Antiretrovirals and diastolic dysfunction

[richvank]

Hi, all.

Here's something to consider in connection with use of antiretroviral therapy in cases of ME/CFS.

As you probably know, Dr. Cheney has found that most of his ME/CFS patients have diastolic dysfunction of the heart.

Diastolic dysfunction is caused by a low rate of production of ATP by the mitochondria.

Dr. John McLaren Howard's testing at Acumen Lab in the UK commonly finds that ATP levels are low in people with ME/CFS due to mitochondrial dysfunction.

I think that all of this is consistent.

O.K., it's known that some of the antiretrovirals can cause mitochondrial problems. AZT is one that is reported to do this.

This raises the question as to whether antiretroviral therapy would interact with existing diastolic dysfunction to cause more serious heart-related problems in ME/CFS patients. I don't know the answer to this, but check out this abstract:

http://thomasland.metapress.com/content/aw730150745q64h8/

This paper reports a high rate of diastolic dysfunction in HIV-infected patients. These patients are apparently on antiretroviral treatment. The abstract mentions that there is an increased risk of cardiovascular disease for HIV-positive patients who are managed on antiretroviral treatment. This study found a high rate of diastolic dysfunction in these patients.

The abstract does not say that the diastolic dysfunction was caused by the antiretrovirals, but given that some of the antiretroviral drugs are known to affect the mitochondria, I think this is something to be concerned about and to explore further.

Perhaps some of the antiretrovirals that have been found to be effective in vitro against the CFS-associated retroviruses do not impact the mitochondria in a deleterious manner. I don't know much about the antiretrovirals. Perhaps others here have information about this.

Best regards,

Rich

 

[IntuneJune]

Rich, thank you for making us aware........ June

 

[Hope123]

This abstract also talks about how the people with heart disease were also more likely to have diabetes, high cholesterol, and high blood pressure so aside from just antiretrovirals and the fact that HIV itself is known to cause cardiomyopathy, there are other factors involved that need to be sorted out.

 

[VillageLife]

Iike dr mikovits said if you have been sick for 20 years not left your bed or house,
these drugs may give you a better quality of life.

 

[Daffodil]

HIV patients on HAART still have some chronic inflammation too, which contributes to cardiac disease.

i have had heart issues ever since starting HAART. i had some before but it seems worse now.

 

[heapsreal]

hi sue, have u had a tilt table test done or been diagnosed with orthostatic intolerence, as this can cause tachycardia and palpitations etc. Antidepressants can worsen orthostatic intolerence as well, sometime even to higher dose or combination of ad's might cause serotonin syndrome which can cause tachycardia and the sweats. Just a thought.

cheers!!!

 

[BEG]

Thanks, Rich, for posting this. I've been tested by a cardiologist and found to have mild Level 1 diastolic dysfunction. I wasn't aware why until reading the article. I should have known. Those mitos seem to be the culprit of a lot of things going on with us.

 

[Chris]

Hi, Rich--many thanks for posting this. I know I too have mild diastolic dysfunction, including severe exercise intolerance, PEM, and OI; maybe I will try Artesunate again, since Cheney reported that it helped with diastolic dysfunction, though I seemed to develop a negative, gut and neurologically based, reaction to it after some improving months. Or just wait till something like Peptide T works out--I saw somewhere that Judy was working with Candace Pert and her (alas privately held) company --might be a promising lead? Best, Chris

 

[xrayspex]

chris and browneyed girl, I am curious what tests did docs do to diagnose your diastolic dysfunction? I saw Cheney once and he told me I have that per his special echo but that isnt really accepted in mainstream world, did you have it figured out in mainstream medicine? Next week I am going to get a pulmonary functioning test I hope that gets at it. I already know I have OH from doing the tilt years ago but I just don't think my b/p quite explains the nature of the oxygen hunger problem I get and I want to get this figured out more after all these years of having to lie down a lot every day. As long as I do tht intermittently can usually keep going but it makes travellng to a nearby city by car just about impossible for something like a museum or mall because there are only benches no public beds!

I am intrigued by the peptide t as well and was just coming here to ask if people heard of this other doc who works with peptides in cancer patients with great success Dr Stanislaw Burzynski? (I think I will post separate about him too)

 

[Navid]

impossible for something like a museum or mall because there are only benches no public beds!

If they won't give us clinical trials...i think we should start protesting for :

Public Beds Now!!!!!!


sorry didn't mean to hijack your thread but i thought your line abt no public beds was funny and so right on!!!! we could do so much more in life if there were public beds every several hundred yards in museums, parks, etc for us to stop and recline, get our heart rates and ans normalized :Retro smile:

thanks for the chuckle....but seriously:

Clinical Trials Now!!!!

