Quantification of Myocardial Oxygen Consumption Using ¹¹C-Acetate

Abstract

Normal cardiac performance reflects the codependency of myocardial mechanical function, oxygen consumption (MVO₂), and blood flow. It is well established that physiological processes directly associated with contraction (e.g., wall stress, shortening, heart rate, and contractility) are major determinants of MVO₂. The rapid cessation of MVO₂ and systolic function with interruption of blood flow (supply) is equally well known. Because of this close coupling of mechanical function, MVO₂, and perfusion, and the primacy of oxidation of substrates for myocardial energy production, most disease processes involving the heart manifest as imbalances in myocardial oxygen supply and demand. For example, it is the imbalance of inadequate myocardial oxygen supply in the face of a given demand that typifies the myocardial manifestations of coronary artery disease. In contrast, in patients with dilated cardiomyopathy, mechanical function is diminished despite adequate oxygen supply.