Volume 13 Supplement 1
Quantification of myocardial oxygen consumption with 17O-CMR: initial study
© Zheng et al; licensee BioMed Central Ltd. 2011
Published: 2 February 2011
Impaired myocardial oxygenation leading to ischemia is central to the pathophysiology of coronary artery disease and an important contributor to other common cardiovascular disease conditions such as left ventricular hypertrophy, dilated cardiomyopathy, renal heart disease and valvular heart disease. Positron Emission Tomography (PET) can quantify myocardial oxygen consumption (MVO2), but has limited applications due to its relatively low spatial resolution, high cost, and ionizing radiation.
This study is aiming to develop a new non-invasive CMR method with the use of 17O based blood tracer to assess myocardial oxygenation and MVO2.
The initial 17O-CMR was performed in normal mongrel dogs (n=3) and myocardial ischemic dogs (n=3). The later dogs includes 70% (n=1) and 100% (n=2) area stenosis in the second diagonal branch of the left descending coronary artery (LAD). The 17O blood tracer was prepared using artificial blood perfluorodecalin emulsion or PFD (OxyToT, Rockland Technimed Ltd, Airmont, NY) and 70% enriched 17O2 gas. Each dog was injected 2 mL/kg 17O-PFD at rest within 30 sec. A novel CMR T1ρ-weighted imaging was performed at baseline and then to monitor the myocardial T1ρ signals for over 30 min after the injection. The 17O2 gas absorbed in PFD will be taken up by the myocardial tissue and converted into H217O water, which will be detected by T1ρ-weighted imaging with a negative contrast. The H217O water concentration can be obtained with the ratio between T1ρ-weighted signals after and before the 17O-PFD injection. MVO2 can be quantified using a new model developed in our laboratory. Quantitative perfusion CMR imaging was also performed at the end of study to confirm the ischemic area.
The 17O-CMR may have potential to provide a direct and non-invasive measurement of the oxygen consumption to facilitate comprehensive evaluations of patients at molecular level with a variety of pathophysiological etiologies.
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.