Risk of stroke in patients with atrial fibrillation -with and without anticoagulation

Previously, I had commented on the risk of stroke in atrial fibrillation patients not treated with oral anticoagulants (OAC).In that commentary I quoted Dr. Overvad -"...current guidelines discrepancies also reflect the fact that the level of stroke risk among men with a score on 1 and women with a score of 2 is on the borderline of where the  impact of anticoagulation  treatment shifts from beneficial to harmful."  His comment seems reinforced by a recent publication in Circulation.

After that commentary I became aware of a very important -and perhaps dogma changing- article published in Circulation by GR Quinn. I added an addendum to that post but  the article is important enough to be highlighted in another commentary. I re-post that addendum here:

"Unfortunately I became aware of the 2016 Circulation article by GR Quinn et al after the above commentary was published.  That very important article  provides good reason to question the dogma that the CHA2DS2-VASc scores translate to fixed stoke rate. It is generally accepted that if a person's stroke rate is estimated to be 1-2% per year then treatment with an OAC offers a  net clinical benefit and that the risk score clearly relates to a quantitative stroke risk, e.g. a CHA2DS2-VASC score of 1 means the person has a risk of about 1 % per year and a score of 2 indicates a risk of 2%. 

However, analysis of 34 studies of patients not treated with anticoagulants demonstrated that the stroke rate varies widely in various cohorts. For example, with a risk score  of 2, 27% of the cohorts reported a stroke risk of less than 1% and 33% reported stroke risk greater than 2% per year. So the correlation between risk score and stroke risk varies with the cohort studied.The numbers from the Northern European studies formed the basis of the alleged relationship between the CHA2DS2-VASc score and annual stroke risk and the North American Cohort analyses indicate significantly lower ( about 1/3 of the European rate) stroke rates for untreated AF.

 Quoting from the authors conclusions: ' The majority of cohorts did not observe stroke rates that would indicate a clear expected net clinical benefit for anticoagulating AF patients with a CHA2DS2-VASc score of 1 or 2.' "


Prediction is difficult, especially the future. Neils Bohr 

The most that can be expected from any model is that it can supply a useful approximation
to reality .   George Box

The old and the new paroxysmal atrial fibrillation- new questions raised by new technology

Paroxysmal atrial fibrillation (PAF) has typically been diagnosed in a patient with cardiac symptoms seeking care for   episodic symptoms  which ultimately- by either  office EKG or some monitoring device shown to have atrial fibrillation ( AF).

The medical literature is conflicted in regard to the risk of PAF versus permanent or persistent AF. It is not surprising that expert opinion in that regard is conflicted as well, While opinions may differ current US guidelines recommend oral anticoagulation( OAC) for PAF patients based on their risk assessment score. Usually the CHA2DS2-VASc score is used and a value of 2  or more would lead to recommendation of OAC.In other words. the same recommendation for persistent or permanent AF applies to PAF.Note this refers to what I will call "clinical PAF"  subclinical PAF (SCAF) has become an  clinical management  issue as huge amounts of data has become available from the rate and rhythm recordings of pace maker patients.

A 2014 report by Vanassche which analyzed data from 6563 AF patients not treated with oral anticoagulants (OAC) determined that stroke risk in permanent AF was roughly twice that of PAF.
They reported that  AF pattern ( PAF versus non PAF )  was the second strongest predictor of stroke second only to previous history of stroke. If their data are  conclusive in this regard that does not necessarily mean that OAC  not be used . Even though the risk of stroke is lower, still the stroke risk may overwhelm the risk of  serious bleeding  from OAC leading  to a positive clinical benefit or trade-off and a reasonable recommendation for OAC.

A new and expanding data base has emerged from the experience of pacemaker (PM) patients. The ability of PMs to store and analyze large amounts of rate and rhythm data has lead to the realization that typically asymptomatic bursts or runs of subclinical atrial fibrillation  are very common in PM patients, values from several studies reporting  an incidence of 30-55%.

The questions arises-is the risk of  these SCAFs equivalent to that of the classically diagnosed PAF. Further, is there value to quantitative the SCAF perhaps in terms of duration or frequency . The literature has adopted the concept of atrial fibrillation burden ( AFB) and several studies have attempted to determine if there is a correlation between PAF ( as in minutes per day) and stroke risk). More importantly  is it possible to find an AFB threshold associated with a clinically important risk of stroke or how much SCAF is necessary to warrant OAC.

In general ,reports  of these attempts  indicate  there is a correlation between PM detected  AFB and stroke risk , however the reports differ in regards to  finding  burden levels that demonstrate an increase hazard ratio- usually in the range of 2 or under (and  sometimes statistically significant and sometimes not). The small number of events of interest-stroke and peripheral emboli- in various duration based subgroups lead to wide confidence intervals and HR values that fluctuate as burden levels increase-sometime being statistically significant at lower levels but  surprisingly not at higher which was the case, for example in the SOS-AF project.

Some of the of  AF burden levels at which a increased hazard ratio (HR) for stroke or other embolic events) have been reported from various studies are shown here: ( note with one exception runs of SCAF less than five or six minutes-depending of the particular study-are not analyzed.) So to date with one recent  exception there is essentially no data on the risk of SCAF events of less than 5 minutes

ASSERT six minutes
TRENDS -5.5 hours
SOS AF - one hour
CARELINK/VA 5.5 hours

These studies were reviewed by Chen-Scarabelli et al in 2015 and also by Camm et al in 2016 and they reached opposing conclusions. Camm's review concluded that data were insufficient to recommend OAC in SCAF while Chen-Scarabelli  and Kenneth  Ellenbogen said that OAC should be initiated on the basis of stroke  risk assessment using the CHA2DS2-VASc score regardless of the mechanism of detection of the atrial fibrillation.

 In the observational TRENDS project, data from 3035 PM patients were analyzed. Those characterized as a "low" AF burden (AFB) ( low is  defined as less than or equal to 5.5 hours on an single day) gave a risk estimate similar to having zero  AF.  An AF burden of greater than 5.5 hours doubled the thromboembolism risk.

