Sparrowhawk
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Forgive me if this is a repost buti found the notes on this blog to be a rich overview of Dr. Cheney s views on CFSME, especially listing cardiac symptomology I had not run into anywhere else. FYI.
http://mdwme.blogspot.com/2013/04/dr-paul-cheneys-latest-observations.html
Great if small output blog as well, by a med student or MD who came down with ME.
Sample text:
Dr. Paul Cheney's Latest Observations, Research, Treatments, and Thoughts on ME/CFS
Dr. Paul Cheney is one of the major players in the ME world. He was an internal medicine doctor in Incline Village when the CFS outbreak occurred there nearly 30 years ago and has been studying the complicated and perplexing disease ever since. Recently (April 2013) Dr. Cheney presented at a conference and his power point slides and audio were recorded and uploaded to youtube. You can see his entire presentation including a question and answer session at the bottom of this post.
The presentation itself is quite lengthy - nearly 2 hours, and the Q&A is about 30 minutes. A summary of the key points (as I see them) is posted below if you do not have the energy or time to listen to the entire recording.
If you have questions like, "what do you think he meant when he said...?" ask in the comments section and I will see if I can figure it out.
A summary will follow each video. Major important points for all 3 videos in my opinion are here:
· ME patients have a cellular energy deficit. This is a compensatory response caused by an inability to deal with the by-products of normal metabolism (energy production). The body decreases energy production so that we do not die from killing off all of our mitochondria with oxidative stress.
· This decreased energy production causes cardiac issues, namely, diastolic dysfunction, which in turn causes significantly decreased cardiac output. Decreased cardiac output manifests itself in multiple ways:
· Compensatory increased systolic squeeze = higher ejection fraction.
· Difficulty perfusing multiple organs especially when standing. POTS and NMH are not purely autonomic problems (as many think), but due to low cardiac output.
· The increased systolic squeeze causes higher than normal pressures in the right ventricle that the tricuspid valve is not really designed to handle - this causes blood to go back the wrong way (tricuspid regurgitation and flow reversal) into the brain (CCSVI) and the liver (CHVI), destroying normal capillary throughput in those organs at least.
· This could explain some of the cognitive, liver (problems with detoxification), and gut issues in ME.
· Physiology of cardiac abnormalities, CCSVI and CHVI:
· Poor redox control → low free energy levels → diastolic dysfunction → low cardiac output → low venous return to the heart → compensatory high ejection fraction → tricuspid regurgitation → flow reversal in inferior and superior vena cava → flow reversal in veins draining brain and liver.
· What causes impaired redox control in the first place? No one knows.
· Very preliminary results using VIP show that it can at least transiently decrease the tricuspid regurgitation and thus flow reversal in the brain and liver, likely by decreasing the pulmonary artery pressure, making it easier for blood to flow in the correct direction.
· A small study in a similar patient population (CIRS-WDB) with VIP had promising results with all patients having increased quality of life and normalization of many inflammatory markers.
http://mdwme.blogspot.com/2013/04/dr-paul-cheneys-latest-observations.html
Great if small output blog as well, by a med student or MD who came down with ME.
Sample text:
Dr. Paul Cheney's Latest Observations, Research, Treatments, and Thoughts on ME/CFS
Dr. Paul Cheney is one of the major players in the ME world. He was an internal medicine doctor in Incline Village when the CFS outbreak occurred there nearly 30 years ago and has been studying the complicated and perplexing disease ever since. Recently (April 2013) Dr. Cheney presented at a conference and his power point slides and audio were recorded and uploaded to youtube. You can see his entire presentation including a question and answer session at the bottom of this post.
The presentation itself is quite lengthy - nearly 2 hours, and the Q&A is about 30 minutes. A summary of the key points (as I see them) is posted below if you do not have the energy or time to listen to the entire recording.
If you have questions like, "what do you think he meant when he said...?" ask in the comments section and I will see if I can figure it out.
A summary will follow each video. Major important points for all 3 videos in my opinion are here:
· ME patients have a cellular energy deficit. This is a compensatory response caused by an inability to deal with the by-products of normal metabolism (energy production). The body decreases energy production so that we do not die from killing off all of our mitochondria with oxidative stress.
· This decreased energy production causes cardiac issues, namely, diastolic dysfunction, which in turn causes significantly decreased cardiac output. Decreased cardiac output manifests itself in multiple ways:
· Compensatory increased systolic squeeze = higher ejection fraction.
· Difficulty perfusing multiple organs especially when standing. POTS and NMH are not purely autonomic problems (as many think), but due to low cardiac output.
· The increased systolic squeeze causes higher than normal pressures in the right ventricle that the tricuspid valve is not really designed to handle - this causes blood to go back the wrong way (tricuspid regurgitation and flow reversal) into the brain (CCSVI) and the liver (CHVI), destroying normal capillary throughput in those organs at least.
· This could explain some of the cognitive, liver (problems with detoxification), and gut issues in ME.
· Physiology of cardiac abnormalities, CCSVI and CHVI:
· Poor redox control → low free energy levels → diastolic dysfunction → low cardiac output → low venous return to the heart → compensatory high ejection fraction → tricuspid regurgitation → flow reversal in inferior and superior vena cava → flow reversal in veins draining brain and liver.
· What causes impaired redox control in the first place? No one knows.
· Very preliminary results using VIP show that it can at least transiently decrease the tricuspid regurgitation and thus flow reversal in the brain and liver, likely by decreasing the pulmonary artery pressure, making it easier for blood to flow in the correct direction.
· A small study in a similar patient population (CIRS-WDB) with VIP had promising results with all patients having increased quality of life and normalization of many inflammatory markers.
