Myocardial oxidative metabolic supply-demand relationships in patients with nonischemic dilated cardiomyopathy

Nonischemic dilated cardiomyopathy (NIDCM) is associated with left ventricular remodeling, hypertrophy, and mitochondrial metabolic abnormalities in vitro. We evaluated the hypothesis that energy supply, as judged by the rate of myocardial oxidative metabolism, is inadequate to meet oxygen demand in patients with NIDCM compared with normal subjects. We used positron emission tomography to determine the myocardial carbon 11 acetate decay rate (k mono) as an index of energy supply, and we compared k mono with the rate-pressure product (RPP) as an index of metabolic demand in 7 patients with NIDCM and 7 normal subjects. The mean k mono value (SEM) was 0.060 ± 0.006 min −1 in NIDCM patients versus 0.054 ± 0.002 in normal subjects ( P = not significant). The RPP was 9949 ± 931 beats/min · mm Hg in NIDCM patients and 6521 ± 476 in normal subjects ( P = .007). The relationship of k mono to this index of demand (k mono/RPP) was 6.2 × 10 −6 in NIDCM patients but was 8.5 × 10 −6 in normal subjects ( P = .003). Thus RPP, as an index of myocardial oxygen demand, was poorly matched by the rate of oxidative metabolism in those patients with NIDCM. The k mono was closely related to RPP in normal subjects ( r = 0.83, P = .02) but not in NIDCM patients. Furthermore, there was no significant relationship between k mono and wall stress as another index of oxygen demand. These results are consistent with a mitochondrial metabolic abnormality in heart failure. This metabolic mismatch detected by positron emission tomography may contribute to the pathophysiology of congestive heart failure and left ventricular remodeling.