scholarly journals Heart Failure With Mid-range Ejection Fraction: Every Coin Has Two Sides

2021 ◽  
Vol 8 ◽  
Author(s):  
Kaiyuan Zhu ◽  
Teng Ma ◽  
Yang Su ◽  
Xin Pan ◽  
Rongrong Huang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Clinical Epidemiology ◽  
Current Knowledge ◽  
Management Strategies ◽  
Cardiovascular Morbidity ◽  
Effective Management ◽  
Aggressive Management ◽  
Cardiovascular Morbidity And Mortality ◽  
Two Sides

This review summarizes current knowledge regarding clinical epidemiology, pathophysiology, and prognosis for patients with HFmrEF in comparison to HFrEF and HFpEF. Although recommended treatments currently focus on aggressive management of comorbidities, we summarize potentially beneficial therapies that can delay the process of heart failure by blocking the pathophysiology mechanism. More studies are needed to further characterize HFmrEF and identify effective management strategies that can reduce cardiovascular morbidity and mortality of patients with HFmrEF.

scholarly journals Targeting Endothelial Function to Treat Heart Failure with Preserved Ejection Fraction: The Promise of Exercise Training

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Andreas B. Gevaert ◽  
Katrien Lemmens ◽  
Christiaan J. Vrints ◽  
Emeline M. Van Craenenbroeck
Keyword(s):  
Heart Failure ◽  
Endothelial Dysfunction ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Current Knowledge ◽  
Beta Blockers ◽  
Preserved Ejection Fraction ◽  
Cellular Mechanisms ◽  
Converting Enzyme Inhibitors ◽  
Reduced Ejection Fraction

Although the burden of heart failure with preserved ejection fraction (HFpEF) is increasing, there is no therapy available that improves prognosis. Clinical trials using beta blockers and angiotensin converting enzyme inhibitors, cardiac-targeting drugs that reduce mortality in heart failure with reduced ejection fraction (HFrEF), have had disappointing results in HFpEF patients. A new “whole-systems” approach has been proposed for designing future HFpEF therapies, moving focus from the cardiomyocyte to the endothelium. Indeed, dysfunction of endothelial cells throughout the entire cardiovascular system is suggested as a central mechanism in HFpEF pathophysiology. The objective of this review is to provide an overview of current knowledge regarding endothelial dysfunction in HFpEF. We discuss the molecular and cellular mechanisms leading to endothelial dysfunction and the extent, presence, and prognostic importance of clinical endothelial dysfunction in different vascular beds. We also consider implications towards exercise training, a promising therapy targeting system-wide endothelial dysfunction in HFpEF.

scholarly journals Cardiovascular morbidity and mortality in patients treated with hemodialysis: Epidemiological analysis

2008 ◽  
Vol 65 (12) ◽  
pp. 893-900 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Mortality Rate ◽  
Cardiovascular Mortality ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass

Background/Aim. Cardiovascular diseases are the leading cause of death in patients treated with hemodialysis (HD). The annual cardiovascular mortality rate in these patients is 9%. Left ventricular (LV) hypertrophy, ischemic heart disease and heart failure are the most prevalent cardiovascular causes of death. The aim of this study was to assess the prevalence of traditional and nontraditional risk factors for cardiovascular complications, to assess the prevalence of cardiovascular complications and overall and cardiovascular mortality rate in patients on HD. Methods. We investigated a total of 115 patients undergoing HD for at least 6 months. First, a cross-sectional study was performed, followed by a two-year follow-up study. Beside standard biochemical parameters, we also determined cardiac troponins and echocardiographic parameters of LV morphology and function (LV mass index, LV fractional shortening, LV ejection fraction). The results were analyzed using the Student's t test and Mann-Whitney U test. Results. The patients with adverse outcome had significantly lower serum albumin (p < 0.01) and higher serum homocystein, troponin I and T, and LV mass index (p < 0.01). Hyperhomocysteinemia, anemia, hypertriglyceridemia and uncontrolled hypertension had the highest prevalence (86.09%, 76.52%, 43.48% and 36.52%, respectively) among all investigated cardiovascular risk factors. Hypertrophy of the LV was presented in 71.31% of the patients and congestive heart failure in 8.70%. Heart valve calcification was found in 48.70% of the patients, pericardial effusion in 25.22% and disrrhythmia in 20.87% of the investigated patients. The average annual overall mortality rate was 13.74%, while average cardiovascular mortality rate was 8.51%. Conclusion. Patients on HD have high risk for cardiovascular morbidity and mortality.

