#67~ Summer OI Tips + Impaired Cardiac Response upon Standing in CFS

In Eastern Medicine it is well known that Summer Time is the time for heart attacks... 
so PLEASE be Gentle with yourselves and follow the Summer Guidelines for 
PWCs that have OI, OK? 
We want to keep you HERE ♥ Happy and smiling ;)


BE SURE if you are in the Northern Hemisphere to 
follow the Normal Summer Regime to help prevent OI
by following some simple Guidelines.

There have been 2 kinds of OI associated with ME/CFS, NMH and POTS.

NMH causes a sudden drop of your "systolic BP" upon standing up...
and even  shows up maybe 5 min later.

POTS/ Postural Orthostatic Tachycardic Syndrome additionally 
causes an increased rapid heartbeat/pulse

cuz your heart is having to work SO much harder to get the 
blood circulating possibly due to low blood volume.

BP name tip reminder: there are 2 numbers 
that comprise your blood pressure as in 120/70. 

The last number is the Diasotlic 
(I remember D=Down/last) 

The First or Top number is the Systolic number.

Many folks even keep a portable BP cuff handy at home 
so they can check their BP on a regular basis

and 
NOT just at the Dr office. 
They have arm and wrist cuffs that are available at amazon.com online

if you can't get out to your local drug store..
Online is a good place to go to ready the brands available 
and compare the prices and read the comments by folks 
that have tried them before.. ;)

As always there are many more "detailed" articles you can read
about these subjects and if these simple rules do NOT handle 
your case of OI or POTS than PLEASE check with your Dr always 
to get proper medical advise to make sure you don't have 
other issues or meds that are interfering with things.


*drinking your 64 oz of water daily. I keep 2 bottles handy that total my daily needs so I don't have to "count glasses."..when my bottles are empty than I know I have had my proper amount for the day.

*if you do not have Hypertension aka High Blood Pressure, then adding Salt to your diet to increase your total blood volume can help maintain a more normal blood pressure if you have OI. This helps keeps your blood circulating better, taxes your heart less and helps get more oxygen to your brain to prevent the OI symptoms..with that said.. NEVER ASSUME and 

always check with your Dr.

I add 2 packets of EmerGenC to my water and salt mixture so I also am getting my electrolytes when I drink my water. I keep one bottle of this mixture handy and then have my additional plain water bottles available also. My salt/EmerGenC bottle lasts about 2 days... and the flavored EmerGenC neutralizes the 

salt taste depending on what flavor you choose ;) 

*Make sure to stay as cool as possible and NOT get over heated.

*When sitting put your legs UP and when lying down prop your head up.

*When standing keep moving, even a little, so you help improve your circulation and avoid blood pooling.

Keep something close by to help you keep your balance if needed..either a wall, a cane or walker, or even a convertible cane with a seat built-in. 
 

*If you tend to get water retention and swollen ankles or legs try wearing some compression socks that can be easily purchased in many places unless you need the HEAVY DUTY compression ones that your Dr can prescribe.

***Hope these tips help you have a Safer more

Enjoyable Summer***

RIP- Dennis Hopper  (May 17, 1936 – May 29, 2010)

Steppenwolf - Born to be wild 1969

                              (Soundtrack of the road film 'Easy Rider')

Thought this was worth sharing.. as many of us have or will have this issue
~ Shared from Co-cure♥

Impaired Cardiovascular Response upon Standing in CFS

[This is probably not the easiest discussion section to fully understand, especially without the tables, graphs, etc. but hopefully many can get the gist of it or some of it.  Check out the extract at least.  It says at the end, "funding was provided by the Medical Research Council, ME Research UK, Irish ME Trust, John Richardson Research Group and CFS ⁄ME Northern Clinical Network", but the (UK) ME Association is also funding important research by Dr. Newton in this area. Tom]


Extract:


" We would therefore suggest that there are a group of patients with CFS who have an underlying cardiac abnormality and it is only on performing
appropriate examination that these high-risk patients will be identified, and understanding of the physiological mechanisms that lead to the abnormality explored. It is unclear what the long-term impact of the cardiac abnormalities will have for those with CFS. However, our findings of reduced survival in those with the fatigue-associated chronic disease and primary biliary cirrhosis [31] and studies confirming a
comparable fatigue phenotype between primary biliary cirrhosis and CFS [32] would point to an (as yet) unidentified  risk for those with CFS, and our findings of cardiac dysfunction in a proportion of patients may suggest the group at increased risk."


