The High-Risk Patient With Heart Failure With Reduced Ejection Fraction: Treatment Options and Challenges

2013 ◽  
Vol 94 (4) ◽  
pp. 509-518 ◽  
Author(s):  
J A Bartos ◽  
G S Francis
Acta Naturae ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 40-51
Author(s):  
A. G. Ovchinnikov ◽  
T. I. Arefieva ◽  
A. V. Potekhina ◽  
A. Yu. Filatova ◽  
F. T. Ageev ◽  
...  

Heart failure withpreserved ejection fraction (HFpEF) is a severe disease with an often unfavorable outcome. The prevalence of HFpEF continues to increase, while effective treatment options remain elusive. All the medical strategies used toimprove the outcome in a heart failure with reduced ejection fraction proved ineffective in HFpEF, which was probably due to the different mechanisms ofdevelopment of these two types of heart failure and the diversity of the HFpEF phenotypes. According to the current paradigm of HFpEF development, a chronic mild pro-inflammatory statecauses a coronary microvascular endothelial inflammation, with further myocardial fibrosis and diastolic dysfunction progression. This inflammatory paradigm of HFpEF has been confirmed with someevidence, and suppressing the inflammation may become a novel strategy for treating and managing HFpEF. This review summarizes current concepts about a microvascular inflammation in hypertrophied myocardium and provides a translational perspective of the anti-inflammatory and immunomodulatory approaches in HFpEF.


Author(s):  
Kazuomi Kario ◽  
Bryan Williams

Heart failure (HF) is a common condition with an increasing prevalence. Despite a variety of evidence-based treatments for patients with HF with reduced ejection fraction, morbidity and mortality rates remain high. Furthermore, there are currently no treatments that have yet been shown to reduce complication and death rates in patients who have HF with preserved ejection fraction. Hypertension is a common comorbidity in patients with HF, contributing to disease development and prognosis. For example, hypertension is closely associated with the development of left ventricular hypertrophy, which an important precursor of HF. In particular, nighttime blood pressure (BP) appears to be an important, modifiable risk factor. Both nighttime BP and an abnormal circadian pattern of nighttime BP dipping have been shown to predict development of HF and the occurrence of cardiovascular events, independent of office BP. Key mechanisms for this association include sodium handling/salt sensitivity and increased sympathetic activation. These pathogenic mechanisms are targeted by several new treatment options, including sodium-glucose cotransporter 2 inhibitors, angiotensin receptor neprilysin inhibitors, mineralocorticoid receptor antagonists, and renal denervation. All of these could form part of antihypertensive strategies designed to control nighttime BP and contribute to the goal of achieving perfect 24-hour BP management. Nevertheless, additional research is needed to determine the effects of reducing nighttime BP and improving the circadian BP profile on the rate of HF, other cardiovascular events, and mortality.


2016 ◽  
Vol 30 (5) ◽  
pp. 541-548
Author(s):  
Shreya Patel ◽  
Keith Veltri

Despite availability of standardized drug therapies with proven beneficial outcomes, heart failure is associated with poor quality of life, increased hospital readmission, and high mortality rate. In the recent years, comprehensive understanding of the pathophysiological mechanisms of heart failure has led to the development and approval of 2 new pharmacological agents, sacubitril–valsartan and ivabradine. These agents are currently approved for use in heart failure with reduced ejection fraction (HFrEF) and present as novel approaches to further improve prognosis and outcomes in patients with HF. They offer alternative treatment options for patients who are intolerant or continue to be symptomatic despite utilization of standard HF drug therapies at optimally tolerated dosages. A review of these 2 novel agents in HFrEF, including information on pivotal trials that led to its approval and its place in therapy for HFrEF, is presented.


Acta Naturae ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 40-51
Author(s):  
A. G. Ovchinnikov ◽  
T. I. Arefieva ◽  
A. V. Potekhina ◽  
A. Yu. Filatova ◽  
F. T. Ageev ◽  
...  

Heart failure withpreserved ejection fraction (HFpEF) is a severe disease with an often unfavorable outcome. The prevalence of HFpEF continues to increase, while effective treatment options remain elusive. All the medical strategies used toimprove the outcome in a heart failure with reduced ejection fraction proved ineffective in HFpEF, which was probably due to the different mechanisms ofdevelopment of these two types of heart failure and the diversity of the HFpEF phenotypes. According to the current paradigm of HFpEF development, a chronic mild pro-inflammatory statecauses a coronary microvascular endothelial inflammation, with further myocardial fibrosis and diastolic dysfunction progression. This inflammatory paradigm of HFpEF has been confirmed with someevidence, and suppressing the inflammation may become a novel strategy for treating and managing HFpEF. This review summarizes current concepts about a microvascular inflammation in hypertrophied myocardium and provides a translational perspective of the anti-inflammatory and immunomodulatory approaches in HFpEF.


ESC CardioMed ◽  
2018 ◽  
pp. 1917-1921
Author(s):  
Francisco J. Martín-Sánchez ◽  
Òscar Miró ◽  
Héctor Bueno

Acute heart failure (AHF) is a potentially life-threatening medical condition requiring emergency hospital evaluation. This chapter highlights aspects of early diagnosis, risk stratification, and treatment. The high-risk patient with AHF is characterized by the presence of severe respiratory failure and haemodynamic instability with or without systemic hypoperfusion, and the presence of potentially life-threatening AHF causes CHAMP (acute Coronary syndrome, Hypertensive emergency, Arrhythmias, acute Mechanical cause, and acute Pulmonary embolism). This high-risk patient is a potential candidate for respiratory and circulatory support, invasive monitoring with an arterial line, and the treatment of CHAMP. After ruling out a high-risk situation, AHF diagnosis must be confirmed with clinical evaluation and additional investigations, including 12-lead electrocardiography, chest X-ray, and laboratory assessment with natriuretic peptide levels. This non-high-risk patient requires non-invasive monitoring and early initiation of appropriate therapy guided by systolic blood pressure.


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