Heart failure is one of the most common cardiovascular disorders worldwide, with high morbidity and mortality. Despite the beneficial effects of the current treatment options in the heart failure population, the prognosis following a diagnosis of heart failure is still poor, with about 50% of patients dying within 5 years. In clinics, heart failure is featured as left-ventricular systolic and/or diastolic dysfunction. Among of all heart failure patients, about half are afflicted with reduced ejection fraction (HFrEF, commonly referred as EF<40%), whereas the other half suffer from heart failure with preserved ejection fraction (HFpEF, EF>50%). Regardless of the debate on whether inflammation is a cause or consequence of heart failure, it has been acknowledged that both HFrEF and HFpEF are accompanied by elevated systemic and myocardial inflammatory response, including cytokines and immune cells.
Acute ischemic and non-ischemic myocardial injury leads to infiltration and recruitment of immune cells to the heart for removal of necrotic cells and myocardial reconstruction. However, HFrEF is induced by the persistent inflammation post-injury. On the other hand, the increased epidemic of HFpEF is associated with the growing prevalence of chronic kidney disease, hypertension, pulmonary disease, obesity, and diabetes mellitus. These comorbidities give rise to low-grade chronic inflammation, contributing to the onset and progression of heart failure. Although the mechanisms underlying the interconnection of inflammation and heart failure have been extensively investigated based on experimental and preclinical models, most therapeutic attempts by targeting inflammation in the heart failure represent neutral or negative effects in clinical trials. The disappointing results can be explained by the diversity and complexity of inflammatory response. Strikingly, the recent CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcome Study) clinical trial study demonstrates an exciting result, with reduced hospitalizations and mortality of heart failure. This promotes the encouraging perspectives that anti-inflammatory and immunomodulatory strategies have a promising therapeutic potential. Therefore, it is essential to further decipher the mechanisms of inflammation-associated heart failure and to explore the therapeutic applications by targeting systemic and cardio-inflammation.
This Research Topic is devoted to encompassing lab-based research and clinical studies of inflammation-associated heart failure, ranging from molecular evidence to the impact on clinical practice. This will provide novel insights into the translational possibility and significance of treatment of heart failure by targeting inflammation in the foreseeable future.
The aim of this Research Topic is to integrate and translate the findings of basic research into clinical medicine on inflammation-related heart failure. It welcomes original papers and review articles on the mechanisms underlying interaction of inflammation with heart failure, manifestation of various modulation (genetic, pharmacologic, lifestyle changing etc), impacts of treatment by targeting cytokines and immune cells, as well as on its therapeutic prospective and clinical implications of heart failure, including discoveries of immune biomarkers and drugs targeting inflammation.
Heart failure is one of the most common cardiovascular disorders worldwide, with high morbidity and mortality. Despite the beneficial effects of the current treatment options in the heart failure population, the prognosis following a diagnosis of heart failure is still poor, with about 50% of patients dying within 5 years. In clinics, heart failure is featured as left-ventricular systolic and/or diastolic dysfunction. Among of all heart failure patients, about half are afflicted with reduced ejection fraction (HFrEF, commonly referred as EF<40%), whereas the other half suffer from heart failure with preserved ejection fraction (HFpEF, EF>50%). Regardless of the debate on whether inflammation is a cause or consequence of heart failure, it has been acknowledged that both HFrEF and HFpEF are accompanied by elevated systemic and myocardial inflammatory response, including cytokines and immune cells.
Acute ischemic and non-ischemic myocardial injury leads to infiltration and recruitment of immune cells to the heart for removal of necrotic cells and myocardial reconstruction. However, HFrEF is induced by the persistent inflammation post-injury. On the other hand, the increased epidemic of HFpEF is associated with the growing prevalence of chronic kidney disease, hypertension, pulmonary disease, obesity, and diabetes mellitus. These comorbidities give rise to low-grade chronic inflammation, contributing to the onset and progression of heart failure. Although the mechanisms underlying the interconnection of inflammation and heart failure have been extensively investigated based on experimental and preclinical models, most therapeutic attempts by targeting inflammation in the heart failure represent neutral or negative effects in clinical trials. The disappointing results can be explained by the diversity and complexity of inflammatory response. Strikingly, the recent CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcome Study) clinical trial study demonstrates an exciting result, with reduced hospitalizations and mortality of heart failure. This promotes the encouraging perspectives that anti-inflammatory and immunomodulatory strategies have a promising therapeutic potential. Therefore, it is essential to further decipher the mechanisms of inflammation-associated heart failure and to explore the therapeutic applications by targeting systemic and cardio-inflammation.
This Research Topic is devoted to encompassing lab-based research and clinical studies of inflammation-associated heart failure, ranging from molecular evidence to the impact on clinical practice. This will provide novel insights into the translational possibility and significance of treatment of heart failure by targeting inflammation in the foreseeable future.
The aim of this Research Topic is to integrate and translate the findings of basic research into clinical medicine on inflammation-related heart failure. It welcomes original papers and review articles on the mechanisms underlying interaction of inflammation with heart failure, manifestation of various modulation (genetic, pharmacologic, lifestyle changing etc), impacts of treatment by targeting cytokines and immune cells, as well as on its therapeutic prospective and clinical implications of heart failure, including discoveries of immune biomarkers and drugs targeting inflammation.
