A poster presentation by Dr. Cheney made at the 1st International XMRV meetings held at the NIH in early September, 2010 was partially summarized by a U-tube video (see http://www.youtube.com/watch?v=S3UwkdzBaro). While the video was in many respects very well done and brings needed attention to CFS and its link to XMRV, there are key misrepresentations made about the poster and what it actually said or implied. This post discusses in detail the good points and bad points of this U-tube presentation which Dr. Cheney knew nothing about and had no hand in it.
Two published studies show that diastolic heart failure (DHF) in the elderly and low birth weights at term in infants have occurred during the same time frame from 1990-2000. No one has an explanation for these anomalies at the ends of the age spectrum in humans but suspect an environmental factor or factors. We have a rising case load of diastolic dysfunction seen in 97% of our CFS cases (ave. age 49) and some appear to have what I would call compensated diastolic heart failure. I would define compensated DHF in CFS as an extremely low cardiac output with a cardiac index (CI) below 2.0 and very poor functional capacity combined with the inability to stand which is the corollary in DHF to the inability to lay down flat in systolic heart failure (SHF). Heart failure patients are typically below 2.0 in CI. I have several CFS patients below that number and they cannot stand still for more than 15-30 seconds without having to sit down or fall down. Walking or moving helps which makes sense as that would increase filling pressures and equivalent to laying down. They might be diagnosed as having orthostatic intolerance by others. These patients are also typically thin or near ideal body weight and have a high catabolic to anabolic ratio on 24 hour urine hormone analysis when I have measured it.
Attached below is an abstract presented at the IACFS meetings in Reno, NV in March 2009. This abstract presents the results of a large (N = 90) study of CFD patients seen at the Cheney Clinic and examines diastolic parameters by echocardiography and compares the results to age and sex matched controls.
Attached below is data abstracted from my current clinic CFS patient population (N=126) that looks at onset date. This looks just like data from my Charlotte practice 15 years ago which showed the peak production year of 1987. It remains the same and suggests CFS is largely a new disorder erupting out of a low level baseline that existed prior to 1980.
I feel strongly that the almost 90% PFO incidence in CFS is largely acquired with the onset of CFS and is not pre-existing except in perhaps 27%. The PFO shunt from right to left will be stronger however, once CFS cardiac physiology is manifest with the near universal (>96%) finding of diastolic dysfunction. I suspect the frequent brain UBO’s on MRI scans are likely a result of this right to left PFO shunting as well as certain symptoms such as migraine and periodic hyperventilation. PFO could also be a factor in sleep apnea pathophysiology. Heavy snoring and airway obstruction is a valsalva maneuver and can cause shunting right to left, particulary if there is also desaturation. Below is an abstract of data on CFS patients at the Cheney Clinic showing an extremely high incidence of PFO using contrast bubble studies.
This discussion presents data on two patients who bring out several interesting features of CFS including problems in the handling of glutathione, poor oxygen transfer off hemoglobin into the cells, PFO with increased risk of brain micro-infarcts and migraine and the effects of Type II AODM on CFS. Also presented are the effects both positive and negative of certain commonly used drugs including modafinil, hydrocodone and benzodiazepines.