title: Impairment of subendocardial perfusion reserve and oxidative metabolism in nonischemic dilated cardiomyopathy.
abstract: BACKGROUND
  Cardiac magnetic resonance (CMR) and [(11)C]acetate positron emission tomography (PET) were used to assess the hypothesis that patients with nonischemic dilated cardiomyopathy (NIDCM) have decreased subendocardial perfusion reserve and impaired oxidative metabolism, consistent with the concept of "energy starvation" in heart failure (HF).
  
  
  RESULTS
  CMR myocardial perfusion was evaluated in 13 NIDCM patients and 15 control subjects with coronary risk factors and normal myocardial perfusion. The NIDCM patients underwent [(11)C]acetate PET. The myocardial perfusion index (MPI) was calculated as the normalized rate of myocardial signal augmentation following gadolinium contrast injection. Hyperemic transmural, subendocardial, and subepicardial MPI were reduced in NIDCM compared with control subjects [0.13 vs 0.18 (P < .001), 0.13 vs 0.17 (P < .001), and 0.13 vs 0.17 (P = .008), respectively]. The subendocardial perfusion reserve was 1.59 ± 0.21 vs 1.86 ± 0.32 for the subepicardium (P = .002), demonstrating reduced perfusion reserve. The myocardial oxidative metabolic rate (kmono) per unit demand (rate-pressure product) was reduced in proportion to perfusion reserve (P = .02) CONCLUSIONS: Impaired subendocardial perfusion reserve in NIDCM confirmed results previously attained only in animal models. Impaired perfusion and impaired oxidative metabolism are consistent with subendocardial energy starvation in HF.
authors: Division of Cardiovascular Medicine, Vanderbilt University School of Medicine, and Cardiology Section, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.
authors: Susan P
authors: SP
authors: Bell
authors: Division of Cardiovascular Medicine, Vanderbilt University School of Medicine, and Cardiology Section, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.
authors: Douglas W
authors: DW
authors: Adkisson
authors: Division of Cardiovascular Medicine, Vanderbilt University School of Medicine, and Cardiology Section, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.
authors: Henry
authors: H
authors: Ooi
authors: Division of Cardiovascular Medicine, Vanderbilt University School of Medicine, and Cardiology Section, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.
authors: Douglas B
authors: DB
authors: Sawyer
authors: Division of Cardiovascular Medicine, Vanderbilt University School of Medicine, and Cardiology Section, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee.
authors: Mark A
authors: MA
authors: Lawson
authors: Division of Cardiovascular Medicine, Vanderbilt University School of Medicine, and Cardiology Section, Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee. Electronic address: marvin.w.kronenberg@vanderbilt.edu.
authors: Marvin W
authors: MW
authors: Kronenberg
mesh_terms: D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis* / Q000378:metabolism*; D003326:Coronary Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D055414:Myocardial Perfusion Imaging / Q000379:methods; D010101:Oxygen Consumption / Q000502:physiology*; D011446:Prospective Studies; D012189:Retrospective Studies
keywords: CMR; fibrosis; heart failure; myocardial blood flow; oxidative metabolism