European Journal of Nuclear Medicine Vol. 29, No. 10, October 2002 Abstract. Idiopathic dilated cardiomyopathy (IDC) is a distinct disease of the myocardium, of unknown etiolo- gy. The disease can occur acutely, or evolve in a sub- acute fashion. IDC is often associated with a substantial impairment of ventricular function, which may recover over time. Although spontaneous recovery of LV func- tion occurs in 20%–45% of newly diagnosed patients, the majority of patients do not do well. IDC has an aver- age 5-year mortality of 20%. Abnormalities of energet- ics, perfusion, and adrenergic control of the myocardium are markers of the status of LV dysfunction. As the heart fails, changes occur in the production and catabolism of high-energy substrates, the efficiency of mitochondrial oxidative processes, the distribution of resting perfusion and coronary vasodilating capacity and the adrenergic receptor density and function. This article reviews the in- formation provided by metabolic and receptor imaging in patients with IDC, and the role the data may play in patient management. Keywords: Idiopathic dilated cardiomyopathy – Meta- bolic imaging – Receptor imaging – Management Eur J Nucl Med (2002) 29:1403–1413 DOI 10.1007/s00259-002-0898-y Idiopathic dilated cardiomyopathy (IDC), a disease of the myocardium associated with cardiac dysfunction, is a distinct form of cardiomyopathy [1] as compared with “specific” forms associated with other recognized car- diovascular or systemic diseases, such as ischemic car- diomyopathy 1 . The annual incidence of IDC ranges from 5 to 8 cases per 100,000 population [2]. However, this is probably an underestimate, because many asymptomatic cases remain unrecognized [3]. Similarly, the natural his- tory of IDC is difficult to determine because progression from asymptomatic left ventricular (LV) dysfunction to overt symptomatic heart failure is unknown. Although spontaneous recovery of LV function occurs in 20%– 45% of newly diagnosed patients, the disease is still characterized by a poor prognosis with an average 5-year mortality of 20% [2]. The pathogenesis of IDC appears to involve a mixture of familial and genetic factors that predispose some pa- tients to the disease and cytotoxic insults from viral in- fections, immune abnormalities or other cardiotoxic agents that function as co-factors in disease causation. Abnormalities of energetics, perfusion and the adren- ergic control of the myocardium are both markers and determinants of the progression of LV dysfunction to- wards heart failure. As the heart fails, alterations occur in the production and catabolism of high-energy sub- strates [4, 5], the efficiency of mitochondrial oxidative processes [6, 7, 8], resting perfusion and coronary vaso- dilating capability [9, 10, 11] and adrenergic receptor density and function [12]. This manuscript reviews the information provided by metabolic and receptor imaging in patients with IDC, and the role the data may play in patient management. Normal myocardial metabolism and metabolic imaging Myocardial metabolism (summarized in Fig. 1, Table 1) [13, 14, 15] can be extensively and quantitatively deter- mined with PET. Since substrate utilization can change as a result of oxygen availability, metabolic imaging is H. William Strauss ( ✉ ) Division of Nuclear Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10016, USA e-mail: straussh@mskcc.org Tel.: +1-212-6397238, Fax: +1-212-7173263 Review article Myocardial metabolic and receptor imaging in idiopathic dilated cardiomyopathy Danilo Neglia 1 , Gianmario Sambuceti 1 , Patricia Iozzo 1 , Antonio L’Abbate 1 , H. William Strauss 2 1 Consiglio Nazionale delle Ricerche (CNR), Institute of Clinical Physiology, Pisa, Italy 2 Division of Nuclear Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10016, USA Published online: 27 July 2002 © Springer-Verlag 2002 1 Ischemic myopathy presents as a dilated cardiomyopathy with impaired contractile performance not explained by the extent of coronary artery disease (CAD) or ischemic damage.