Orthostasis & heart abnormalities
We now know that many ME/CFS patients have orthostatic intolerance – the inability to stand upright for long without symptoms such as dizziness, altered vision, nausea, fatigue, neurocognitive difficulties, headache, sweating or pallor (see our article, “Standing up for ME”). For the past few years, researchers at the Miwa Naika Clinic in Toyama, Japan have been investigating both orthostatic intolerance and heart function in ME/CFS. In a paper in 2011, they described a sub-group of patients with relatively small hearts in whom orthostatic intolerance was associated with a low ‘cardiac output’ (the amount of blood pumped by the heart in a certain time). The team have recently extended their investigations to include a larger group of patients plus a comparison group of healthy people, and the results have just been published in the journal ‘Heart and Vessels’.
For their study, they recruited 40 ME/CFS patients (defined using the ICC-ME 2011 criteria) and 40 healthy controls. Orthostatic intolerance was assessed from self-reported symptoms, plus changes in blood pressure and heart rate, during a 10 minute standing-up test. Also, cardiac measurements, such as mass and volume of the left ventricle of the heart; its ejection fraction (the amount of blood ejected per minute); stroke volume (the volume of blood pumped by the heart with each beat); and cardiac index (the heart’s performance relative to the size of the person) were determined using ECG monitoring.
Interestingly, 4 of the patients were unable to stand up quickly, and so could not undergo the 10-minute standing-up test. However, of the remainder, 35 (97 %) were found to have orthostatic intolerance on the stand up test, even though only 70% had reported having symptoms of orthostatic intolerance in their everyday lives. In most of these patients, orthostatic intolerance took the form of POTS (i.e. an increase in heart rate or 30 beats/min or more, or a heart rate of 120 beats/min or more during the 10-minute standing test). As regards the cardiac and circulation measurements, most were significantly smaller in the ME/CFS group than in the healthy people. In fact, it was far more common for patients to have a small left ventricle diameter (<40 mm) in the ‘end-diastolic’ phase of the heart just before a contraction than healthy people (45 versus 3%), and to have a low cardiac index (53 versus 8%).
The high incidence of orthostatic intolerance found by the Japanese research group certainly accords with what we know from Western patients; in fact, orthostatic intolerance is found in so many patients that it may very well serve as a definable subset in its own right, and might even be seen as diagnostic if the underlying mechanisms could be understood (see “Impaired cardiovascular response to standing”). Sadly, orthostatic symptoms have not yet been incorporated into official clinical and diagnostic guidelines, such as the NICE Guideline in the UK.
As regards cardiovascular measurements, other investigators have also reported a reduced cardiac volumes in ME/CFS patients (e.g., Hollingsworth in 2012, funded by ME Research UK; and Hurwitz in 2010), and it is certainly feasible that an impairment of flow, particularly to the brain, could be involved in the fatigue and other symptoms that they experience. As the researchers point out, ME/CFS is associated with a “variety of possible cardiovascular complaints, including chest pain, palpitations, dyspnoea, cold feet, dizziness and fainting”, and while these are not necessarily attributable to cardiovascular dysfunction, they might certainly be related to the reduced cardiac ‘preload’, as seen in the present study (preload relates to the volume of blood inside the ventricle of the heart just before contraction).
Though these results are intriguing, several questions remain. The researchers have shown that orthostatic intolerance occurs alongside cardiac anomalies, but we do not know if the two phenomena were significantly linked in this group of patients. It is possible that information on possible correlations will become the subject of a separate scientific paper in the near future, and these may support the team’s previous findings suggestive of a link. Also, these results relate to a Japanese population with ME/CFS, and it will be important to test whether similar cardiac abnormalities – relatively small hearts with a correspondingly reduced cardiac output – are also observable in Western populations. SOURCE