Impaired Cardiac Function study in Journal of Internal Medicine:

[Gamboa]

There is a new study released July 27, 2011 in the Journal of Internal Medicine. It concludes that , surprise, surprise, that ME patients have " markedly reduced cardiac mass and blood pool volumes...". Article below:


Impaired Cardiac Function in Chronic Fatigue Syndrome Measured Using Magnetic Resonance Cardiac Tagging Source: Journal of Internal Medicine, Jul 27, 2011

by Kieren G Hollingsworth, et al.
July 29, 2011

Objectives: Impaired cardiac function has been confirmed in patients with chronic fatigue syndrome (CFS).

Magnetic resonance cardiac tagging [aka electromechanical heart mapping] is a novel technique that assesses myocardial wall function in vivo.

We hypothesized that CFS patients may have impaired development and release of myocardial torsion and strain. [Note: The heart not only contracts but rotates as it pumps.]

Methods: Cardiac morphology and function was assessed using magnetic resonance imaging and cardiac tagging methodology in 12 CFS (Fukuda) and 10 matched controls.

Results: Compared to controls the CFS group had substantially reduced LV [left ventricular] mass (reduced by 23%), end diastolic volume (30%), stroke volume (29%), and cardiac output (25%).

Residual torsion at 150% of the end-systolic time was found to be significantly higher in the CFS patients (5.31.6o) compared to the control group (1.70.7o, p=0.0001).

End diastolic volume index correlated negatively with both torsion to endocardial strain ratio (TSR) (r =-0.65, p=0.02) and the residual torsion at 150% end systolic time (r=-0.76, p=0.004), so decreased end diastolic volume is associated with raised TSR and torsion persisting longer into diastole. Reduced end diastolic volume index also correlated significantly with increased radial thickening (r=-0.65, p=0.03) and impaired diastolic function represented by the ratio of early to late ventricular filling velocity (E/A ratio, r=0.71, p=0.009) and early filling percentage (r=0.73, p=0.008).

Conclusion: CFS patients have markedly reduced cardiac mass and blood pool volumes, particularly end diastolic volume: this results in significant impairments in stroke volume and cardiac output compared to controls. The CFS group appeared to have a delay in the release of torsion.

Source: Journal of Internal Medicine, Jul 27, 2011. DOI: 10.1111/j.1365-2796.2011.02429.x. Hollingsworth KG, Hodgson T, Macgowan GA, Blamire AM, Newton JL. Newcastle Magnetic Resonance Centre, Institute of Cellular Medicine, and Institute for Ageing and Health, Campus for Ageing and Vitality, and Institute of Human Genetics, Newcastle University; Department of Cardiology, Freeman Hospital, Newcastle upon Tyne, UK. [Email: k.g.hollingsworth@ncl.ac.uk]

 

[WillowJ]

Very nice addition to my collection; thanks for posting.

I'm interested in the new technique. I hear echocardiogram isn't all that accurate. There are alternatives, but it's nice to have another paper to say, here is an alternative appropriate for this disease.

 

[ixchelkali]

One of the things that makes this interesting is that it came out of the UK, from Newcastle University. It sounds similar to what Paul Cheney says he's found in his practice.

 

[taniaaust1]

What a great new study..

Its so great that a decent study has come out of UK. Maybe this will help in some way to change the UK situation.

 

[laura]

Thanks for posting! I am always glad to see research that closely links to our symptoms and demonstrates what we intuitively know to be so.

 

[In Vitro Infidelium]

There is a new study released July 27, 2011 in the Journal of Internal Medicine. It concludes that , surprise, surprise, that ME patients have " markedly reduced cardiac mass and blood pool volumes...". Article below:


Impaired Cardiac Function in Chronic Fatigue Syndrome Measured Using Magnetic Resonance Cardiac Tagging Source: Journal of Internal Medicine, Jul 27, 2011 by Kieren G Hollingsworth, et al. July 29, 2011

http://onlinelibrary.wiley.com/doi/...ionid=1FF117C6F5FD1E325A9E8F43FF1F9FA8.d03t04

The abstract does not specify if screening on the basis of activity levels pre morbidity in the patients or in the controls, was undertaken. Chronic low level activity is associated with loss of heart muscle mass as the individual ages (Regular exercise can help preserve/build heart mass ), so subject selection could greatly affect results. If selection were on the basis of typical age profiles (40 +) and included patients who had been housebound/bed bound for may years, then the results may simply reflect an effect of being chronically ill, rather than having any relationship to initial causation. Of course this is still important information for both researchers and M.E/CFS affected people but it may not mean what we may like it to mean.

IVI

 

[In Vitro Infidelium]

I am always glad to see research that closely links to our symptoms and demonstrates what we intuitively know to be so.

In science it's called confirmation bias, finding significance on the basis of a narrow perspective.

