Editorial: Cardiac energetic efficiency and cardiometabolic diseases

Increasing evidence have suggested that a compromised myocardial energetics is implicated in the pathogenesis of cardiovascular disease including ischemic cardiomyopathy, left ventricular hypertrophy and heart failure. The present Research Topic collects some of the last investigations evaluating the mechanisms underlying the link between an altered myocardial energetic efficiency and cardiovascular diseases, and the utility of pharmacological and non-pharmacological approaches targeting cardiac energetic metabolism to counteract cardiovascular disease progression. The compilation starts with a cross-sectional study conducted by Liu et al. evaluating the association between coronary microvascular dysfunction and altered heart energetic efficiency and contractility. The Authors report that subjects with coronary microvascular dysfunction, defined as a reduced coronary flow reserve, exhibit a reduction in global work index, global contractive work, and global work efficiency and a higher global waste work, suggesting that coronary microvascular dysfunction may affect myocardial energetic efficiency and contractility. Additionally, the Authors also demonstrate that a reduced myocardial global work and efficiency may be a predictor of coronary microvascular dysfunction with a good diagnostic capacity, thus indicating that a compromised cardiac mechano-energetic efficiency may be a diagnostic tool for early identification of individuals with coronary artery disease. Energetic metabolism of heat is a dynamic process depending of the availability of oxygen and several metabolic substrates such as glucose, fatty acids, ketone bodies and ammino acids. In order to gain insight into the metabolic alterations associated to a worse prognosis in subjects with coronary artery diseases, Na et al. conducted an observational study on 5,935 patients admitted to the cardiovascular department of Guang'anmen Hospital who were diagnosed with coronary heart disease and subdivided into two groups according to the occurrence of adverse myocardial events (MACEs) during the hospitalization. The Authors found that age, blood glucose, fatty acid, albumin, and ApoA1 levels at admission were associated with an increased risk of MACEs during the hospitalization. Decreased levels of blood glucose were associated with an increased risk of MACEs, whereas higher levels of glucose, making this energetic substrate more easily available, were protective. Higher levels of fatty acids and decreased values of Apo A1 were associated with an increased risk of MACEs, probably due to the accumulation of lipids in conditions of oxygen deprivation and their toxic effects on the heart. Additionally, decreased albumin concentrations were found to predict MACEs occurrence, indicating that a decreased availability of ammino acids for energetic supply may aggravates cardiac damage in conditions of myocardial hypoperfusion. The results of this study not only provide evidence that several energetic substrate changes occur in the heart of subjects with coronary artery disease but also demonstrate that metabolic alterations may predict MACEs, thus representing a tool for a better cardiovascular risk stratification and a potential therapeutic target. Amongst chemical compound able to positively modulate energetic metabolism, polyphenols have attracted considerable attention. In their review Hedayati et al. describe the various benefic properties of polyphenols, including anti-inflammatory, antioxidant, antiapoptotic, and antiatherogenic effects thus suggesting that polyphenols may be promising adjutant approaches in the treatment of cardiovascular disease and heart failure. The collection also includes preclinical studies with translational impact, providing new insights and interesting tools for clinical research on this topic field. Raposo et al. report that intracoronary transfer of xenogeneic Human umbilical cord matrix-mesenchymal stromal cells (hUCM-MSC), shortly