Heart failure with preserved ejection fraction: controversies, challenges and future directions

Heart ◽  
2018 ◽  
Vol 104 (5) ◽  
pp. 377-384 ◽  
Author(s):  
Rosita Zakeri ◽  
Martin R Cowie
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Management Strategies ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Protein Kinase G ◽  
Preserved Ejection Fraction ◽  
Future Directions ◽  
Novel Treatments ◽  
Inflammatory State

Heart failure with preserved ejection fraction (HFpEF) comprises almost half of the population burden of HF. Because HFpEF likely includes a range of cardiac and non-cardiac abnormalities, typically in elderly patients, obtaining an accurate diagnosis may be challenging, not least due to the existence of multiple HFpEF mimics and a newly identified subset of patients with HFpEF and normal plasma natriuretic peptide concentrations. The lack of effective treatment for these patients represents a major unmet clinical need. Heterogeneity within the patient population has triggered debate over the aetiology and pathophysiology of HFpEF, and the neutrality of randomised clinical trials suggests that we do not fully understand the syndrome(s). Dysregulated nitric oxide–cyclic guanosine monophosphate–protein kinase G signalling, driven by comorbidities and ageing, may be the fundamental abnormality in HFpEF, resulting in a systemic inflammatory state and microvascular endothelial dysfunction. Novel informatics platforms are also being used to classify HFpEF into subphenotypes, based on statistically clustered clinical and biological characteristics: whether such subclassification will lead to more targeted therapies remains to be seen. In this review, we summarise current concepts and controversies, and highlight the diagnostic and therapeutic challenges in clinical practice. Novel treatments and disease management strategies are discussed, and the large gaps in our knowledge identified.

scholarly journals Clinical epidemiology of heart failure with preserved ejection fraction (HFpEF) in comparatively young hospitalized patients

2016 ◽  
Vol 202 ◽  
pp. 918-921 ◽  
Author(s):  
Michael Zacharias ◽  
Samuel Joffe ◽  
Elizabeth Konadu ◽  
Theo Meyer ◽  
Michael Kiernan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Clinical Epidemiology ◽  
Hospitalized Patients ◽  
Preserved Ejection Fraction

scholarly journals Recognition, Diagnosis, and Management of Heart Failure with Preserved Ejection Fraction

2018 ◽  
Vol 12 (1) ◽  
pp. 8-12
Author(s):  
Meshal Soni ◽  
Edo Y Birati
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Diagnostic Criteria ◽  
Paradigm Shift ◽  
Management Strategies ◽  
Clinical Syndrome ◽  
Treatment Modalities ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
The Common

The clinical syndrome of heart failure with preserved ejection fraction (HFpEF) is unique in terms of etiologies, diagnostic criteria, costs, and treatment modalities when compared to heart failure with reduced ejection fraction. There is an emerging paradigm shift that recognizes the clinical syndrome of HFpEF and its various phenotypes. Understanding these HFpEF phenotypes is crucial to understanding the pathophysiology of HFpEF, which in turn can further guide our management strategies. This review outlines the diagnostic criteria, introduces the common clinical phenotypes, and discusses treatments currently utilized in practice for the management of HFpEF.

scholarly journals A Clinical Review of Ventricular Arrhythmias in Patients with Congestive Heart Failure

2019 ◽  
Author(s):  
Noel Boyle
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Ventricular Arrhythmias ◽  
Beta Blockers ◽  
Management Strategies ◽  
Significant Risk ◽  
Holter Monitoring ◽  
Current Evidence ◽  
Compensatory Mechanisms ◽  
Ventricular Ejection Fraction