31 Jones DEJ, Bhala N, Burt JA, Goldblatt J, Newton JL. Four year follow up of fatigue in a geographically defined primary biliary cirrhosis patient cohort. Gut 2006;55:536–41.


32 Jones DEJ, Gray JC, Newton JL. Perceived fatigue is comparable between difference disease groups. QJM 2009;102:617–24.


-----------------
Discussion


We have demonstrated that the skeletal muscle bioenergetic abnormality recently described in patients with CFS [1] associates with a similar cardiac bioenergetic abnormality. This impairment is associated with an increase in cardiac contractility on standing (i.e. the heart has to work harder for the same
degree of physiological stress), the severity of which associates with symptoms on standing in those with CFS.


Our study provides a significant way to defining a bioenergetic phenotype in those with CFS, which appears to be systemic and associates with the symptoms on standing frequently described by those with CFS. The finding of varying degrees of muscle abnormality may account for the contradictory results
in the previous CFS muscle literature [25–29] and underlines the need for a whole organ systematic approach to studies in CFS. Clearly, from this data, the cardiac status of the CFS population recruited for a given study will matter. If our CFS patients are considered as a single group, then oxidative muscle
metabolism is not significantly impaired compared with controls, as we had previously reported [1], and this would not change by recruiting greater numbers: division by cardiac status, however, suggests the presence of subgroups within the population, one of which has impaired oxidative muscle metabolism.
Within the observation that the maximal oxidative function is impaired, it is not possible to determine from these MRS experiments whether this is due to primary mitochondrial defects or alterations in muscle blood flow. Given the relationship between autonomic parameters and cardiac metabolism, the latter may well be true: further large studies are required to
confirm the true prevalence of this bioenergetic phenotype in CFS with subsequent interventional studies to explore this relationship.

We had previously reported abnormalities in proton efflux in the CFS group as a whole [1] while end-exercise and minimum pH were not significantly different. Stratification by cardiac energetics helps us to explore this further and suggest that the impaired cardiac energetic group are weaker and less able to
access anaerobic pathways, therefore producing less acid during exercise and having smaller proton effluxes post-exercise.


Considering the high prevalence of orthostatic symptoms in CFS [2], it was no surprise to find strong correlations between cardiac bioenergetics and cardiovascular responses to standing. The relationship between cardiac contractility on standing and
symptoms was an important finding as it suggests that symptoms in those with CFS are potentially modifiable by treatment of the underlying cardiac abnormality. These abnormalities were CFS-specific, as there were no such correlations in the control population.


At this stage, we have not proven causation, and it is difficult to determine whether the impaired cardiac bioenergetics in CFS ⁄ME represent 'cause' or 'effect'. Two mechanisms are possible.
First, those with CFS have an intrinsic cardiac abnormality [30] that leads to impaired functional cardiac impairment, subsequent hypotension and reduced organ perfusion, all of which manifests as the characteristic symptoms of CFS. Alternatively,
afterload abnormalities involving impaired vascular
response to orthostatic pooling may lead to a secondary cardiac dysfunction. Our findings of a relationship between total peripheral resistance and cardiac bioenergetics would support this alternative hypothesis, but further work is needed to elucidate
each of these mechanisms completely.


When we considered cardiac energy metabolism in the
whole CFS patient group, this appeared to be mixed, with many individuals falling in the normal range with some individuals showing impairment. This suggests that within the symptom complex of CFS, there is a group of patients in whom an actual cardiac abnormality is present (defined by the presence of PCr ⁄ATP ratio < 1.6 [17]). The heterogeneity of patients included in CFS studies is well recognized, however,
despite the usage of specific diagnostic criteria for inclusion, and we could not symptomatically differentiate between the normal and impaired cardiac energetic group. This underlines how important it is to correctly characterize patients with CFS and to study the underlying physiological parameter rather than the symptom complex. We would therefore suggest that there are a group of patients with CFS who have an underlying cardiac abnormality and it is only on performing appropriate examination that these high-risk patients will be identified, and understanding of the physiological mechanisms that lead to the abnormality explored. It is unclear what the long-term impact of the cardiac abnormalities will have for those with CFS. However, our findings of reduced survival in those with the fatigue-associated chronic disease
and primary biliary cirrhosis [31] and studies confirming a comparable fatigue phenotype between primary biliary cirrhosis and CFS [32] would point to an (as yet) unidentified risk for those with CFS, and our findings of cardiac dysfunction in a proportion of patients may suggest the group at increased risk.