Also a sub-study of the TRENDS project showed that 29 of the 40 patients who had a embolic event had no AF detected in the 30 day period  preceding the event suggesting that the relationship between AF and stroke may not be a simple as the former invariably causing the latter.  


As Glotzer and his co-authors in the TRENDS project emphasized, the available data-even combining data from several studies as  was done in the SOS AF project- do not necessarily make it possible define a "safe "AFB that confers no risk greater than observed with no AFB. The event rates ( i.e stroke and other embolism events) are low in all of these studies, lower than predicted based on a widely accepted 4% per year rate in atrial fibrillation patients) and this  limits statistical precision and produces wide confidence limits as well as limits the number of threshold ranges that can be analyzed with the expectation of statistical significance.

 Small numbers in each  duration subgroup lead to results that sometimes seem counter intuitive- for example : In the SOS AF a statistically increased HR was found for the five minutes cutoff and the one hour cutoff but not the six hours or 12 hour or 23 hour. A long duration would have been thought to impair a higher HR.

The RATE RHYTHM study was designed to determine if there is a definable burden of AFIB that will be predictive of thromboembolic events. At this writing I have only access to an abstract of the findings. I believe that the investigators found there were no risk for bursts of atrial fibrillation less than 20 seconds. . 


The data indicate  that the risk of PM detected SCAF is lower than the clinically detected classical PAF but there is a  correlation between SCAF and stroke risk and SCAF is an independent risk factor for or  predictor of stroke. ( An independent risk factor is not necessarily causal- see here) .  Of course  the question is with the variable  coarse- grain risk values derived from any of  these studies is anticoagulation for these SCAF warranted and in that regard there is not unanimity of expert opinion.

Guidelines ,with the exception of the Canadian Cardiovascular Society guidelines, do not recommend  specifically to give OAC for device-detected AF. The Canadians suggested that OAC could be given to patients 64 and older with a CHADS score one or more who have SCAF episodes lasting a day or more  or for those with a shorter interval if they have recently had a cryptogenic stroke. ( ref 1)

A number of researchers have argued that randomized trials are needed to determine the clinical  benefit for OAC in PM detected   PAF. Two such trials are now in progress The ARTESIA project aims to enroll 4000 patients and randomize patients with at least one episode equal to or greater than 6 minutes of AF  to either apixaban or aspirin. 2019 is the projected end date.  Note even after this trial is complete there will still not be any RCT level evidence about what to do with patients  with AF burdens of less than 6 minutes per day.  The NOAH project will compare edoxaban or aspirin/placebo in patients over 65 years of age with one additional CHA2DS2VASc risk factor.

RCTs do seem to be needed, I believe we have learned all we can from the type the observational trials mentioned above and expert opinion differs regarding the management of SCAAF detected by PM recordings. An optimistic view is that these 2 RCTS may allow recommendations regarding OAC and device detected to move past battling expert opinion and trying to tease clinical truth from conflicting observational data.


1.Verma A et al 2014 Focused update of the Canadian Cardiovascular  Society Guidelines for the Management of Atrial fibrillation. Can J Cardiol. 2014 30 114-1130

update 12/16/16 A paragraph inadvertently omitted was added. 
addendum 1/18/17 and 2/4/17  several minor changes made in syntax and typos corrected.

How do patients with atrial fibrillation do when not treated with anticoagulants?

Clinical guidelines and conventional medical wisdom all recommend oral anticoagulation (OAC) for patients with atrial fibrillation who are determined to have an increased risk of stroke according to widely used risk indicator tools. Usually the CHA2DS2-VASc risk assessment tool is used and for   patients with a risk score of greater  than  or equal 2 ,OAC is generally recommended.European and Canadian and U.S.  guidelines differ  in regard to recommendations for risk score of 1. For risk categories 0 and 1 there are no randomized clinical trials demonstrating the net clinical benefit of OAC . Those recommendations are driven simply observational trials and  expert option seems to vary geographically.


 According to a 2016 article by Overvad et al :. "current guidelines discrepancies also reflect the fact that the level of stroke risk among men with a score of 1 and women with a score of 2 is on the borderline of where the impact of anticoagulation treatment shifts from beneficial to harmful."( ref 2)
In simple terms-it is a close call. 

 The clinical issue is the trade off between OAC reduction in ischemic stroke risk and the risk of serious bleeding complications the worse of which is intracranial hemorrhage. Importantly and perhaps ironically the higher the CHA2DS2 score , the higher the risk of major hemorrhage. Analysis (ref 1)  of over 44 thousand in the Military Health System patients with non-valvular atrial fibrillation over a 2.5 year period treated with rivaroxaban demonstrated a strong relationship between the risk score and the risk of major bleeding.So the patients at the highest risk of stroke are  the same people who have the highest risk of major hemorrhage.,especially those with the high vascular disease components of the risk score score.The data indicated that while the risk of hemorrhage increases with the risk score the stroke risk increases more so it is generally believed that there is net clinical benefit even at the highest hemorrhage risk levels.

Hess et al published a study focused on data from a outcomes registry for patients with atrial fibrillation in part to determine if patients with afib were being treated according to  accepted guidelines.(American Journal of Medicine 2016 , Nov 22).See here for link to abstract.

There were 9555 patients with afib and 1846 of those were not being treated with OAC even though they had a CHA2DS2-Vasc score greater than 2.

Interestingly the stroke risk in those not treated compared with those who were treated was not statistically significantly elevated.. The adjusted HR was 1.18 with a 95% Confidence interval of 0.91--1.54.

It is often stated that risk of stroke in afib patients is increased by a factor of 3- 5 (based on Framingham data) and that OAC may decrease that risk by 60% or more.Yet in this large data base OAC did not seem to bring about that degree of benefit. However, absence of OAC was associated with a statistically significant increase in risk of death. ( HR 1..22 (1.05--1.41).