Heart failure is an increasingly prevalent condition, which is associated with ventricular arrhythmias. The reduction in cardiac pumping efficiency leads to the activation of several compensatory mechanisms. These mechanisms eventually lead to cardiac remodelling and a decline in haemodynamic status, contributing to the formation of a substrate conducive to arrhythmias, including increased automaticity, triggered activity, and, most commonly, re-entry circuits. In turn, ventricular arrhythmias can lead to the worsening of heart failure. A diagnosis of heart failure and ventricular arrhythmias is obtained using the patient’s history, examination findings, and investigation results. A key tool in this is echocardiogram imaging, which visualises the cardiac chambers, determines ventricular ejection fraction, and identifies structural abnormalities. A reduction in ejection fraction is a significant risk factor for the development of ventricular arrhythmias. Arrhythmias are diagnosed by ECG, Holter monitoring, and telemetry or event monitoring, and should initially be treated by optimising the medical management of heart failure. Anti-arrhythmic drugs, including beta-blockers, are usually the first-line therapy. Sudden cardiac death is a significant cause of mortality in heart failure patients, and implantable cardioverter defibrillator devices are used in both primary and secondary prevention. Anti-arrhythmic drugs and catheter ablation are important adjunctives for minimising shock therapy. In addition, autonomic modulation may offer a novel method of controlling ventricular arrhythmias. The objective of this review is to provide a practical overview of this rapidly developing field in relation to current evidence regarding the underlying pathophysiology, burden of disease, and management strategies available.

New insights into SERCA2a gene therapy in heart failure: pay attention to the negative effects of B-type natriuretic peptides

2018 ◽  
Vol 55 (5) ◽  
pp. 287-296 ◽  
Author(s):  
Yuting Zhai ◽  
Yuanyuan Luo ◽  
Pei Wu ◽  
Dongye Li
Keyword(s):  
Heart Failure ◽  
Gene Therapy ◽  
Gene Transfer ◽  
Ejection Fraction ◽  
Current Knowledge ◽  
Potential Interaction ◽  
Future Research ◽  
Therapeutic Effects ◽  
Reduced Ejection Fraction ◽  
Negative Results

Sarcoplasmic/endoplasmic reticulum calcium ATPase 2a (SERCA2a) is a target of interest in gene therapy for heart failure with reduced ejection fraction (HFrEF). However, the results of an important clinical study, the Calcium Upregulation by Percutaneous Administration of Gene Therapy in Cardiac Disease (CUPID) trial, were controversial. Promising results were observed in the CUPID 1 trial, but the results of the CUPID 2 trial were negative. The factors that caused the controversial results remain unclear. Importantly, enrolled patients were required to have a higher plasma level of B-type natriuretic peptide (BNP) in the CUPID 2 trial. Moreover, BNP was shown to inhibit SERCA2a expression. Therefore, it is possible that high BNP levels interact with treatment effects of SERCA2a gene transfer and accordingly lead to negative results of CUPID 2 trial. From this point of view, effects of SERCA2a gene therapy should be explored in heart failure with preserved ejection fraction, which is characterised by lower BNP levels compared with HFrEF. In this review, we summarise the current knowledge of SERCA2a gene therapy for heart failure, analyse potential interaction between BNP levels and therapeutic effects of SERCA2a gene transfer and provide directions for future research to solve the identified problems.

scholarly journals Pregnancy-Associated Myocardial Infarction

2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Marysia S. Tweet ◽  
Jennifer Lewey ◽  
Nathaniel R. Smilowitz ◽  
Carl H. Rose ◽  
Patricia J.M. Best
Keyword(s):  
Myocardial Infarction ◽  
Current Knowledge ◽  
Treatment Strategies ◽  
Cardiovascular Morbidity ◽  
Diagnostic Evaluation ◽  
Morbidity And Mortality ◽  
Cardiovascular Morbidity And Mortality ◽  
Consensus Statements

Pregnancy-associated myocardial infarction is a primary contributor to maternal cardiovascular morbidity and mortality. Specific attention to the cause of myocardial infarction, diagnostic evaluation, treatment strategies, and postevent care is necessary when treating women with pregnancy-associated myocardial infarction. This review summarizes the current knowledge, consensus statements, and essential nuances.

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