Heart failure: is there an energy deficit contributing to contractile dysfunction?

Heart failure involves complex changes in energy metabolism. Researchers have long debated whether these changes cause or result from the condition. Prior work shows altered myocardial energy metabolism in both animals and humans. However, the role of these changes remains unclear. Some studies suggest energy deficits may contribute to contractile dysfunction. Others argue these changes are adaptive responses. The creatine kinase system links energy production to mitochondrial function. In acute heart failure, reduced creatine phosphate may reflect increased oxygen demands. Yet, chronic heart failure presents different patterns.

This review examines whether energy deficits contribute to heart failure. The goal is to clarify the role of the creatine kinase system and high-energy phosphates. The focus is on acute and chronic heart failure states. The authors aim to distinguish between energy deficit and energy reserve depletion. They also explore mitochondrial diseases and stunned myocardium. The review evaluates how energy metabolism changes affect contractile function. The goal is to determine if these changes are harmful or protective. The authors seek to resolve whether these alterations drive or result from heart failure.

The authors conducted a literature review of animal and clinical studies. They analyzed the creatine kinase system's role in energy metabolism. They compared acute and chronic heart failure cases. The review included mitochondrial diseases and stunned myocardium. The authors examined how energy reserves affect contractile function. They evaluated whether energy deficits or reserves are primary factors. The study focused on mass action ratios and ATP/ADP dynamics. The authors synthesized findings from in vitro and in vivo experiments.

In acute heart failure, reduced creatine phosphate reflects increased oxygen demands. The creatine kinase system supports mitochondrial respiration under stress. Chronic heart failure shows reduced energy reserves but not energy deficits. This reduction may lower contractile reserve during stress. The mechanisms linking energy reserves to contractile dysfunction remain unclear. Mitochondrial diseases often present with neurological symptoms, not cardiac ones. Stunned and hibernating myocardium show prolonged dysfunction despite reversible damage. The reduced energy reserve may either worsen heart failure or protect the heart from overload.

The authors suggest energy deficits are not the main issue in chronic heart failure. Instead, reduced energy reserves may limit contractile function during stress. They propose this mechanism could explain reduced contractile reserve. However, the exact cause of this limitation remains unknown. The authors also note mitochondrial diseases may involve cardiac complications. Stunned and hibernating myocardium remain poorly understood in terms of triggers. The reduced energy reserve may act as a protective mechanism in some cases. The findings highlight the need for further research into energy metabolism in heart failure.