About this Research Topic
Heart failure is a major health and socio-economic problem with 26 million people worldwide suffering from this condition. Additionally, an ageing population is contributing to an increased burden of comorbidities, prevalence and incidence. Of these patients suffering from heart failure, it is estimated that half have preserved ejection fraction (HFpEF). This clinical phenotype remains a diagnostic and therapeutic challenge.
Impaired left ventricular relaxation and increased filling pressure represents the hallmarks of diastolic dysfunction underlying the pathophysiology of HFpEF. There are multiple mechanisms, including functional and structural abnormalities, able to explain these findings. The understanding of the molecular mechanisms, determining the onset and worsening of HFpEF, represents a crucial challenge for clinicians, playing a key role in patient assessment and the development of novel treatments.
The neurohumoral and sympathetic nervous systems seem not to play a crucial role in HFpEF, as treatments targeting these pathways do not show beneficial effects in these patients, in contrast to HFrEF. Recent data has directed attention to the role of inflammation in HFpEF as a cause of alterations in the extracellular matrix and functional abnormalities in diastolic function. A better understanding of the underlying molecular mechanisms may increase the accuracy in diagnosis and evaluation leading to the development of novel therapeutic options.
Led by a team of subject experts, this Research Topic will provide clinicians with the most recent updates on the mechanisms underlying the impairment of diastolic dysfunction with particular interest to the role played by inflammation. The Topic Editors encourage submission of articles focused on pathophysiology, diagnostic assessment and treatment options. Manuscript types may include but are not limited to, original articles, state-of-the-art reviews, meta-analyses, and case reports addressing these themes.
Impaired left ventricular relaxation and increased filling pressure represents the hallmarks of diastolic dysfunction underlying the pathophysiology of HFpEF. There are multiple mechanisms, including functional and structural abnormalities, able to explain these findings. The understanding of the molecular mechanisms, determining the onset and worsening of HFpEF, represents a crucial challenge for clinicians, playing a key role in patient assessment and the development of novel treatments.
The neurohumoral and sympathetic nervous systems seem not to play a crucial role in HFpEF, as treatments targeting these pathways do not show beneficial effects in these patients, in contrast to HFrEF. Recent data has directed attention to the role of inflammation in HFpEF as a cause of alterations in the extracellular matrix and functional abnormalities in diastolic function. A better understanding of the underlying molecular mechanisms may increase the accuracy in diagnosis and evaluation leading to the development of novel therapeutic options.
Led by a team of subject experts, this Research Topic will provide clinicians with the most recent updates on the mechanisms underlying the impairment of diastolic dysfunction with particular interest to the role played by inflammation. The Topic Editors encourage submission of articles focused on pathophysiology, diagnostic assessment and treatment options. Manuscript types may include but are not limited to, original articles, state-of-the-art reviews, meta-analyses, and case reports addressing these themes.
Keywords: HFpEF, diastolic dysfunction, Extracellular matrix, congestion, inflammation
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