Goldkorn ◽  
Robert Klempfner ◽  
Yael Peled ◽  
...  

2019 ◽  
Vol 19 (21) ◽  
pp. 1878-1901 ◽  
Author(s):  
Yue Zhou ◽  
Jian Wang ◽  
Zhuo Meng ◽  
Shuang Zhou ◽  
Jiayu Peng ◽  
...  

Chronic Heart Failure (CHF) is a complex clinical syndrome with a high incidence worldwide. Although various types of pharmacological and device therapies are available for CHF, the prognosis is not ideal, for which, the control of increased Heart Rate (HR) is critical. Recently, a bradycardic agent, ivabradine, is found to reduce HR by inhibiting the funny current (If). The underlying mechanism states that ivabradine can enter the Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels and bind to the intracellular side, subsequently inhibiting the If. This phenomenon can prolong the slow spontaneous phase in the diastolic depolarization, and thus, reduce HR. The clinical trials demonstrated the significant effects of the drug on reducing HR and improving the symptoms of CHF with fewer adverse effects. This review primarily introduces the chemical features and pharmacological characteristics of ivabradine and the mechanism of treating CHF. Also, some expected therapeutic effects on different diseases were also concluded. However, ivabradine, as a typical If channel inhibitor, necessitates additional research to verify its pharmacological functions.


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