4.5 Article

MR augmented cardiopulmonary exercise testing-a novel approach to assessing cardiovascular function

Journal

PHYSIOLOGICAL MEASUREMENT
Volume 36, Issue 5, Pages N85-N94

Publisher

IOP PUBLISHING LTD
DOI: 10.1088/0967-3334/36/5/N85

Keywords

CMR; exercise; cardio pulmonary exercise test

Funding

  1. Great Ormond Street Children's Charity
  2. British Heart Foundation
  3. UK national institute of health research (NIHR)
  4. British Heart Foundation [PG/11/98/29201, PG/10/76/28545, FS/08/012/24454] Funding Source: researchfish
  5. Great Ormond Street Hospital Childrens Charity [V1404] Funding Source: researchfish

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The purposes of this study were: (1) to evaluate feasibility and acceptability of MRI augmented cardiopulmonary exercise testing (MR-CPET) in healthy adults and (2) to test whether peak values obtained at conventional and MR-CPET correlate and to demonstrate variation in peak oxygen consumption (VO2) relates to both peak cardiac output (CO) and peak oxygen extraction (Delta cO(2)). Seventeen healthy adults underwent CPET and MR-CPET using an MR compatible ergometer and CPET system customised for MR use. Continuous aortic flow measurement used a validated UNFOLD-SENSE spiral phase contrast magnetic resonance (PCMR) sequence. Fifteen of 17 volunteers completed exercise; exclusions were due to claustrophobia and inability to effectively master exercise technique. Measures of acceptability were lower but still satisfactory for MR-CPET. There were strong correlations between conventional and MR-CPET for peak VO2 (r = 0.94, p < 0.001); VCO2 (r = 0.87, p < 0.001) and VE (r = 0.88, p < 0.001). Multiple linear regression analysis demonstrated peak CO and Delta cO(2) were independent predictors of peak VO2 measured during MR-CPET (beta = 0.73 and 0.38 p < 0.0001) and conventional CPET (beta = 0.78, 0.28 p < 0.0001). MR-CPET is feasible, acceptable and demonstrates physiology not apparent with conventional CPET. MR-CPET allows differentiation of the contributions of CO and Delta cO(2) to variation in peak VO2. We believe that this will be useful in understanding the origin of reduced exercise capacity in cardiac disease.

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