 

[urbantravels]

Ahahaha, that made me laugh. Because this is what I decided after an emergency room visit this summer: Gurneys are awesome! I would totally love to be pushed around everywhere on a gurney. That would be the best way to see a museum!

 

[xrayspex]

haha yea I know, its anice thought, if it was socially acceptable to lie down without being looked at like a derelict, hell I lie down anyway always on my layovers at airports, I have to plan my trips that way to make it cross country.

So I dont know if I should go forward with my pulmonary functioning test or not, if its worth it or could end up being another useless thing that looks like I am healthy. I do have neurally mediated hypotension from 96 tilt test but that doesnt satisfy my frustration with the oxygen hunger problem not sure explains it cus I had low b/p before cfs but not a problem and I want to explore thru mainstream med Cheneys idea that i have diastolic dysfunciton.

 

[natasa778]

some interesting bits on carnitine lowering HAART toxicity

L-Carnitine Reduces Lymphocyte Apoptosis and Oxidant Stress in HIV-1-Infected Subjects Treated with Zidovudine and Didanosine
http://www.liebertonline.com/doi/abs/10.1089/15230860260196191

Acetyl-l-carnitine: a pathogenesis based treatment for HIV-associated antiretroviral toxic neuropathy. http://www.ncbi.nlm.nih.gov/pubmed/15238773

Long-term effect of acetyl-L-carnitine for antiretroviral toxic neuropathy. http://www.ncbi.nlm.nih.gov/pubmed/16566084

L-carnitine enhances the pace and degree of recovery of the AZT-associated destruction of human myotubes, restores and preserves the structure of mitochondria, mobilizes the endomyotubular fat, and allows the regeneration of myofibrils, even if AZT treatment continues. The findings may have potential clinical implications in improving the myotoxicity of AZT in patients with AIDS when the administration of AZT treatment must continue..... http://www.ncbi.nlm.nih.gov/pubmed/7967528

 

[natasa778]

another one, this time on mildronate (which is an inhibitor of carnitine synthesis! confused? I know I am :Retro smile


Mitochondria as the target for mildronate's protective effects in azidothymidine (AZT)-induced toxicity of isolated rat liver mitochondria.
Abstract
Previously mildronate, an aza-butyrobetaine derivative, was shown to be a cytoprotective drug, through its mechanism of action of inhibition of carnitine palmitoyltransferase-1, thus protecting mitochondria from long-chain fatty acid accumulation and subsequent damage. Recently in an azidothymidine (AZT)-induced cardiotoxicity model in vivo (in mice), we have found mildronate's ability of protecting heart tissue from nuclear factor kappaB abnormal expression. Preliminary data also demonstrate cerebro- and hepatoprotecting properties of mildronate in AZT-toxicity models. We suggest that mildronate may target its action predominantly to mitochondria... http://www.ncbi.nlm.nih.gov/pubmed/18508390

 

[Chris]

Hi, XraySpecs--sorry, I have not been checking this thread recently--so here is a belated partial answer to your question about diagnosing diastolic dysfunction. I had several echocardiograms over the last years (had cardiac surgery for a stenotic aortic valve in 2004, so this is regular maintenance stuff). The echo I had in Dec 2005 was done by a first rate cardiologist in Montreal, who noted that "the filling was perhaps acceptable considering patient's age"--i.e. not very good, but passable. At that point my E to A ratio was .9--normal is considered around 1.4. After CFS struck in 2006, my echos have recorded ratios of .75 and then .8. The cardios here in Victoria dismiss this aspect of cardiac performance, but I think they are wrong. So I trust my Montreal cardio, Cheney, and my symptoms--acute OI, which according to Cheney's last DVD is the peculiar sign of diastolic dysfunction. On a couple of those echos I also had chaotic wall motion, again specific to dd according to Cheney. He also reports that the heart squeezes harder to make up for reduced stroke volume, and he has seen ejection fractions as high as 80%; mine is usually around 70%, high enough to make the cardios around here think my heart is doing just fine--the hell with my symptomes. You might get hold of Cheney's DVD, "CFS: Is Oxygen the Problem, " still available quite cheaply, I think.

It is pretty technical, and I have no idea whether you will be able to make a doc pay attention to it, but it does contain some really good observations on heart function in CFS.
Apologies again for the lateness of this reply! Best, Chris