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Cardiac dysfunction and orthostatic intolerance in patients with myalgic encephalomyelitis

Discussion in 'Latest ME/CFS Research' started by Ecoclimber, Apr 18, 2014.

  1. Ecoclimber

    Ecoclimber Senior Member

    Heart Vessels. 2014 Apr 16. [Epub ahead of print]
    Cardiac dysfunction and orthostatic intolerance in patients with myalgic encephalomyelitis and a small left ventricle.
    Miwa K.
    Author information
    • Department of Internal Medicine, Miwa Naika Clinic, 1-4-3 Shintomicho, Toyama, 930-0002, Japan,
    The etiology of chronic fatigue syndrome (CFS) is unknown. Myalgic encephalomyelitis (ME) has been recently postulated to be the cause of CFS. Orthostatic intolerance (OI) has been known as an important symptom in predicting quality of life in CFS patients. Cardiac function may be impaired in patients with ME.

    The presence or absence of OI was determined both symptomatically and by using a 10-min stand-up test in 40 ME patients. Left ventricular (LV) dimensions and function were determined echocardiographically in the ME patients compared to 40 control subjects.

    OI was noted in 35 (97 %) of the 36 ME patients who could stand up quickly. The mean values for the cardiothoracic ratio, systemic systolic and diastolic pressures, LV end-diastolic diameter (EDD), LV end-systolic diameter, stroke volume index, cardiac index and LV mass index were all significantly smaller in the ME group than in the controls. Both a small LVEDD (<40 mm, 45 vs. 3 %) and a low cardiac index (<2 l/min/mm2, 53 vs. 8 %) were significantly more common in the ME group than in the controls.

    Both heart rate and LV ejection fraction were similar between the groups. In conclusion, a small LV size with a low cardiac output was common in ME patients, in whom OI was extremely common. Cardiac dysfunction with a small heart appears to be related to the symptoms of ME.
    ahimsa, Valentijn, Tito and 2 others like this.
  2. anciendaze

    anciendaze Senior Member

    This is very similar to the 95% Dr. Cheney observed in the patients who had been with him for 20 years who had diastolic dysfunction. I suspect the problem is actually the result of long illness in which the left ventricle does not fill properly because the muscle does not relax completely during diastole. We still don't know what we would have seen in these patients prior to onset.

    My own guess is that diastolic dysfunction is part of a pathological process which includes endothelial dysfunction. Even this is likely not the beginning of the problem. I'm looking for an immune defect which even precedes gastrointestinal trouble reported in sudden onset. Once this develops, and immune response to all the microbes in the gut starts striking out in many directions, a whole new layer of complications comes into existence.

    If this were only an obscure problem of a tiny minority of people, I could understand that researchers would hesitate to tackle the problem. What we still don't know is what happens to those whose medical history follows other branches of this pathology. I predict we will find more common, and serious, pathologies sharing the same root cause. We already have strong indications of abnormalities in cardiac, immune, neurological and metabolic functions. This covers a great deal of the biomedical landscape. If you want to explore blank spots on the map, not already trampled by other explorers, this is an opportunity.
    NK17, Valentijn, Tito and 4 others like this.

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