Ketone bodies can become a major source of adenosine triphosphate production during stress to maintain bioenergetic homeostasis in the brain, heart, and skeletal muscles. In the normal heart, ketone bodies contribute from 10% to 15% of the cardiac adenosine triphosphate production, although their contribution during pathologic stress is still not well-characterized and currently represents an exciting area of cardiovascular research. This review focuses on the mechanisms that regulate circulating ketone levels under physiologic and pathologic conditions and how this impacts cardiac ketone metabolism. We also review the current understanding of the role of augmented ketone metabolism as an adaptive response in different types and stages of heart failure. This analysis includes the emerging experimental and clinical evidence of the potential favorable effects of boosting ketone metabolism in the failing heart and the possible mechanisms of action through which these interventions may mediate their cardioprotective effects. We also critically appraise the emerging data from animal and human studies which characterize the role of ketones in mediating the cardioprotection established by the new class of antidiabetic drugs, namely sodium-glucose co-transporter inhibitors.

酮体可以成为压力期间产生三磷酸腺苷的主要来源，以维持大脑、心脏和骨骼肌的生物能量稳态。在正常心脏中，酮体占心脏三磷酸腺苷产量的 10% 至 15%，尽管它们在病理应激期间的贡献仍未得到充分表征，并且目前代表了心血管研究的一个令人兴奋的领域。本综述侧重于在生理和病理条件下调节循环酮水平的机制以及这如何影响心脏酮代谢。我们还回顾了目前对增强酮代谢作为不同类型和阶段心力衰竭的适应性反应的作用的理解。该分析包括新出现的实验和临床证据，表明促进衰竭心脏中酮代谢的潜在有利影响，以及这些干预措施可能通过其调节其心脏保护作用的可能作用机制。我们还批判性地评估了来自动物和人类研究的新数据，这些数据表征了酮在介导由新型抗糖尿病药物（即钠-葡萄糖协同转运蛋白抑制剂）建立的心脏保护作用中的作用。