In vivo 2D mapping of impaired murine cardiac energetics in NO‐induced heart failure

31 P MRS studies in humans have shown that an impairment of cardiac energetics is characteristic of heart failure. Although numerous transgenic mouse models with a heart‐failure phenotype have been generated, current methods to analyze murine high‐energy phosphates (HEPs) in vivo are hampered by limited spatial resolution. Using acquisition‐weighted 2D 31 P chemical shift imaging (CSI) at 9.4 Tesla, we were able to acquire 31 P MR spectra over the entire thorax of the mouse with high spatial resolution in defined regions of the heart (the anterior, lateral, posterior, and septal walls) within a reasonable acquisition time of about 75 min. Analysis of a transgenic cardiomyopathy model (double mutant: cardiospecific inducible nitric oxide synthase (iNOS) overexpression and lack of myoglobin (tg‐iNOS + /myo −/− ) revealed that cardiac dysfunction in the mutant was associated with an impaired energy state (phosphocreatine (PCr)/adenosine triphosphate (ATP) 1.54 ± 0.18) over the entire left ventricle (LV; wild‐type (WT): PCr/ATP 2.06 ± 0.22, N = 5, P < 0.05), indicating that in the absence of efficient cytosolic NO scavenging, iNOS‐derived NO critically interferes with the respiratory chain. In vivo data were validated against 31 P MR spectra of perchloric acid extracts (PCr/ATP: 1.87 ± 0.21 (WT), 1.39 ± 0.17 (tg‐iNOS + /myo −/− , N = 5, P < 0.05). Future applications will substantially benefit studies on the cause‐and‐effect relationship between cardiac energetics and function in other genetically well‐defined models of heart failure. Magn Reson Med 57:50–58, 2007. © 2006 Wiley‐Liss, Inc.