About this Research Topic
Heart failure (HF) represents a public health problem of enormous importance, affecting more than 30 million people worldwide with a steadily rising prevalence. HF is among the leading causes of hospitalization and mortality, especially with a growing aging population.
Despite improvements in cardiovascular medicine, including diagnostic procedures and treatments, HF, with mortality rate higher than many cancers, remains a challenge for scientific community.
It is clear that continuing research is vital to address unmet needs in this highly important field. Novel and alternative approaches will be essential for the care of HF patients in which current therapies improve symptoms but do not address the very mechanisms of the disease.
The observation that chronic HF can progress to a more advanced stage despite optimal medical treatment has directed research into additional pathways and mechanisms that contribute to the development and progression of HF.
The fact that treatment is not always effective in prolonging life highlights how prevention should be a priority, in particular for subjects at high risk of developing HF. To this end, awareness of the disease and its effects on millions of people is still poor and more and more efforts should be made to convey the message that prevention is fundamental and that healthy lifestyle reduces the risk and saves lives.
The scientific community clearly recognizes that the HF syndrome is not only a consequence of the reduced systolic performance. In fact, several new hypotheses have been advanced to understand the underlying processes leading to diastolic dysfunction and HF in the heterogenous population with multi-morbidities.
Fortunately, the field is not static. In recent years, we have witnessed the introduction of the combination sacubitril/valsartan as a new pharmacological approach in the management of HF. There has been enormous effort to explore novel agents targeting cytokine signaling and inflammatory process emerging as potential driving force of the pathophysiologic continuum. Other approaches aim at improving myocardial contractility by the modulation of sarcoplasmic-endoplasmic reticulum calcium ATPase 2a (SERCA 2a), ryanodin receptor or calcium/calmodulin-dependent kinase II. Finally, targeting myocardial fibrosis, interstitial remodeling and promoting efficient myocardial repair draws understandable attention.
This Research Topic addresses issues relevant to cardiovascular disease pathophysiology and management through a series of Perspectives, providing an input from leading basic, translational and clinical researchers in the field of cardiovascular medicine.
Despite improvements in cardiovascular medicine, including diagnostic procedures and treatments, HF, with mortality rate higher than many cancers, remains a challenge for scientific community.
It is clear that continuing research is vital to address unmet needs in this highly important field. Novel and alternative approaches will be essential for the care of HF patients in which current therapies improve symptoms but do not address the very mechanisms of the disease.
The observation that chronic HF can progress to a more advanced stage despite optimal medical treatment has directed research into additional pathways and mechanisms that contribute to the development and progression of HF.
The fact that treatment is not always effective in prolonging life highlights how prevention should be a priority, in particular for subjects at high risk of developing HF. To this end, awareness of the disease and its effects on millions of people is still poor and more and more efforts should be made to convey the message that prevention is fundamental and that healthy lifestyle reduces the risk and saves lives.
The scientific community clearly recognizes that the HF syndrome is not only a consequence of the reduced systolic performance. In fact, several new hypotheses have been advanced to understand the underlying processes leading to diastolic dysfunction and HF in the heterogenous population with multi-morbidities.
Fortunately, the field is not static. In recent years, we have witnessed the introduction of the combination sacubitril/valsartan as a new pharmacological approach in the management of HF. There has been enormous effort to explore novel agents targeting cytokine signaling and inflammatory process emerging as potential driving force of the pathophysiologic continuum. Other approaches aim at improving myocardial contractility by the modulation of sarcoplasmic-endoplasmic reticulum calcium ATPase 2a (SERCA 2a), ryanodin receptor or calcium/calmodulin-dependent kinase II. Finally, targeting myocardial fibrosis, interstitial remodeling and promoting efficient myocardial repair draws understandable attention.
This Research Topic addresses issues relevant to cardiovascular disease pathophysiology and management through a series of Perspectives, providing an input from leading basic, translational and clinical researchers in the field of cardiovascular medicine.
Keywords: heart failure, translational research, cardiovascular pharmacology, therapeutic options, therapeutic targets
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