Impaired cardiovascular response to standing in chronic fatigue syndrome.
BACKGROUND
Impaired skeletal muscle metabolism is recognized in chronic fatigue syndrome (CFS). This study examined the relationship between skeletal and cardiac muscle function and symptoms on standing in CFS using magnetic resonance spectroscopy (MRS) and impedance cardiography.


METHODS
Phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio by cardiac MRS, PCr/ADP and proton efflux by muscle MRS were performed in 12 CFS (Fukuda) and 8 controls. Head up tilt (HUT) and cardiac contractility (left ventricular work index, LVWI) (n = 64 CFS and matched controls) were found. Fatigue impact was accessed by Fatigue Impact Scale and orthostatic symptoms by Orthostatic Grading Scale (OGS).


RESULTS
Cardiac PCr/ATP correlated with measures of muscle bioenergetic function (half-time PCr recovery [kappa = -0.71, P = 0.005] and half-time ADP recovery [kappa = -0.60, P = 0.02]) suggesting that the muscle and cardiac bioenergetic function correlate in CFS. Four of 12 (33.3%) CFS patients had PCr/ATP values consistent with significant cardiac impairment. Those with impaired cardiac energy metabolism had significantly reduced maximal and initial proton efflux rates (P < 0.05). Cardiac PCr/ATP ratio correlated with myocardial contractility (LVWI) in response to standing (P = 0.03). On HUT, LVWI on standing was significantly higher in CFS (P = 0.05) with symptoms on standing (OGS) occurring in 61/64 (95%) (vs. 25/64 [39%] controls; P < 0.0001). OGS scores were significantly higher in those with abnormal LVWI responses to standing (P = 0.04), with the LVWI on standing correlating with OGS scores (r(2) = 0.1; P = 0.03). HUT was positive in 19 (32%).


CONCLUSIONS
Skeletal muscle and cardiac bioenergetic abnormalities associate in CFS. Cardiac bioenergetic metabolism associates with increase in cardiac contractility on standing. Haemodynamic assessment in CFS is well tolerated and safe with a high diagnostic yield comparable with unexplained syncope.
Hollingsworth
Kieren G
KG
Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.
Jones
David E J
DE
Taylor
Roy
R
Blamire
Andrew M
AM
Newton
Julia L
JL
D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D004734:Energy Metabolism; D005221:Fatigue / Q000503:physiopathology; D015673:Fatigue Syndrome, Chronic / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006334:Heart Function Tests; D006439:Hemodynamics; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D011187:Posture; D055815:Young Adult
D010725:Phosphocreatine; D000255:Adenosine Triphosphate