Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function

Abstract

The study examined whether deficits in cardiac output and blood volume in a CFS (chronic fatigue syndrome) cohort were present and linked to illness severity and sedentary lifestyle. Follow-up analyses assessed whether differences in cardiac output levels between CFS and control groups were corrected by controlling for cardiac contractility and TBV (total blood volume). The 146 participants were subdivided into two CFS groups based on symptom severity data, severe (n=30) and non-severe (n=26), and two healthy non-CFS control groups based on physical activity, sedentary (n=58) and non-sedentary (n=32). Controls were matched to CFS participants using age, gender, ethnicity and body mass. Echocardiographic measures indicated that the severe CFS participants had 10.2% lower cardiac volume (i.e. stroke index and end-diastolic volume) and 25.1% lower contractility (velocity of circumferential shortening corrected by heart rate) than the control groups. Dual tag blood volume assessments indicated that the CFS groups had lower TBV, PV (plasma volume) and RBCV (red blood cell volume) than control groups. Of the CFS subjects with a TBV deficit (i.e. > or = 8% below ideal levels), the mean+/-S.D. percentage deficit in TBV, PV and RBCV were -15.4+/-4.0, -13.2+/-5.0 and -19.1+/-6.3% respectively. Lower cardiac volume levels in CFS were substantially corrected by controlling for prevailing TBV deficits, but were not affected by controlling for cardiac contractility levels. Analyses indicated that the TBV deficit explained 91-94% of the group differences in cardiac volume indices. Group differences in cardiac structure were offsetting and, hence, no differences emerged for left ventricular mass index. Therefore the findings indicate that lower cardiac volume levels, displayed primarily by subjects with severe CFS, were not linked to diminished cardiac contractility levels, but were probably a consequence of a co-morbid hypovolaemic condition. Further study is needed to address the extent to which the cardiac and blood volume alterations in CFS have physiological and clinical significance.

Altered immune pathway activity under exercise challenge in Gulf War Illness: An exploratory analysis

“…All control subjects were screened as sedentary based on their response to a questionnaire upon recruitment. This was subsequently confirmed by the aerobic capacities obtained (VO2 max) (Hurwitz et al, 2010). Adjusted maximum VO2 levels were comparable between GWI and control groups but were significantly lower for the CFS disease control group (p < 0.05).…”

Small Heart With Low Cardiac Output for Orthostatic Intolerance in Patients With Chronic Fatigue Syndrome

“…11 Following our reports, Hurwitz et al reported that severe CFS patients have lower cardiac volume assessed by echocardiography and lower total blood volume, plasma volume, and red blood cell volume measured by dual tag blood volume assessments than controls, suggesting a comorbid hypovolemic condition. 18 Interestingly, in 2003 Peckerman et al reported that, using impedance cardiography in the supine and standing positions, cardiac output is significantly lower in a severe CFS group than in controls and less-ill patients. 19 Many CFS patients have low cardiac output, and the resulting low circulatory flow state may make it difficult for patients to meet the demands of daily activity, and it may also lead to fatigue and other conditions.…”

Chronic fatigue syndrome: comments on deconditioning, blood volume and resulting cardiac function

“…The interesting paper in the present issue of Clinical Science by Hurwitz et al [1] entitled ‘Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function’ is important because it aligns current thinking regarding CFS (chronic fatigue syndrome) with ongoing work concerning circulatory regulation, particularly as it relates to decreased overall blood volume and issues of orthostatic intolerance. In addition, despite significant cardiac findings, the paper [1] effectively puts to rest arguments in favour of a causative role for heart disease in CFS.…”