So how do patients do  with atrial fibrillation  not treated  with OAC ? Based on this observational data- better than you might expect. On the other hand if we look at older data from a randomized clinical trial published in 1991 ( SPAF trial) the stroke risk per year for the placebo arm was 6.3% versus the warfarin  arm which was 2.3% and surprisingly the aspirin  arm was 3.6%.Later studies never confirmed the value of aspirin  in stroke prevention in afib but the SPAF numbers conform with the broad brush comments that the risk of stroke is about  three to five times and the risk reduction from OAC may be in the 40-60% range. The BAFTA study not only failed to show the value of aspirin in stroke reduction in afib patients but demonstrated that in older patient s ( over 75 years of age) aspirin caused a similar risk of intracranial bleeding as warfarin.


So the question remains why did the patients without treatment do so well in Hess's data or maybe the real life treatment of afib with OAC is much less impressive than it  is in randomized clinical trials or maybe there are so many potential biases in observational big data exercises  that solid "take home" messages are difficult to find and/or rely upon..

And things get even murkier or perhaps more clear when Dr. H. Kamel  discusses challenges to the notion that the risk of stroke in afib is in fact  solely due to   thrombi in the left atrium and proposes  that things are much more complicated including the notion that at least sometimes a stroke can cause an atrial thrombus. It is well known that stroke can precede the onset of afib.He and coauthors discuss a new model for stroke and afib in which both afib and emboli are downstream  effect of abnormal atria substrate (an atrial myopathy).This model might explain why stroke  risk is not eliminated by rhythm control strategies and why stroke can predate afib and generally the poor temporal relationship that exist between afib onset and stroke and why some reports do not show a dose response relationship between afib duration and stroke(.However, other reports such as the TRENDS data do show  dose response relationship .)

Drs Akar and Marieb make similar comments and say in part "...AF may simply be a marker of underlying conditions that causes stroke as opposed to an active participant in the stroke  pathogenesis"

 In short, they are saying  there   is reason to believe there is much  more to it than simply that afib cause thrombi in the left atrium and the clot embolizes  to the brain. although no one is saying that does not happen (" Atrial Fibrillation and Thrombogenesis:Innocent bystander or guilty accomplice", JACEEP 2015, 2015;1(13) p 218.

Another article  (ref 3) tends to support the notion that there is more to afib and stroke than the century old model that the former simply  leads to the later.Boriani published a study evaluating the risk of stroke in men and women with pacemakers and found that atrial fibrillation of at least five minutes occurred in 44% of 2398 patients and that a higher atrial fibrillation burden was not associated with a higher stroke risk. Confirming other studies this analysis found the stroke and TIA risk in women was twice that on men.

 references

1.Peacock,WF et al CHA2DS2-VASc Scores and Major Bleeding in Patients with Nonvalvular Atrial Fibrillation Who are Receiving Rivaroxaban.Annals of Emergency Medicine, published online, accessed  12/4/16

2. Overvad TF et al. "Treatment thresholds for stroke prevention in atrial fibrillation :observations on the CHA2DS2-VASC Score" Euro Heart Journal-Cardiovascular pharmacology Published on line August 2016

3. Boriani, G et al " The increased risk of stroke/transient ischemic attack in women with a cardiac implantable electronic device is not associated with a higher atrial fibrillation burden. Europace: 2016, dec 28.

"Truth is much too complicated to allow anything but approximations" John Von Neumann 


Addendum: 12/22/2016. Unfortunately I became aware of the 2016 Circulation article by GR Quinn et al after the above commentary was published.  That very important article  provides good reason to question the dogma that the CHA2DS2-VASc score translate to fixed stoke rate. It is generally accepted that if a person's stroke rate is estimated to be 1-2% per year then treatment with an OAC offers a a net clinical benefit and that the risk score clearly relates to a quantitative stroke risk, e.g. a CHA2DS2-VASC score of 1 means the person has a risk of about 1 % per year and a score of 2 indicates a risk of 2%. 
 However, analysis of 34 studies of patients not treated with anticoagulants demonstrated that the stroke rate varies widely in various cohorts. For example, with a risk score  of 2, 27% of the cohorts reported a stroke risk of less than 1% and 33% reported stroke risk greater than 2% per year. So the correlation between risk score and stroke risk varies with the cohort studied.The numbers from the Northern European studies formed the basis of the alleged relationship between the CHA2DS2-VASc score and annual stroke risk and the North American Cohort analyses indicate significantly lower ( about 1/3 of the European rate) stroke rates for untreated AF.
 Quoting from the authors conclusions: " The majority of cohorts did not observe stroke rate that would indicate a clear expected net clinical benefit for anticoagulating AF patients with a CHA2DS2-VASc score of 1 or 2."
  

Set point theory of threshold of physical actiivity to maximize the "health span"

Dr. Lazarus and Harridge from King's college in London have suggested that by observing the trajectory of decline in physiological parameters in highly trained athletes we are observing the diminution  of function due solely to aging. In other words, there is no confounding issue of inactivity's effect of time related losses in function.

They talk about a "set point" for optimal exercise  and a threshold of physical activity that is needed  to age optimally and to thereby optimize the so called health span.Exercise above this hypothetical set point would increase a person's athletic performance but may not positively affect health.

This is reminiscent of Busse's 1969  concept of primary and secondary aging wherein such things as exercise ( I suppose the nebulous optimal amount) and eating right ( if we can ever figure out what that is exactly) would would minimize secondary aging  but primary aging would trudge along unimpeded.

Is Medicine increasingly less about physicians and patients and more about "Big Medicine"?

