Impaired cardiac function in chronic fatigue syndrome measured using magnetic resonance cardiac tagging

Abstract. Hollingsworth KG, Hodgson T, MacGowan GA, Blamire AM, Newton JL (Institute of Cellular Medicine, Campus for Ageing and Vitality; Institute of Genetic Medicine; and Institute for Ageing and Health, Campus for Ageing and Vitality; Newcastle University, Newcastle, UK). Impaired cardiac function in chronic fatigue syndrome measured using magnetic resonance cardiac tagging. J Intern Med 2012; 271 : 264–270. Objectives. Impaired cardiac function has been confirmed in patients with chronic fatigue syndrome (CFS). Magnetic resonance cardiac tagging is a novel technique that assesses myocardial wall function in vivo. We hypothesized that patients with CFS may have impaired development and release of myocardial torsion and strain. Methods. Cardiac morphology and function were assessed using magnetic resonance imaging and cardiac tagging methodology in 12 CFS patients (Fukuda) and 10 matched controls. Results. Compared to controls, the CFS group had substantially reduced left ventricular mass (reduced by 23%), end‐diastolic volume (30%), stroke volume (29%) and cardiac output (25%). Residual torsion at 150% of the end‐systolic time was found to be significantly higher in the patients with CFS (5.3 ± 1.6°) compared to the control group (1.7 ± 0.7°, P = 0.0001). End‐diastolic volume index correlated negatively with both torsion‐to‐endocardial‐strain ratio (TSR) (r = ?0.65, P = 0.02) and the residual torsion at 150% end‐systolic time (r = ?0.76, P = 0.004), so decreased end‐diastolic volume is associated with raised TSR and torsion persisting longer into diastole. Reduced end‐diastolic volume index also correlated significantly with increased radial thickening (r = ?0.65, P = 0.03) and impaired diastolic function represented by the ratio of early to late ventricular filling velocity (E/A ratio, r = 0.71, P = 0.009) and early filling percentage (r = 0.73, P = 0.008). Conclusion.  Patients with CFS have markedly reduced cardiac mass and blood pool volumes, particularly end‐diastolic volume: this results in significant impairments in stroke volume and cardiac output compared to controls. The CFS group appeared to have a delay in the release of torsion.