Abstract 10150: Is the Myocardium Oxygen Deprived in Non Ischemic Heart Failure?
Background: Microvascular dysfunction is present in dilated cardiomyopathy (DCM). However, it is not known whether it severe enough to result in ischemia on a tissue level. Furthermore, deranged cardiac energetics is a hallmark of DCM, however whether this is ischemia-driven is unknown.
We asked whether, in the absence of epicardial coronary artery disease, the failing myocardium is oxygen deprived.
Methods: Twenty six subjects (14 DCM; 12 normal) were studied at a 3Tesla MR system, with acquisition of BOLD (T2 sequence for assessment of oxygenation change) and first-pass perfusion (0.03 mmol/kg Gd-DTPA bolus) at stress and rest (4-6 minutes i.v. adenosine, 140μg/kg/min). Signal intensity change (SIΔ) and myocardial perfusion reserve index (MPRI) were measured from BOLD and perfusion images, respectively.
As BOLD does not measure absolute levels, to test if deoxygenation exists at rest, we performed 31P MR spectroscopy (PCr/ATP) before and after 4 hours of oxygen via facemask.
Results: During stress there were equivalent rises in rate pressure product (DCM 76±15%, normal 79±9%, P=0.84).
There was no significant difference in BOLD SI[[Unable to Display Character: ▵]] (BOLD SI[[Unable to Display Character: ▵]] DCM: 17±3%, normal: 20±2%, P=0.38). For comparison, BOLD SI[[Unable to Display Character: ▵]] in CAD was previously reported as 3±9%.
MPRI was significantly reduced in DCM (DCM: 1.51 ± 0.11; normal 1.86±0.10 P=0.03).. LGE burden did not correlate with MPRI (R=0.03 P=0.65) or BOLD (R=0.10 P=0.18).
Resting PCr/ATP was reduced in DCM (1.72±0.09, normal 2.11±0.06, P=0.01). With oxygen supplementation, there was no change in PCr/ATP (1.74±0.08, P=0.96). There was also no effect of oxygen on systolic function (EF pre oxygen 37±3%, post oxygen 38±3%, P=0.56)
Conclusion: This is the first report of a direct comparison between perfusion and oxygenation in DCM. Our results show a dissociation between microvascular dysfunction and oxygenation, suggesting that impairment of perfusion is not severe enough to cause deoxygenation during stress.
We demonstrate that cardiac energetics are unaffected by oxygen supplementation, suggesting that there is no significant deoxygenation at rest.
This suggests that novel treatments for non-ischemic heart failure should focus directly on cardiomyocyte function rather than oxygen delivery and microvascular function.
- © 2013 by American Heart Association, Inc.