By "big medicine", I mean to refer collectively to the large organizations that form much of the medical landscape in the U.S. These organizations are: insurance companies,HMOs,Big Pharma (large pharmaceutical companies ) and corporate not - for -profit hospitals and now ACOs.For economy of key strokes let us call it Bigmed. (Of course, not for profit needs to be in air quotes,)

Increasingly Bigmed controls the practice of medicine. This is not breaking news. Dr.Roy M. Poses has been writing and speaking about this issue for years. In 2003 he published an article describing the results of interviews he had with a number of physicians who expressed this key idea. "Medicine had been taken over by large organizations which did not honor the core values of physicians."

Poses has been prolific and tireless in efforts to address these (and other) threats to health care's core values and many of his commentaries can be read on the blog "Health care Renewal"

Now there are some other physicians joining the discussion.Dr. S. Supri and K. Malone have published an important commentary in the American Journal of Medicine in part striking similar themes to Dr. Poses.

Remember when the economist Alain Enthoven  rallied against the power of individual physicians , comparing the situation to that of herding cats , animals notoriously resistance to herding.Well, now the hospitals and clinics and other health care facilities are swarming with herds of  docile  trained cats who have not only leaned to dutifully bend over computers and enter required "quality" data  but also have  leaned helplessness. 

More evidence of brain damage in NFL players

More evidence of   the brain damage that occurs  in  professional football players   was presented at the 2016 meeting of the American Academy of Neurology.See here.

Abnormalities in diffusion tensor imaging (DTI) and standard MR were found in a number of former NFL players . DTI reflects abnormalities in water molecule movement in white matter tracts. Dr. Francis Conidi studied 40 retired players 17 of which had positive findings on DTI .The average time in the league was 7 years and the average number of reported concussion was 8. Most of the players with findings were lineman. Linemen are less likely to sustain the very hard impacts that cause concussions and broken necks  but just watch  line play in a game for a few minutes and you can easily see the number of sub concussive head impacts that routinely  occur.

addendum: 12/27/16 On a recent Sunday night football ( or was it Monday or Thursday) I noticed the pre game comments by the announcer pointing out that 3 of one team's starting lineup would not play because they were on the concussion "protocol". Several years ago those players would likely be in the lineup. The point being concussions are very common and a short while ago no one cared.

What works best-HIIT,SIT or MICT for various aspects of the training effect?

HIIT is high intensity interval  training or interval training in which the person exercises to at least 80% of his maximal heart rate and often to 80-90% SIT is sprint interval training in which one goes all out exercising to the maximal possible.MICT ( moderate intensity continuous training) is the traditional aerobic exercise training in which the person does not get much over 50-60% of his maximal oxygen uptake.

There is not much  really new to HIIT or SIT other than the names. Roger Bannister did not invent the technique but he certainly used it in the preparation for his race ( 1954)  that broke the four minute mile. He would run ten quarter mile intervals in 59 seconds each jogging in between each. Today his training might be characterized at high intensity , low volume.


An excellent review on these 3 types of training and the important effect of exercise intensity is found in  a review by Maclnnis and Gibala (1) Gibala is Chair of the Department  of Kinesiology at McMaster University and has written extensively about high intensity interval training.

 The authors review aspects of the three training modes on mitochondrial proliferation,increases in capillary density and increases in V02 max. And the winners are for two of the three are SIT and HIIT.Only  in regard to increases in capillary density brought about by training does MICT hold an advantage but even that is in dispute as some studies show HIIT is just as good.

 In regard to all three it seems that the data strongly suggest that the key variable is intensity not duration nor frequency of training.See here for a 2016 lecture by Gibala outlining the case of interval training and the argument that intensity is the key variable.

Interval training is no longer just inside baseball type talk among athletes and coaches but has becoming mainstream in the world of rehabilitation , for example in cardiac ( see here) and pulmonary patients( see here), type 2 diabetes (see here)and heart failure patients.




(1) Maclnnis MJ and Gibala,MJ Physiological adaptations to interval training and the role of exercise intensity.J. of Physiology 2016,October 17 

Run like a Keyan or maybe better a Kalenjin

Occasionally while  running in the park I will see a T-shirt that says "Run Like a Keynan". A more precise and accurate phrasing might read "Run like a Kalenjin"

Indeed most runners might admire or envy the impressive running speed and endurance that Kenyan runners  have demonstrated

The Kakenjin tribe in Kenya account for only 12% of the total population of the county, but about 75% of the elite Kenyan runners are Kalenjins.

Danish researchers attempted to determine why Kenyans are so good at endurance running events. They found that the Kenyans do not have a higher maximal oxygen uptake (V02Max) nor a higher aerobic threshold than other elite endurance athletes  but that they simply were more efficient runners. This the researcher attributed to their body type, specifically long thin legs.That does not mean that Kalenjins do not have a high 02 max,They certainly do but that is not their distinguishing
characteristic.  Long thin legs and high V02 max and efficiency  seem to be the keys.

Exercise capacity of octogenarians and age related decline in exercise capacity

A great source for information about the exercise capacity of octogenarians is a 2013 article by Scott Trappe and co-authors.( Trappe,S et al , New records in aerobic power among octogenarian lifelong endurance athletes. JAAP, vol 114, no 1, 3-10.) See here.

The authors studied 9 life long and still competitively active  elite endurance athletes and compared their aerobic capacity as well as myocellular markers of oxidative metabolism with 6 age matched healthy non exercisers.

The V02 max (maximal oxygen uptake ) in the group of athletes was 38 plus/minus 2.1 ml/kilo/minute versus 21 plus minus 1 for the sedentary group. The authors reviewed other published data on aerobic capacity in untrained 80 year olds and found:

1) In 195 men  the average V02max was 21 plus/minus 4
2) In  269 women the average V02max was 18 plus/minus 4

These values are comparable to Trappe's non-exercising  subjects while his athletes  were said to have the highest values reported in a group of octogenarians.(There are some individual case reports with values this high and higher-see below)

Having monitored several hundred stress tests using the Bruce protocol I find it helpful to put these 02max values in that context.