Intuition as a faculty no doubt confered evolutionary advantage on our Pleistocene ancestors by increasing the probability of success in survival behaviours such as finding water in arid climates or avoiding encounters with lions, but human intuition is frequently fooled by finding significance where no significance exists. Human intuition has been very, very poor at leading us to the the reality of the Universe which we inhabit and it seems unlikely to help in understanding the nature of disease.

IVI

 

[RustyJ]

In science it's called confirmation bias, finding significance on the basis of a narrow perspective.

Intuition as a faculty no doubt confered evolutionary advantage on our Pleistocene ancestors by increasing the probability of success in survival behaviours such as finding water in arid climates or avoiding encounters with lions, but human intuition is frequently fooled by finding significance where no significance exists. Human intuition has been very, very poor at leading us to the the reality of the Universe which we inhabit and it seems unlikely to help in understanding the nature of disease.

IVI

How ironic. I read Laura comment differently. I thought she was referring to a wider context; that it was good to hear about biological symptoms being tied to the disease, contrary to prevailing psychiatry bias in the UK, rather than the narrow view that she intuitively believed this heart issue was connected to me/cfs.

But I guess it depends on your perspective.

 

[eric_s]

Interesting research. It seems there have been a number of good studies recently. I hope they will do another study with a bigger sample size and where they try to find out if or how much of what they observed could be due to deconditioning (or maybe they have already adressed that in the full text). I like those new techniques, finally they might have the tools necessary to find out what's wrong.

 

[CBS]

The abstract does not specify if screening on the basis of activity levels pre morbidity in the patients or in the controls, was undertaken.

Then I suggest that you might want to read more than the abstract. All controls were sedentary and the control BMI's were marginally higher than those of the patients.

... Of course this is still important information for both researchers and M.E/CFS affected people but it may not mean what we may like it to mean.

IVI

If you had read more than the abstract - including the Results and Discussion sections you would know that the authors interpret their findings, not as pointing to a conditioning issue but rather, as a likely blood volume issue and that the changes seen are consistent with compensation for a chronic state of hypovolemia (perhaps it might help to think of increased residual torsion at 150% of the end-systolic time as the heart's attemtp to squeeze on last drop from the bottle).

That said, nice (but poorly placed) lecture on confirmation bias. Shall I go into my own speech on reading too much into abstracts?

Any author worth reading will tell you that there are no perfect studies. To me, the more intelligent question is: Do you know how to identify what can be learned from a study (and then use it it to build upon previous knowledge) while at the same time being able to separate out what isn't supported by the data?

 

[eric_s]

But what exactly is a sedentary control? Are there healthy people who live a life that is comparable to people with ME/CFS? I didn't read the full text, but if somebody could comment on that, that would be welcome. They often mention sedentary controls, but i don't know what type of person that is.

 

[Esther12]

Getting controls suitable to rule out the affects of deconditioning in CFS is difficult. More and more researchers seem to be trying though, and remember that many CFS patients have a fair amount of functionality still. It could be that the sickest patients are unlikely to be able to take part in research of this sort.

 

[RustyJ]

According to Wessely me/cfs patients can be sedentary controls, if the condition is regarded as psychiatric. lol.

 

[CBS]

The critical point here is that there was a unique type of wall thickening (radial) and residual torsion, consistent with over compensation for low blood volume. This is inconsistent with deconditioning, in someways the opposite. In a number of conditions of "inefficiency" the heart over compensates in a similar manner. That is not a difference attributable to a subtle (or not so subtle) difference between control and patient activity levels/conditioning. It's a pumping issue and the authors are saying that it is consistent with too little blood (low volume) to satisfy the body's needs so it overcompensates. They propose looking for ways to raise blood volume in CFS (ME) patients.

 

[fla]

The critical point here is that there was a unique type of wall thickening (radial) and residual torsion, consistent with over compensation for low blood volume. This is inconsistent with deconditioning, in someways the opposite. In a number of conditions of "inefficiency" the heart over compensates in a similar manner. That is not a difference attributable to a subtle (or not so subtle) difference between control and patient activity levels/conditioning. It's a pumping issue and the authors are saying that it is consistent with too little blood (low volume) to satisfy the body's needs so it overcompensates. They propose looking for ways to raise blood volume in CFS (ME) patients.

Exactly CBS. With the energy production so low in M.E. and consequently the heart output being significantly lower, the brain has no choice but to increase the heart rate to compensate (POTS in M.E. is an energy problem not a problem with the control system).

For me, sitting up requires the heart rate to go at a jogging level and standing/walking requires a heart rate of an all out sprint. Mostly bedbound, my leg muscles are deconditionned but my heart on the contrary is overworked by simply doing minor daily activities like showering/eating/going to the washroom...

