Cardiac Metabolism in Heart Failure

Background: While the causes of heart failure (HF) are diverse, the available evidence suggests that HF is essentially a metabolic disease. In HF, there is a significant decrease in the rate of fatty acid oxidation both in absolute terms and as a fraction of myocardial oxygen consumption. There is evidence that sequestration of free CoA (limiting the formation of acetyl-CoA) and accumulation of toxic intermediates of lipid metabolism, could be involved in the pathophysiology of HF.

Project: We will study the changes in myocardial metabolism in patients with 2 different forms of LV dysfunction: pressure overload due to aortic stenosis and volume overload due to ischemic cardiomyopathy. First, we will study the metabolic changes at the time of diagnosis by comparing metabolite concentrations in arterial and coronary sinus blood.

Clinical perspective: Even with the best state of the art and guideline-recommended therapy, HF is still associated with an annual mortality of 10%. Pharmacologic modulation of impaired fatty acid and carbohydrate metabolism represents a novel strategy in the treatment of HF. A better insight into metabolic changes in LV dysfunction could open the way to personalized treatment of HF based on an integrative approach linking metabolic and cardiac performance data.