The Bruce protocol has 3 minutes stages and after each the treadmill pace and inclination increase:

Stage I 1.7 mph 10% grade using 5 METS  and requiring 17.5 ml 02/kilo/mi

Stage II 2.5 mph 12%                    7 METs                          24.5

Stage III 3.4 mph 14%                    9 METS                        31.5

Stage IV    4,2    mph 16%               13 METS                        45


Stage V    5 mph  18%                     15 Mets                          52

Stage VI     5,5 mph   20%               18 METS                       68



A MET is the resting oxygen uptake of 3.5 ml 02/kilo/min.

Based on these values many or maybe most of the male non athlete   octogenarians would complete Stage I while a number  of the females might not .Most of Trappe's athletes would likely complete Stage 111 .

One of Trappe 's'subjects was 91 years old , a former Olympic champion  ( ok he is not an octogenarian)  had an amazing  aerobic capacity of 36! He should complete stage 3 and into stage 4.

Using time estimates from Tim Noakes book (footnote 1   ) you can guesstimate  running and marathon times from aerobic capacity or  at least get a estimate of the aerobic capacity that is required to run at a given speed. An  02 capacity of 30-32 would be required to complete the 26.2 marathon in about 5.5 hours.

Ed Whitlock, dob 1931, was the first man to run a marathon in less than 3 hours at age 70 marathon.It probably takes a 02 Max of 60 to run a sub three hour marathon.

There are real life 80 year  people who complete marathons. For example, 4 men all aged 80 finished the Houston Marathon in times ranging from 4:23 to 5:40  in 2016 .The winner in this group probably has a 02 max of about 40 ( using the table from footnote 1).Also there were three 80 year olds who completed the NY City Marathon in 2016 with times ranging from 5:03 to 5:37.

In 2011, Ed Whitlock at age 80 ran the Toronto Marathon in 3:15corresponding to a 02 uptake of 50-53. This is  comparable to the report by Trive Karlsen who measured the max 02 uptake on an 80 year old Norwegian at 50 and claimed that as a world record for an 80 year old.See here. There are  a few other octogenarians who have run a sub-four hour marathon, Ed Benham ran 3:48 at age 82. and Harold Willson who did 3:58 at age 80 . These are times  probably requiring an 02 Max of around 40.

(See addendum below for update on Ed Whitlock)

,
In regard to the non superathlete male octogenarians , their average 21 ml/kilo/min aerobic capacity should allow them to be able to walk at a fifteen minute per mile pace  ( which is a fairly brisk walking  pace) which probably requires about 17 ml  02/kilo/min as does playing double tennis, doing light yard work ,etc. and a lot more than whittling on the park bench.Finishing Stage II suggests adequate 02 capacity to run a fifteen mile. (Walking a fifteen minute mile requires about 70% as much 02 uptake as does running a mile.)

It seems more than reasonable to assume that these octogenarian marathon finishers has in their youth 02 max values just as impressive for their ages then as they are now and likely could have run a marathon in less than 2 1/2 hours.

The conventional thinking is that from about age 45 to age 70 a persons aerobic capacity declines somewhere between 5% and 10 % per decade. Some studies have shown and other studies have presented contradictory evidence  that those who continuously train aerobically  have a lower rate of decline. ( Personal note-A rough calculation based on my marathon times suggest that my decline was slightly over the 10% per decade number)

Some of subjects in the non athletic group had V02 max values approaching the range that have been proposed as a threshold value for independent living(18 ml/kilo/min) and as a threshold for disability assessment ( 15 ml/kilo/min) refs 2 and 3

The lower the 02 max, the higher percentage of it is used  for the typical  activities of everyday life leading to fatigue and predisposition to inactivity and deconditoning. Further the increased oxygen consumption  attendant to trauma , acute illness and surgery may push someone with a 18 -20 02 max over into the disabled category .

addendum: 10/19/2016- Ed Whitlock,at 85 years old, finished a marathon In Toronto in 3 hours and 56 minutes -over a half hour quicker than the previous record for that age for the marathon.

 On March 13, 2017 Ed Whitlock died of prostate cancer at age 86.

footnotes:

 1.Table 2.3 page 66, Forth Edition of "Lore of Running " Tim Noakes

2 Jackson, AS et al Effect of lifestyle and aging on the longitudinal change in respiratory fitness. Arch Int Med. 2009,169 ,1781

3 Putz, C et al  Incremental shuttle and six minute waking tests in the assessment of functional capacity.in Chronic Heart Failure.Can J Cardiol 2008 24 (2) 131-134



Addendum: 3/19/18 Having just discovered the "VDOT" tables and an  on line calculator devised by noted running coach Jack Daniel and having compared those values with estimated values  based on the Bruce protocol results including my own I believe that in the future I will be using those rather than those found in Noakes table 2.3.

Exercise intensity and risk of atrial fibrillation-a possible gender specific effect

Dr, S. Moharty  et al have presented a meta-analysis on the relationship between exercise level and risk of atrial fibrillation (AF). In what is the largest data analysis to date on this topic they found that  women's risk of AF is reduced at all levels of exercise while in men low and moderate levels of exercise seem protective risk of AF increases at the highest levels.

The term coined by Jim Manzi,( ref 5)  "high causal density", seems appropriate in regard to the etiology of AF. Both inactivity and allegedly " too much exercise" both increase the risk of AF as do aging,obesity, alcohol , hypertension ,  perhaps pericardial fat deposition. and apparently being too tall as well as a number of other putative risk factors.The trick is to figure out what is "too much". Moharty's paper suggests there may be  no "too much" for women ,at least they did not demonstrate a threshold, a claim  which I believe has not been made before.

Reviewing 22 studies (665,750 subjects) they found:

1) In men moderate exercise was protective ,OR .72 , while vigorous exercise increased AF risk with an OR of 3.30 (1.97--4.63). When the authors excluded some small case control studies that had very wide confidence intervals the estimated  risk level was reduced but not eliminated to OR of 2.45 ( 1.1-3.8)


2 )In women moderate exercise was protective with an OR of 0.91 while vigorous exercise seemed even better with an OR of  0.72. So for them more was better without discernable  limit?

