Abstract 16976: Derangements in Cardiac Oxidative Metabolism in Humans With Dilated Cardiomyopathy

• Published in: Circulation (New York, N.Y.) Vol. 142; no. Suppl_3 Suppl 3; p. A16976
• Main Authors: Clark, Daniel, Davogustto, Giovanni E, Bell, Susan P, MALLUGARI, RAVINDER, Bradham, William S, Lawson, Mark, Gupta, Deepak K, Kronenberg, Marvin W
• Format: Journal Article
• Language: English
• Published: by the American College of Cardiology Foundation and the American Heart Association, Inc 17.11.2020
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.142.suppl_3.16976

IntroductionDilated cardiomyopathy (DCM) is associated with impaired myocardial perfusion reserve and impaired myocardial oxidative metabolism. However, the association between myocardial perfusion reserve and oxidative metabolism, is not fully understood.HypothesisReduced myocardial perfusion reserve is associated with reduced myocardial oxidative metabolism.MethodsUsing non-invasive cardiac imaging, we studied 8 DCM patients and 14 normal subjects. Myocardial perfusion reserve index (MPRI) was calculated using cardiac magnetic resonance as the normalized rate of myocardial signal augmentation following gadolinium contrast injection between rest and regadenoson induced stress. Resting oxidative metabolism was calculated as the myocardial mono-exponential decay rate (Kmono) of [C]acetate by positron emission tomography normalized per unit demand (rate-pressure product, RPP) (Kmono/RPP).ResultsMPRI was lower in DCM compared to controls (1.25 ± 0.22 vs 1.59 ± 0.49, p=0.038). Similarly, Kmono/RPP was lower in DCM compared with normal subjects (0.6x10e-3 ± 0.15 x10e-3 vs 1.2x10e-3 ± 0.9x10e-3, p<0.0001). There was a linear relation between Kmono and RPP in normal subjects. However, DCM patients showed no increase in Kmono regardless of RPP (Figure 1A). Kmono/RPP was not significantly related to MPRI in either group (Figure 1B).ConclusionsPatients with DCM exhibit markedly impaired myocardial oxidative metabolism compared to normal subjects. However, this impairment was not quantitatively related to impaired myocardial perfusion reserve. Of the various mechanisms that could explain decrease in oxidative metabolism in DCM, these data suggest that reduced myocardial perfusion is not the principal driver of impaired oxidative metabolism.