This study has examined the tolerability and diagnostic
potential of assessment protocols that examine haemodynamic responses to immediate and prolonged standing in CFS and, for the first time, examines the relationship between measures of cardiovascular function, cardiac energetics at rest and muscle
energetics under exercise in CFS patients. HUT is one of the assessment modalities of choice in the evaluation of those with unexplained syncope, and is recommended in national and international guidelines [33–35]. In contrast, the UK NICE CFS guidelines [36] actively discourage the assessment by HUT.

This is surprising considering the apparent pathophysiological overlap between neurally mediated hypotension and CFS [37,38,39]. Our study confirms a comparatively high diagnostic rate in CFS particularly in those with a history of syncope. We would recommend therefore that referral for cardiovascular
testing, including HUT testing, is encouraged in those where symptoms on standing are predominant, and particularly where there is a history of syncope or presyncope. Importantly, our positivity rate in our control group was similar to previous controls [40].


This study has some limitations. The study group could
clearly be considered to be self-selected, and as a result biased, as they were recruited via the local patient support group. However, all participants had been seen within a local CFS service within 2 years and been diagnosed with the formal Fukuda criteria. A further limitation is that this study cannot establish a
direction of causality for the associations seen in cardiac metabolism, skeletal muscle metabolism and autonomic function. The findings are, however, consistent with a model in which a cardiovascular impairment might lead to impaired oxidative function, perhaps through impaired venous run-off post-exercise.

Our future work will involve assessing groups of newly diagnosed CFS patients to determine their cardiac and muscle phenotypes and following them through time. In addition, largescale bioenergetic phenotyping of cohorts of patients with CFS are required with a view to understanding those biomarkers that are unique to CFS, which will subsequently allow the development of investigative treatment algorithms specific to this disease.


Sources of funding
Funding was provided by the Medical Research Council, ME Research UK, Irish ME Trust, John Richardson Research Group and CFS ⁄ME Northern Clinical Network.


Author contributions
None of the funders contributed to the design, performance or interpretation of the results of this study.
---------------
'Impaired cardiovascular response to standing in Chronic Fatigue Syndrome' Hollingsworth KG, Jones DE, Taylor R, Blamire AM, Newton JL. Eur J Clin Invest. 2010 May 20. [Epub ahead of print]


Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.


http://www.ncbi.nlm.nih.gov/pubmed/20497461


[TK: I've spaced this out a little]


Abstract


Background:
Impaired skeletal muscle metabolism is recognized in chronic fatigue syndrome (CFS).


This study examined the relationship between skeletal and cardiac muscle function and symptoms on standing in CFS using magnetic resonance spectroscopy (MRS) and impedance cardiography.


Materials and methods:
Phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio by cardiac MRS, PCr/ADP and proton efflux by muscle MRS were performed in 12 CFS (Fukuda) and 8 controls.


Head up tilt (HUT) and cardiac contractility (left ventricular work index, LVWI) (n = 64 CFS and matched controls) were found.


Fatigue impact was accessed by Fatigue Impact Scale and orthostatic symptoms by Orthostatic Grading Scale (OGS).


Results:
Cardiac PCr/ATP correlated with measures of muscle bioenergetic function (half-time PCr recovery [kappa = -0.71, P = 0.005] and half-time ADP recovery [kappa = -0.60, P = 0.02]) suggesting that the muscle and cardiac bioenergetic function correlate in CFS.


Four of 12 (33.3%) CFS patients had PCr/ATP values consistent with significant cardiac impairment.


Those with impaired cardiac energy metabolism had significantly reduced maximal and initial proton efflux rates (P < 0.05).


Cardiac PCr/ATP ratio correlated with myocardial contractility (LVWI) in response to standing (P = 0.03).


On HUT, LVWI on standing was significantly higher in CFS (P = 0.05) with symptoms on standing (OGS) occurring in 61/64 (95%) (vs. 25/64 [39%] controls; P < 0.0001).


OGS scores were significantly higher in those with abnormal LVWI responses to standing (P = 0.04), with the LVWI on standing correlating with OGS scores (r(2) = 0.1; P = 0.03). HUT was positive in 19 (32%).


Conclusions:
Skeletal muscle and cardiac bioenergetic abnormalities associate in CFS.


Cardiac bioenergetic metabolism associates with increase in cardiac contractility on standing.


Haemodynamic assessment in CFS is well tolerated and safe with a high diagnostic yield comparable with unexplained syncope.


PMID: 20497461 [PubMed - as supplied by publisher]