- Oral presentation
- Open Access
Patients with Dilated Cardiomyopathy (DCM) have appropriate myocardial oxygenation response to vasodilator stress
© Dass et al; licensee BioMed Central Ltd. 2013
- Published: 30 January 2013
- Perfusion Image
- Dilate Cardiomyopathy
- Segment Model
- Rate Pressure Product
- Microvascular Dysfunction
Microvascular dysfunction in non-ischemic DCM is well established. Despite this, little is known about whether this microvascular dysfunction is severe enough to result in ischemia on a tissue level and thus contribute to the observed derangement of cardiac energetics which is also a hallmark of DCM.
We hypothesized that in DCM the oxygen response of the myocardium to moderate stress is appropriate despite the presence of microvascular dysfunction.
Baseline characteristics of subjects
Male, n (%)
Ejection fraction (%)
LV Mass index
NYHA Class 1/2/3/4 (n)
ACE/ARB, n (%)
B-Blockers, n (%)
Spironolactone, n (%)
Digoxin, n (%)
Loop diuretic, n (%)
The baseline characteristics are summarized in table 1. During stress there were equivalent rises in rate pressure product in all groups, (normal 73±20%, DCM 74±50%, P=0.31).
In DCM, there was no significant difference in BOLD SIΔ from normals (BOLD SIΔ DCM: 16±13%, normal: 19±13%, P=0.56). For comparison, BOLD SIΔ in ischemic segments in patients with CAD was previously reported as 3.43±9.18%.
MPRI was significantly reduced in DCM (DCM: 1.52 ± 0.49; normal 1.89±0.29 P=0.03). On a segmental basis, there were no significant correlations between BOLD SIΔ and MPRI (R=0.06, P=0.43) and between BOLD SIΔ and LGE (R= 0.08, P=0.28).
This is the first report of a direct comparison between myocardial perfusion and oxygenation in DCM. Our results demonstrate dissociation between perfusion and oxygenation in DCM, suggesting that the impairment of perfusion is not severe enough to cause deoxygenation during vasodilator stress.
The lack of correlation of BOLD SIΔ and LGE suggests that the development of fibrosis in DCM is not oxygen dependant.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.