Previous studies were conflicting with some showing in men the so called J or U shaped curve while others claimed greater physical activity was associated with a lower risk of AF. i.e. a continuing downsloping risk curve as exercise levels increase. Moharty's study indicates that in women the curve is continuously down sloping and supported the existence of a  U-shaped curve in men.

 Intensity levels of exercise in most (all?) of the studies is at best a "coarse grain" indication. Some  of the exercise levels were based on the subjects' declaration of  their exercise level. In Anderson's study of cross country skier exercise  level was defined as finishing one race versus those who finished 5 or more. In some trials AF was self reported, in others AF was  physician confirmed. Often exercise level reflects duration of exercise per week with no consideration of level of intensity of exercise and  some times quantified by number of endurance events completed usually without consideration of intensity, i.e completion times.

The effect of men's age on risk of AF at various exercise levels is also a consideration. At least it seemed to be in Aizer's paper. This was an analysis of AF in men in a post hoc analysis of the randomized aspirin study as part of the Physicians health study. (Ref 1) The only increased AF  risk was shown in men less than age fifty at the highest self reported exercise level.Suggested non-causal explanations for this include survivor effect and the increased risk of so called lone-AF in otherwise healthy runners  typically occuring in a younger or middle aged man 

Another study presented data that suggested increased risk of AF in younger but not older men. This study  by Nikola Drca from Sweden  was a long term followup of 44,000 men with retrospective estimates of their exercise levels. Those 30 year olds who exercised more than 5 hours per week has an increased RR (1.19) but that was not the case for fifty year olds.  Again, could this be a survivor effect or a high number of so-called "lone parasympathetic AF" in the younger runners? Here we have the relative risk of less than 2, a topic I have ranted about before. An age differential effect was not mentioned in Moharty's paper.

Being the pattern seeking story telling creatures that people are ( ref 4) there are bound to be speculations as to why/how this purported  gender difference could occur. Here is one such such speculation found in a 2011 article by Wilhelm ( ref 3). The authors compared male and female non elite runners and found that the men has subtle changes in diastolic function, slightly large left atria ,changes in heart rate variability and higher BP during exercise, a constellation of findings arguably making male runners, holding training levels constant, more at risk for AF and in fact 4 of the 70 men  studied did have episodes of paroxysmal AF.

How to determine where moderate ( and allegedly therefore benefit) ends and excessive ( and allegedly therefore harm) begins either with group data or for an individual is the problem, one that I suspect is not solvable.



ref
1. Aizer,a et al. Atrial fibrillation is association with different levels of exercise at different ages in men. Heart 2014;100, 1037-1042.

2.Drca, N Atrial fibrillation is associated with different levels of physical activity at different ages in men. Heart, 2014 ,100 (13), p 1037

3. Wilhelm, M et al.Gender Differences of atrial and ventricular remodeling and autonomic tone in non elite athletes.American Coll cardio nov15,2011, vol 108, pg 1489


4."Humans are pattern seeking story telling creatures and are quite adept at telling stories about patterns whether they are true or not.: Usually attributed to  Michael Sherma.The phrase became a theme for Ed Lemer, UCLA economist, in his Book "Macroeconomic Patterns and Stories.


5."Uncontrolled:The surprising payoff of trial-and-error" Jim Manzi ,2012 Basic Books

Endurance exercise athletes heart works differently from the untrained but how much is training and how much genetic?

People who do endurance exercise training may re-model their hearts in a way that not surprisingly facilitates exercise but also this may have public health implications in regard to
the increasing incidence and prevalence of diastolic heart failure, more properly labelled as HFpEF(heart failure with preserved ejection fraction.

The exercise physiology party  line had been for years-probably fifty or more- that as one increases his level of exercise, both heart rate  and stroke volume (SV) increase together up to a point. That point is around a heart rate of around 120 or a work load of about 40% of  02Max at which time the SV levels off. The thinking was that at higher heart rates diastolic filling time will become  so limited that SV would flatten out at a relatively low heart rate More recent data indicate that while  that pattern is what happens when the untrained person exercises , a different pattern has been observed in ( at least some) well trained endurance athletes and this difference may be due in part to impressive diastolic function .

The endurance athlete continues to increase the SV to levels higher than the text book limit of a heart rate of 120  and several authors including Gledhill et al ( ref 1 below) showed no plateau to the SV in heart rates up to 200 beat per minute in trained endurance athletes. Their ability to continually  increase stroke volume was attributed to not only enhanced ventricular emptying but to a even greater increase in ventricular filling. The left ventricular ejection time was longer and the diastolic or filling time was shorter. Not only could they push blood out better they could suck blood into the ventricle even  better.

This enhanced ventricular filling make the endurance  trained group better able to use the Frank Starling mechanism. ( Shifting the curve up and to the left) Further the greater blood volume seen in endurance athletes helps maintain adequate filling pressure and end diastolic volume given the shortened filling times that occur with heart approaching 200 beats per minutes. The greater ability to empty out the ventricle leads to a greater recoil from a lower end systolic volume with a greater suction effect enabling better filling.

The athletes were able to , for example, refill the ventricle with each 188 ml stroke volume in 0.1 sec.

Levine and co workers have shown similar patterns of  enhanced diastolic function in older endurance athletes.  (ref 2)

 Gledhill compared young ( average age 22) untrained subjects with a 02 max of about 40 with a trained group with  02 max of 60 plus. ( Group average for  the untrained was 44 versus 68 in the trained). So the trained group has 02 max values typically associated with folks who can run a sub-three hour marathon.  A trained person with a baseline of 44 V02 max  would be expected to be able to run a marathon in under 4.5 hours. (Estimates are from data of Davies and Thompson as depicted in table 2.3 in Noakes' Lore of  Running, 3rd edition.) Obviously Gledhill's endurance trained group  were rather far out on the curve of ability to exercise  and though they trained hard you have to wonder how high was their 02 max before training.

