More on Research dealing with CFISD severity and cardiac function. Dr Klimas one of the authors is an expert HIV, CFIDS, Gulf War Illness Researcher in Florida and is highly respected internationally.
Gulf War veterans have experienced cardiac palpitations but no real detailed research has been done on this complaint of Gulf War Veterans.
There has been one study by Dr Berg, et al, that was on hypercoagulation in gulf war veterans. That was an independently done study no funding from government sources. Dr Ronald Bach, VA funded researcher, and an outstanding individual has completed one study and we are waiting anxiously for his publication of his study.
Many veterans that were health care providers themselves noticed early on from their return that the RBC on their own tests showed a shift downward from their values prior to the war. They also noticed changes in Sedimentation rates. But to see these changes you would have to be asute to go back to prewar physical lab work and compare to post war to see the subtle changes that were dramatic. One researcher from Australia also looked at shape of RBC and found shapes of RBC had been changed. They were no longer spherical.
Another interesting clinical test could be done! Draw arterial and venous oxygen levels at the same time. I encourage VA clinicans to get involved and look for the keys that are there and available in the clinical setting to help gulf war veterans. This is not that expensive to do!
With so many young age group dying the VA must immediately launch an investigation and find answers. Are they dying from Cancers or Cardiacs or what? Many veterans have gotten Social Security or found ways to use Tricare and their records may be in civilian hospitals. It is your sworn duty to provide the best care and find answers and this doesnt mean saying it is psychosomatic, PTSD, anxiety attacks etc. It means trying everything else before you send them off to a Psych consult or adding another Psychotrophic drug. Many of our veterans have reported being on 14-18 prescriptions are you really telling me you have checked for all medication side effects and interactions of multiple drugs.
You still have to have a license to practice medicine and that means you are potentially a Malpractice Case.
Clin Sci (Lond). 2009 May 26. [Epub ahead of print] Links
Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function.Hurwitz BE, Coryell VT, Parker M, Martin P, Laperriere A, Klimas NG, Sfakianakis GN, Bilsker MS.
This study examined whether deficits in cardiac output and blood volume in a Chronic Fatigue Syndrome (CFS) cohort were present and linked to illness severity and sedentary lifestyle. Follow-up analyses assessed whether differences between CFS and control groups in cardiac output levels were corrected by controlling for cardiac contractility and total blood volume (TBV). The 146 participants were subdivided into two CFS groups based on symptom severity data, severe (n=30) vs. non-severe (n=26), and two healthy non-CFS control groups based on physical activity, sedentary (n=58) vs. non-sedentary (n=32). Controls were matched to CFS participants using age, sex, ethnicity and body mass. Echocardiographic measures indicated that the severe CFS participants displayed 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 CFS groups had lower TBV, plasma volume (PV) and red blood cell volume (RBCV) than control groups. Of the CFS subjects with a TBV deficit (i.e., >/=8% below ideal levels), the mean +/-SD percent deficit in TBV, PV and RBCV were 15.4+/-4.0, 13.2+/-5.0, and 19.1+/-6.3, respectively. Lower CFS cardiac volume levels were substantially corrected by controlling for prevailing TBV deficits, but were not affected by controlling for cardiac contractility. 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 LV mass index. Therefore, the findings indicate that lower cardiac volume levels, displayed primarily by persons with severe-CFS, were not linked to diminished cardiac contractility levels, but were likely a consequence of a comorbid hypovolemic condition. Further study is needed to address the extent to which the CFS cardiac and blood volume alterations have physiological and clinical significance
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