Heart Failure with Preserved Ejection Fraction

Abstract

Heart failure with preserved ejection fraction (HFpEF) has recently emerged as a major cause of cardiovascular morbidity and mortality. Contrary to initial beliefs, HFpEF is now known to be as common as heart failure with reduced ejection fraction (HFrEF) and carries an unacceptably high mortality rate. With a prevalence that has been steadily rising over the past two decades, it is very likely that HFpEF will represent the dominant heart failure phenotype over the coming few years. The scarcity of trials in this semi-discrete form of heart failure and lack of unified enrolment criteria in the studies conducted to date might have contributed to the current absence of specific therapies. Understanding the epidemiological, pathophysiological and molecular differences (and similarities) between these two forms of heart failure is cornerstone to the development of targeted therapies. Carefully designed studies that adhere to unified diagnostic criteria with the recruitment of appropriate controls and adoption of practical end-points are urgently needed to help identify effective treatment strategies.

Optimising Management of Patients with Heart Failure with Preserved Ejection Fraction in Primary Care (OPTIMISE-HFpEF): rationale and protocol for a multi-method study

“…Understanding of underlying pathophysiological processes continues to develop through research, and varying models have been proposed to explain the abnormal cardiac structure and function observed. 2,4,8 The current preferred paradigm is that microvascular endothelial inflammation, driven by coexisting conditions, leads to myocardial inflammation and fibrosis that in turn results in increased oxidative stress and alterations in cardiomyocyte signalling. 2,8 Diagnostically, while definitions and criteria have been tightened, universal consensus and a definitive algorithm are lacking.…”

“…2,4,8 The current preferred paradigm is that microvascular endothelial inflammation, driven by coexisting conditions, leads to myocardial inflammation and fibrosis that in turn results in increased oxidative stress and alterations in cardiomyocyte signalling. 2,8 Diagnostically, while definitions and criteria have been tightened, universal consensus and a definitive algorithm are lacking. [9][10][11] In treatment terms, evidence-based pharmacological therapies and device options are limited and developments lag behind those observed in HFrEF.…”

“…As HFpEF is set to become the dominant form of HF, it is vital that effective primary care-based programmes of identification and management are developed. The OPTIMISE-HFpEF programme of research aims to fill this void by: (1) finding out what patients and providers want; (2) understanding what people with HFpEF are like in the UK, through detailed phenotypic characterisation of a large cohort; and (3) exploring common problematic areas like transitions of care (any move from one care setting to the next, most often hospital to home), hospitalisations, and the support of carers (see Table 1). Results generated will be synthesised, and both face-to-face and online consensus methods employed to develop and refine an optimised programme of management.…”

“…1 Half of all HF cases may be attributable to HFpEF, and prevalence is rising at a rate of 1% annually. [1][2][3] Although mortality for all-cause HF in the UK has modestly improved, no treatment has yet been shown to improve mortality and morbidity in HFpEF. 4,5 Lack of evidence for pathophysiological mechanisms underpinning the disease, effective pharmacotherapies, and disease management programmes specifically targeting HFpEF hamper progress.…”

The Effect of YiQiFuMai on Ischemic Heart Failure by Improve Myocardial Microcirculation and Increase eNOS and VEGF Expression

“…After acute myocardial infarction, myocardial fibrosis and cardiac dilatation occur gradually in the infarcted myocardium, eventually leading to heart failure [1]. Coronary ischemia causes hemodynamic disorder, excessive neuroendocrine activation and abnormalities in energy metabolism, which aggravate ventricular remodeling and cardiac dysfunction [2].…”