Heart failure (HF) is a complex clinical syndrome occurring as a consequence of a reduced ability to pump blood under normal preload condition. It is a worldwide global pandemic, with increasing prevalence and high morbidity and mortality. In clinics, HF is classified in 3 categories according left ventrricular Ejection fraction (EF): HF with reduced ejection fraction (HFrEF, commonly <40%), HF preserved ejection fraction (HFpEF, >50%) and the newly renamed HF with midly reduced ejection fraction (HFmrEF, 40-49%). Notably, patients with HFpEF represent approximately 50% of all HF cases.
During the last 30 years a plethora of data from animal models have provided advancements in our understanding of the mechanism behind the physiopathology of HFrEF at the molecular and cellular levels. Meanwhile, clinicians have developed and used different therapeutic strategies for treating HFrEF.
Disappointingly, effective therapies for patients with HFrEF are not adequate for patients with HFpEF. Indeed, the pathophysiology of HFpEF remains uncertain. At the clinical level, diastolic dysfunction is observed. It is now clear that HFpEF is not a disorder due only to abnormality in the left ventricular diastolic function, but also triggered by comorbidities and other contributing factors such as aging, lifestyle and genetic predisposition.
There is a clear need for a better understanding of HFpEF to be able to develop new therapies. Therefore, it is essential to further decipher HFpEF from molecular level to the level of the patient.
Regarding basic and translational studies, new animal models involving both haemodynamic and metabolic disease are needed. While at the clinical level, diagnosis and therapeutics must improve.
We encourage investigators to submit original (basic, translational, and clinical) research articles, clinical trials and reviews to this Research Topic with the purpose to address mechanistic insights and decipher novel diagnostic tools and new treatments for HFpEF.
Specific sub-topics include, but are not limited to the following areas:
- Basic and translational studies on HFpEF
- Experimental animal models that can recapitulate HFpEF
- Clinical studies on HFpEF
- Electrophysiological studies that charaterize HFpEF
- Studies on cardiac arrhythmias associated with HFpEF
- Novel treatment strategies on HFpEF
- Genetics and mechanistically based studies in human HFpEF patients
- New signalling pathways and potential therapeutic targets in HFpEF
Heart failure (HF) is a complex clinical syndrome occurring as a consequence of a reduced ability to pump blood under normal preload condition. It is a worldwide global pandemic, with increasing prevalence and high morbidity and mortality. In clinics, HF is classified in 3 categories according left ventrricular Ejection fraction (EF): HF with reduced ejection fraction (HFrEF, commonly <40%), HF preserved ejection fraction (HFpEF, >50%) and the newly renamed HF with midly reduced ejection fraction (HFmrEF, 40-49%). Notably, patients with HFpEF represent approximately 50% of all HF cases.
During the last 30 years a plethora of data from animal models have provided advancements in our understanding of the mechanism behind the physiopathology of HFrEF at the molecular and cellular levels. Meanwhile, clinicians have developed and used different therapeutic strategies for treating HFrEF.
Disappointingly, effective therapies for patients with HFrEF are not adequate for patients with HFpEF. Indeed, the pathophysiology of HFpEF remains uncertain. At the clinical level, diastolic dysfunction is observed. It is now clear that HFpEF is not a disorder due only to abnormality in the left ventricular diastolic function, but also triggered by comorbidities and other contributing factors such as aging, lifestyle and genetic predisposition.
There is a clear need for a better understanding of HFpEF to be able to develop new therapies. Therefore, it is essential to further decipher HFpEF from molecular level to the level of the patient.
Regarding basic and translational studies, new animal models involving both haemodynamic and metabolic disease are needed. While at the clinical level, diagnosis and therapeutics must improve.
We encourage investigators to submit original (basic, translational, and clinical) research articles, clinical trials and reviews to this Research Topic with the purpose to address mechanistic insights and decipher novel diagnostic tools and new treatments for HFpEF.
Specific sub-topics include, but are not limited to the following areas:
- Basic and translational studies on HFpEF
- Experimental animal models that can recapitulate HFpEF
- Clinical studies on HFpEF
- Electrophysiological studies that charaterize HFpEF
- Studies on cardiac arrhythmias associated with HFpEF
- Novel treatment strategies on HFpEF
- Genetics and mechanistically based studies in human HFpEF patients
- New signalling pathways and potential therapeutic targets in HFpEF