The authors of this and several similar articles hoped to study how fitness levels modify the heart and vascular system response to exercise. However the authors realized that this type of cross-sectional study cannot tease out the effect of  training from the effect of genetic endowment,
 
Quoting Gledhill:

"It is not possible to state with certainty ,based on these findings, that the difference in cardiac function between endurance trained athletes and normally active individuals is an adaptation to endurance training, a consequence of genetics or a combination of these influences."

 So far all of this seems little more than inside baseball physiology talk but could there be a broader significance ?

A optimistic " maybe" seems to be the view of Dr. Benjamin Levine of Southwestern Medical School (see reference number 3).

Levine's et al showed that there was some preservation of diastolic function-i.e ventricular compliance as measured by echocardiography  (E/a ratio etc) as a function of the amount of long standing aerobic exercise and it seemed proportional to the amount of exercise. Long term exercisers had better compliance ( aka measure of ventricular stiffness) while measurements of "relaxation" decreased in the exercisers to about the same degree with aging  as the sedentary group-this was measured by the relaxation time (IVRT) of the left ventricle.IVRT is the time between closure of the aortic valve and the opening of the mitral valve.

On the other hand, Hirofumi Tanaka et al from Colorado  (see reference 4) concluded that the compliance was not preserved in the long term exercisers ( though I believe  some of his data was not really inconsistent with that hypothesis) while  there was a beneficial modulation of the age associated stiffness in the large elastic arteries ( as measured by the aortic pulse wave velocity)

 Levine ( reference 5) has suggested that the long term endurance exercise ( maybe as "little" as 2-3 hours per per week) can prevent the decrease in left ventricular compliance associated with aging and/or inactivity and perhaps have important implication for prevention of cardiovascular disease ( ie. HFpEF or diastolic heart failure).  While, in my opinion,the evidence for this is a something less than overwhelmingly convincing this  is a  reasonable possibility and it would be very nice to think so, particularly to someone who has done a lot of running over the years.


A mechanism by which exercise may help to maintain  ventricular compliance has been outlined by Hyo-Bum Kwak ( ref 6) on the basis of rat research into apoptosis or programmed cell death and exercise. Myocytes decrease in the aging heart and this is in part thought be due to a mitochondrial-mediated apoptotic pathway. Kwak has shown that exercise training decreased these apoptotic pathways .



 "Reason is, and ought only  to be, the slave of the passions and can never pretend to any other office than to serve and obey them." David Hume "Treatise on Human Nature"circa 1738.


references:

 1.Gledhill, N. et al  Endurance athlete's stroke volume does not plateau:major advantage in diastolic function.Medicine and Science in Sports and exercise,26, pp 1116-1121, 1994

2.Levine, BD et al. Left ventricular pressure volume and Frank-Starling relations in endurance athletes.Circulation 84:1016-1023.1991

3.Prasad,A The Effects of Aging and Physical Activity on Doppler measurements of diastolic function. Am J Cardiol 2007, 99, 1629

4.Tanaka, H Endurance exercise performance in Master's athletes age-associated changes and underlying physiological mechanisms.  J Physiol 586, 2008, 555-58

5.Bhella, P Impact of Lifelong exercise "dose"on left ventricular compliance and distensibility
JACC 641257-1266,2014

6. Kwak,H , Effects of aging and exercise training on apoptosis in the heart. J exer Rehabil 2013 apr 212-219


addendum several additions made to introduction to text-2/4/17

Health care with other people's money- what could be wrong with that?

Paying for health care with other people's money-what could possibly go wrong?

Dr. Paul Hsieh answers the question posed in the title in a commentary in Forbes. See here.

He outlines four important ominous consequences of basing health care on spending other people's money.

  This excellent article should be read in its entirety but let me briefly  comment on the first in the list.

"Doctors will be increasingly expected to save money for the system  ."

This is already happening.Various medical professional organizations are re-writing traditional medical ethics, pushing the fiduciary duty of the physician to the patients into the memory hole and substituting the bogus concept of the physician as a steward of society's medical resources which at least one physician's organization (the ABIM Foundation) has strangely linked to social justice. I have ranted about this before but the caravan rolls on and increasingly  the rhetoric  in various medical forums emphasizes saving money for the system. It seems that the medical professional elite would have us believe that the road to social justice is for physicians to follow guidelines, which may not be designed for patient benefit alone but also for cost containment for the third party payers.

The medicine of the collective is replacing the medicine of the individual. This is being promoted in part by what I have called the progressive medical elite who, to a frightening degree, seem to occupy the leadership positions in many influential medical organizations . Their unspoken mantra is that medical care is too complex and too important to be left to the individual patient and his physician. Wise leaders with ideas need to be in charge. Of course, it is promoted by the third party payers, private and public, who may well consider the medical professional  elite in this ethical paradigm shift as useful idiots.

 The third party payers and the professional medical elite have attempted to turn traditional medical ethics around so that the fiduciary duty to the patient is somehow replaced by an ethical duty to save money and the whole flim-flam activity is sprinkled with non sequiturs  about social justice. Social justice is typically taken to mean redistribution and if cost to the system is reduced it is difficult to see wherein the redistribution lies if everyone gets less.Everyone, of course, except the third party payers.

  In regard to private property the owners have the incentive to be a "good steward" of their resources.You have to ask what is the incentive of physicians to act as stewards of a mythical  collectively owned resource? If everyone owes it , no one owns it and no one has the incentive to care for it.

