Abstract 20180: Reduced Subendocardial Perfusion Correlates with Impaired Energy Supply-Demand Relations in Patients with Non-Ischemic Dilated Cardiomyopathy.
Introduction: Myocardial energy starvation is thought to be important in the pathophysiology of congestive heart failure. We previously reported impaired subendocardial perfusion reserve in humans with non-ischemic dilated cardiomyopathy (NIDCM), providing a mechanism for energy starvation. Separately we showed lower energy supply vs. demand in NIDCM. To further investigate this mechanism we employed cardiovascular magnetic resonance imaging (MRI) and positron emission tomography (PET) to test the hypothesis that impaired subendocardial myocardial perfusion reserve is related to abnormal energy supply-demand relations in NIDCM and is thus a factor in energy starvation.
Methods: The [11C] acetate decay rate (kmono) was measured by PET as an index of myocardial oxygen supply in 10 patients with NIDCM, and the product of systolic blood pressure and heart rate (RPP) was an index of oxygen demand. Using MRI, the myocardial perfusion index (MPI) was derived as the ratio of the upslope of myocardial signal augmentation during the first-pass wash-in of gadolinium contrast normalized to the LV blood pool signal. The % change in MPI was calculated between rest and the peak hyperemic effect of adenosine.
Results: The LV ejection fraction was 38 ± 2.5% (Mean ± SEM). From rest to stress, the % change of subendocardial MPI was 63.9 ± 11.3 and subepicardial was 96.7 ± 21.5. The ratio of kmono to RPP was 5.77 × 10–6 ± 4.7 × 10 −7. There was a moderately strong correlation between kmono/RPP and the % change in subendocardial MPI (r=0.71, p=0.009). In conclusion, subendocardial perfusion reserve is impaired in patients with NIDCM. This impairment is quantitatively related to the ratio of myocardial energy supply to demand. Thus, we propose that the inability to increase perfusion in the subendocardium during vasodilator stress is partially responsible for energy starvation in patients with NIDCM.
- © 2010 by American Heart Association, Inc.