Obesity cardiomyopathy was described as a collection of cardiac structural and functional abnormalities that could arise even in the absence of increased afterload and underlying organic heart disease. However, co-existing systemic hypertension, diabetes mellitus, and sleep apnoea syndrome were recognized as aggravating factors. Intriguingly, whilst in patients with chronic heart failure obesity may be protective (‘obesity paradox’), weight reduction was proposed to improve obesity-related cardiovascular disease and premature atherosclerosis.

Rayner et al. provides much needed, valuable insight into human obesity DCM, a highly prevalent disease burden in our society, yet it leaves some important questions unanswered. Despite the importance of the myocardial PCr/ATP ratio and CK flux, alone they cannot explain the complex pathophysiology underlying the concept of the obesity paradox in DCM. Indeed, many confounding factors, such as secretory function of adipose tissue and the functional status of other metabolic organs (liver and skeletal muscle), may play important roles in the pathogenesis and progression of DCM.

In addition, it is not yet clear whether the myocardial PCr/ATP ratio and CK flux are sufficient to decide on an optimal treatment strategy. There is a long way ahead to better define patient groups before the key observations of this elegant study by Rayner and colleagues can be translated into clinical recommendations.




Disease Condition ,Coronary Artery Disease,Myocardial Infarction