Abstract 4028: Impaired Subendocardial Perfusion in Human Non-Ischemic Dilated Cardiomyopathy: A mechanism for Energy Starvation
Introduction Energy starvation has long been thought to be a major factor in the pathophysiology of congestive heart failure. Studies in animals have shown decreased subendocardial perfusion relative to the subepicardium in models of non-ischemic dilated cardiomyopathy (NIDCM), providing a mechanism for energy starvation. PET studies in patients have shown decreased transmural perfusion, but cannot resolve subendocardial flow. Thus, we employed cardiovascular magnetic resonance imaging (MRI) to assess the hypothesis that patients with NIDCM have decreased subendocardial perfusion reserve as a mechanism of energy starvation.
Methods Myocardial perfusion MRI was performed using adenosine infusion and gadolinium injection in 5 patients with NIDCM and 6 normal subjects. We employed the normalized slope of myocardial signal augmentation to derive the myocardial perfusion index (MPI).
Results The LV mass index in the NIDCM patients was 83.8±5.9g (mean [±SEM]) (compared to 48.7±3.2 in normals, p=0.008) and the LV ejection fraction was 38±3% vs. 71±4% in normals (p=0.0002). Subendocardial MPI was greater during adenosine infusion in normals compared to patients with NIDCM (0.17±0.02 vs. 0.11±0.1 [p=0.047]). However, in the subepicardium, the MPI was similar in normals and NIDCM (0.15±0.02 vs. 0.12±0.1 [p=0.19]). In NIDCM, the MPI increased significantly during adenosine infusion in the subendocardium (from 0.9±0.1 at baseline to 0.11±0.1 during adenosine infusion [p=0.024]) and in the subepicardium (from 0.80.1 to 0.12±0.1 [p=0.013]), with a greater increase in the subepicardium than the subendocardium (p=0.003).
Conclusions The subendocardial myocardial perfusion index is lower in patients with NIDCM compared to normal subjects during adenosine infusion, and in NIDCM, the vasodilatory response to adenosine is impaired in the subendocardium when compared to the subepicardium. This study provides the first human evidence of impaired subendocardial perfusion in non-ischemic heart failure, confirms results previously attained only in animal models, and provides a mechanism for energy starvation in heart failure.