Indeed, metabolic-related cardiomyopathy is a large spectrum of functional and structural myocardial dysfunctions encompassing heart failure with preserved ejection fraction (HFpEF) and coronary heart diseases without angioplasty procedure evidence of coronary lesions. As all, such conditions have common hyperglycemia-mediated physiopathologic pathways made up by: a) myocardial tissue inflammation, b) enhanced oxidative stress, c) impaired trans-membrane ion fluxes, d) declined myocardial wall elasticity.
One can also not exclude that heart failure with reduced ejection fraction (HErEF) might be just a worsening effect over the time of a progression of HFPEF due to: a) an unappropriated therapy (such as undertreatment per se or inaccuracy of the drug/s used); b) impaired microvascular circulation with a further worsening of the ventricular wall contraction power and secondary decline in stroke volume.
Understanding the interplay between metabolic disturbances and inflammatory processes, which underlies the pathogenesis of metabolic-related cardiomyopathy, is clinically relevant to improve diagnosis, management and consequently minimize the current unacceptably high mortality rates. Both inflammation and metabolism interact over the course of cardiomyopathy progression, and likely impact its treatment and prevention. Despite metabolic diseases being an important aetiology of cardiomyopathy, there are few dedicated pieces of research that aim to understand the etiologic-specific diagnosis and clinical management of this syndrome. Today, it is known that progressive pathologic changes in cardiac metabolism may precede myocardial dysfunction, indicating that metabolic remodelling is an important early event in the progression of cardiomyopathy. Consequently, the identification of metabolic abnormalities may be able to prevent or ameliorate disease progression.
Moreover, hyperglycemic patients can form proteins alteration resulting from their glycosylation in presence of high glucose concentrations that can be converted in stable covalent adducts called advanced glycosylation end products (AGEs). AGEs can influence the development of cardiovascular complications associated with hyperglycemia. AGE prevention is emerging as a novel therapeutic intervention for the treatment of cardiovascular complications such as acute myocardial infarction in the presence of hyperglycemia.
This Research Topic aims to provide further insights: to better understand and support the causal, mechanistic role of metabolic inflammation, including hyperglycemia-mediated physio-pathologic pathways, in the development of metabolic related cardiomyopathy; to propose a framework that shows how metabolic comorbidities profoundly impact cardiac metabolism and inflammatory pathways; to provide clinical evidence for the best diagnosis and clinical management of metabolic related cardiomyopathy.
Indeed, metabolic-related cardiomyopathy is a large spectrum of functional and structural myocardial dysfunctions encompassing heart failure with preserved ejection fraction (HFpEF) and coronary heart diseases without angioplasty procedure evidence of coronary lesions. As all, such conditions have common hyperglycemia-mediated physiopathologic pathways made up by: a) myocardial tissue inflammation, b) enhanced oxidative stress, c) impaired trans-membrane ion fluxes, d) declined myocardial wall elasticity.
One can also not exclude that heart failure with reduced ejection fraction (HErEF) might be just a worsening effect over the time of a progression of HFPEF due to: a) an unappropriated therapy (such as undertreatment per se or inaccuracy of the drug/s used); b) impaired microvascular circulation with a further worsening of the ventricular wall contraction power and secondary decline in stroke volume.
Understanding the interplay between metabolic disturbances and inflammatory processes, which underlies the pathogenesis of metabolic-related cardiomyopathy, is clinically relevant to improve diagnosis, management and consequently minimize the current unacceptably high mortality rates. Both inflammation and metabolism interact over the course of cardiomyopathy progression, and likely impact its treatment and prevention. Despite metabolic diseases being an important aetiology of cardiomyopathy, there are few dedicated pieces of research that aim to understand the etiologic-specific diagnosis and clinical management of this syndrome. Today, it is known that progressive pathologic changes in cardiac metabolism may precede myocardial dysfunction, indicating that metabolic remodelling is an important early event in the progression of cardiomyopathy. Consequently, the identification of metabolic abnormalities may be able to prevent or ameliorate disease progression.
Moreover, hyperglycemic patients can form proteins alteration resulting from their glycosylation in presence of high glucose concentrations that can be converted in stable covalent adducts called advanced glycosylation end products (AGEs). AGEs can influence the development of cardiovascular complications associated with hyperglycemia. AGE prevention is emerging as a novel therapeutic intervention for the treatment of cardiovascular complications such as acute myocardial infarction in the presence of hyperglycemia.
This Research Topic aims to provide further insights: to better understand and support the causal, mechanistic role of metabolic inflammation, including hyperglycemia-mediated physio-pathologic pathways, in the development of metabolic related cardiomyopathy; to propose a framework that shows how metabolic comorbidities profoundly impact cardiac metabolism and inflammatory pathways; to provide clinical evidence for the best diagnosis and clinical management of metabolic related cardiomyopathy.