Research abstract:

Elevated brain natriuretic peptide levels in chronic fatigue syndrome associate with cardiac dysfunction: a case control study Cara Tomas, Andreas Finkelmeyer, Tim Hodgson, Laura MacLachlan, Guy A MacGowan, Andrew M Blamire, Julia L Newton in BMJ Openheart 4:2 2017

Key questions
What is already known about this subject?

• Structural and functional cardiac abnormalities have been reported in chronic fatigue syndrome (CFS).
• Magnetic resonance spectroscopy studies have suggested a subclinical cardiomyopathy in some of those with CFS.

What does this study add?

• Brain natriuretic peptide (BNP) levels were significantly higher in CFS compared with matched controls.
• There were significantly lower cardiac volumes in those with higher BNP levels in both end-systolic and end-diastolic volumes.
• There were no relationships between fatigue severity, length of illness and BNP levels confirming that our findings are unlikely to be related to deconditioning.

How might this impact on clinical practice?

• This study confirms an association between reduced cardiac volumes and BNP in CFS.
• Lack of relationship between length of disease suggests that findings are not secondary to deconditioning.
• Further studies are needed to explore the utility of BNP to act as a stratification paradigm in CFS that directs targeted treatments.

Objectives:

To explore levels of the brain natriuretic peptide (BNP) and how these associate with the cardiac abnormalities recently identified in chronic fatigue syndrome (CFS).

Methods:

Cardiac magnetic resonance examinations were performed using 3T Philips Intera Achieva scanner (Best, Netherlands) in CFS (Fukuda) participants and sedentary controls matched group wise for age and sex. BNP was also measured by using an enzyme immunoassay in plasma from 42 patients with CFS and 10 controls.

Results:

BNP levels were significantly higher in the CFS cohort compared with the matched controls (P=0.013). When we compared cardiac volumes (end-diastolic and end-systolic) between those with high BNP levels (BNP>400 pg/mL) and low BNP (<400 pg/mL), there were significantly lower cardiac volumes in those with the higher BNP levels in both end-systolic and end-diastolic volumes (P=0.05). There were no relationships between fatigue severity, length of disease and BNP levels (P=0.2) suggesting that our findings are unlikely to be related to deconditioning.

Conclusion:

This study confirms an association between reduced cardiac volumes and BNP in CFS. Lack of relationship between length of disease suggests that findings are not secondary to deconditioning. Further studies are needed to explore the utility of BNP to act as a stratification paradigm in CFS that directs targeted treatments.