 

[RustyJ]

The critical point here is that there was a unique type of wall thickening (radial) and residual torsion, consistent with over compensation for low blood volume. This is inconsistent with deconditioning, in someways the opposite. In a number of conditions of "inefficiency" the heart over compensates in a similar manner. That is not a difference attributable to a subtle (or not so subtle) difference between control and patient activity levels/conditioning. It's a pumping issue and the authors are saying that it is consistent with too little blood (low volume) to satisfy the body's needs so it overcompensates. They propose looking for ways to raise blood volume in CFS (ME) patients.

I assume that even after raising blood volume with medications, the wall thickening etc would persist for some time and would continue to compound problems? Perhaps that would mitigate the effects of such medications, and cause conflicting results in patients, as reported?

 

[kday]

In science it's called confirmation bias, finding significance on the basis of a narrow perspective.

Intuition as a faculty no doubt confered evolutionary advantage on our Pleistocene ancestors by increasing the probability of success in survival behaviours such as finding water in arid climates or avoiding encounters with lions, but human intuition is frequently fooled by finding significance where no significance exists. Human intuition has been very, very poor at leading us to the the reality of the Universe which we inhabit and it seems unlikely to help in understanding the nature of disease.

IVI

Hmmm.... I would have to disagree.

While I don't have a solution to the problem, it has been my intuition that led me the right direction. I use my intuition when comes to evaluating what meds and supplements work, and what doesn't. I can find plenty of abnormalities on lab tests, but for the most part, I see them as pretty much useless. I even had what looks like chronic liver disease on an ultrasound when labs were normal. I had to go doctor to doctor and finally convinced one to just order it.

This illness has brought me a great sense of intuition not something I really knew I had.

I also had pericarditis when all the medical professionals kept trying to convince me it was GI. I was never hesitant to tell them they were wrong, and after running the appropriately tests, it was clearly evident that I was right all along.

I think members of the medical community are the ones that really lack intuition (in general).

But at the same time, I think the average person that hasn't experience a chronic condition isn't very intuitive when it comes to their health.

 

[Chris]

Eric--a belated reply to your query about what constitutes a "sedentary control" in this study--they specify that "all control subjects performed less than 30 mins exercise three times per week." Wish I could do that much in one session! It does seem a very interesting paper--helps explain how I have a high ejection fraction, but still can't exercise worth a damn. May try my own home-made version of this new in process Nancy Klimas thing, but it seems very close to what I have been doing, with not much to show for it. But I have bought a heart rate monitor, and will see what light that can throw on my situation and the process of trying to increase my exercise capacity without provoking a crash.
Chris

 

[In Vitro Infidelium]

The critical point here is that there was a unique type of wall thickening (radial) and residual torsion, consistent with over compensation for low blood volume. This is inconsistent with deconditioning, in someways the opposite. In a number of conditions of "inefficiency" the heart over compensates in a similar manner. That is not a difference attributable to a subtle (or not so subtle) difference between control and patient activity levels/conditioning. It's a pumping issue and the authors are saying that it is consistent with too little blood (low volume) to satisfy the body's needs so it overcompensates. They propose looking for ways to raise blood volume in CFS (ME) patients.

So decreased ventricular mass is incidental ? a function of low blood volume ? I don't understand why the decreased VM would be judged not to be the precurser of the radial thickening. And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? - the high urinary output reported by many M.E/CFS sufferers would seem inconsistent with classic hypovolaemia. The charistics seen in the M.E/CFS cohort may be indicative of symptom causation, but I don't how the observation couldn't be explained as being a particular subset of responses to sedentary living. It would be interesting to see this study repeated in young people with M.E who have been diagnosed within the previous 12 months, and who prior to becoming ill had been active - this would rule out aging dependent effects and mnimise sedentary effects.

IVI

 

[RustyJ]

So decreased ventricular mass is incidental ? a function of low blood volume ? I don't understand why the decreased VM would be judged not to be the precurser of the radial thickening. And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? - the high urinary output reported by many M.E/CFS sufferers would seem inconsistent with classic hypovolaemia. The charistics seen in the M.E/CFS cohort may be indicative of symptom causation, but I don't how the observation couldn't be explained as being a particular subset of responses to sedentary living. It would be interesting to see this study repeated in young people with M.E who have been diagnosed within the previous 12 months, and who prior to becoming ill had been active - this would rule out aging dependent effects and mnimise sedentary effects.

IVI

So does this mean you have discovered a new disease - a never before seen response to sedentary living in a sub-set of me patients, which does not appear at all in the sedentary controls, nor in previous studies of sedentary lifestyle? Well done.

Mind you, there has not been any correlation of urinary irregularities with other symptoms within any one subset, or with me on the whole.

What does it matter if this is the cause of only a subset?

There are always two sides to looking at an issue. The destruction way is to keep tearing at these sorts of studies, and at the small hopes of patients. The constructive way is to build on these studies to help explain to the rest of us who are perhaps not so qualified how they could lead to some of the symptoms we have.