Reliable hot spot inflammation imaging with fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) in suspected cardiac infection, cardiac sarcoidosis, or vulnerable coronary plaque is only possible when physiologic myocardial FDG uptake can be adequately suppressed. The gamut of perfusion-metabolism patterns possible in cardiac sarcoidosis 1 combined with the erratic and real possibility of inadequate suppression of normal myocardial FDG uptake is a sure recipe for head scratching and challenging image interpretation. A number of preparation methods aimed at suppressing physiologic myocardial glucose utilization have been described without clear consensus on the optimal method. In the present issue of the Journal of Nuclear Cardiology, Osborne and colleagues (doi:10.1007/s12350-016-0502-7) review various preparation protocols and success rates achieved in published studies for FDG cardiac PET and provide useful practical recommendations.A brief overview of cardiomyocyte metabolism is essential to appreciate the challenges and rationale of interventions. The heart uses various substrates as energy sources including free fatty acids (FFAs), glucose, and lactate. In the fasting condition, the normal myocardium utilizes FFAs as the major energy source (90%). Other sources include glucose and lactate.2 Postmeals or in the dysfunctional myocardium (example ischemic heart disease), myocardial metabolism shifts to glucose per the glucose-fatty acid cycle.2,3 Elevated blood insulin and glucose levels with decreased FFAs lead to a relative rise in myocardial glucose consumption. In contrast, during fasting, there is an increase in FFAs with decrease in insulin and glucose levels, shifting myocardial energy consumption away from glucose and toward FFAs. Hence interventions that facilitate myocardial FFAs metabolism while at the same time suppress physiologic glucose metabolism are imperative for successful FDG PET cardiac inflammation imaging. These include avoidance of strenuous exercise prior to imaging (to prevent skeletal muscle glucose utilization), high-fat with low (less than 5 g)-or no carbohydrate diet (to increase blood FFAs and minimize glucose and insulin levels), addition of a high-fat drink to this diet prior to FDG injection (to elevate blood FFAs), fasting for 4-18 hours (to decrease blood glucose and insulin levels and increase FFAs), and certain pharmacologic maneuvers. The latter include unfractionated heparin which induces lipolysis and up to fivefold increase in blood FFAs 4 and calcium channel blockers which reduce myocardial FDG uptake.5 Most studies combine two or more interventions with the goal of complete suppression of normal cardiac FDG uptake.Tang and colleagues in a meta-analysis involving 16 studies and 559 patients evaluated for cardiac sarcoidosis examined various patient preparations that impact the diagnostic performance of FDG PET. They conclude that duration of fasting and heparin administration significantly affected the diagnostic odds ratio (P = .01 and .04, respec...