The notion of "the system" [in regard to medical care] while a rhetorically useful notion for a certain agenda, is basically fallaciously  aggregating elements that do not belong together. In short, there is no system for health care just as there is no car delivery system or a home building system. It makes no sense to speak of the situation in which someone buys a new car as a cost to the car supply system or a person buying a home as a cost to the home supply system.All of these are transactions in which there are buyers and sellers and exchanges take  place.Mr Jones gets a CT  of  the abdomen.. This is not a cost to any system. It is a cost to Jones and/or his insurance company while to the providers of care it is a payment. One person's cost is another person's income.To call this a cost to a system is nonsense.Unless all the health care is provided, operated and owned by  a single entity, usually the government., then the services provided  could be considered  a cost to the system.

Who gains from acceptance of this bogus notion of physicians as stewards of some mythical collectively owned medical resources? The third party payers for whom the gain is obvious and the medical elite progressives who stand to gain from their position of prestige  as experts and rule makers  and the rest of us, real physicians and patients,  lose.

So, in summary there is no medical care system to which a cost is charged with every medical care transaction and secondly the physician as steward concept is completely contradictory to the traditional role of the physician as the fiduciary agent of the patient .

What is going on with the price of the Epipen?

 Scott Alexander on his blog Slate Star Codex offers this insightful explanation of what is going on with the price of the Epipen and why are there not cheaper substitutes available in the US. Actually Alexander tells us this is one.See here.

John Goodman tells a similar story here.


Disclaimer:
 I have never actually used an Epipen but in an ill planned effort to dispose of an out of date pen I managed to drive the needle through my thumb.

New high school football season advice-don't let your babies grow up to be defensive backs

 Extracted from an article  from AANS regarding traumatic brain injury (TBI) data from 2012:

Defensive backs in American football are at the greatest risk for both fatal head injury and serous cervical spine injury.:

"The majority of catastrophic injuries occur while playing defensive football. In 2012, two players were on defense and one was in a weight lifting session. Since 1977, 228 players with permanent cervical cord injuries were on the defensive side of the ball and 55 were on the offensive side with 44 unknown. Defensive backs were involved with 34.6 percent of the permanent cervical cord injuries followed by member of the kick-off team at 9.2 percent and linebackers at 9.5 percent."

Spending even a small amount of time watching high school,college and professional football on TV makes it seem obvious that the vast majority of high impact collisions occur in the defensive zone involving defensive backs and either runners or receivers and on kickoffs.Quarterbacks receive many hits with the helmets impacting the ground and have a significant risk of concussion but apparently have  lower risk of fatal injury or injury leading to permanent disability.Offensive and defensive  linemen may receive more sub-concussive head blows over a game or a season and whatever the long term consequences of that may be  seem less likely to regularly  be involved in high impact collisions and therefore less at risk for serious brain or cervical spine injury. There is a reason for ambulances to be  parked near the playing field of high school football games attesting to the cognitive dissonance of some of  the  parents cheering them on.The EMTs are not on site to help manage sprained ankles.

Don't let your babies grow up to be defensive backs.

Notice: This is a lightly edited and altered version of an earlier commentary on this blog. As  I see high school kids  on the practice field in early August in Texas with heat indices pushing 105 my antipathy to high school and youth football  flares again.

Another football season begins, what do we know about sports related head trauma

What do we know about head trauma in high school and college football?

Mild Traumatic Brain Injury ( mTBI) encompasses the clinical entity of concussion. Concussion is defined as a trauma induced alteration of mental status with or without loss of consciousness.

Considerable research has been published regarding concussion and recently  research has been published about the multiple blows to the head that occur in all levels of football in  the absence of a recognized concussion. These "sub-concussive blows" have become the target for various types of brain imaging and cognitive function testing and the results have raised concern about the long term effects on the brains of highs school and college players.

 Some of what we know is :

1.While conventional MRIs and CTs in concussed high school and college football players are normal , Diffusion Tensor Imaging (DTI) and functional MRI have shown abnormal findings some of which may persist for weeks or months. Additionally subtle impairments of verbal memory and other cognitive tests have been reported in concussion cases persisting past the time during which the player has any symptoms.The long term significance of these finding is not known.

2.Similar imaging findings and cognitive testing results are being reported in high school and college players after a season of participation in football even thought the players had no reported concussive event.

3.We know that football helmets do not prevent concussions.

4.We know that at least  some  college level contact sport athletes decades later show abnormal white matter by Diffusion tensor imaging and lowered test results on cognitive testing but again we don't know if these changes are a predictor of later symptoms of CTE.

 Some of  what we don't know is :

1.We do not know what pathological changes underlie the imaging findings. Do the scan results indicate transient damage and tissue repair without likely long term sequelae? Is there a recognizable subset of these players with these findings who if  they continue to be exposed to multiple head blows over many years will develop Chronic Traumatic encephalopathy (CTE)? How can those who may be destined to develop CTE be distinguished from the vast majority of players who never will  have those problems

From  the wide range of head hit exposures in those NFL players who have been diagnosed with CTE the obvious implication is that there must be a fairly wide range of thresholds. There are reports of NFL players with as little as five years of play showing  typical pathological findings at autopsy. Further there has been at least one case of a college player diagnosed with CTE.


2.the long term cognitive changing on various tests  and brain imaging abnormalities have been   demonstrated  in  contact sport athletes in college and high school who did not experience a concussion.

 After the last high school football season ending there were reports of 13 fatalities.   This is about average for the years following the meaningful changes made in the rules and the instruction of techniques of blocking and less dangerous ways to tackle. Better helmets probably prevent skull fractures but not concussions.Can you imagine the outcry if high school boys were forced to take part in an activity that results in deaths each year?

See here for details  of some  of those deaths. Tragically it seems that two were due to heat stroke, all were not due to head injury.In reading over the cases it seems reasonable to designate two of the deaths to the second hit syndrome.

You see the same parents who carefully made sure their kids did not ride tricycles without  wearing helmets are some of the same ones watching and yelling at Friday night football games and probably do not see the irony  of common practice of there being an ambulance at the stadium. If their son is the victim of the second hit syndrome, probably an ambulance won't help.

Note: Much of this posting is a rewrite of another commentary from last year which I shamelessly re-post  now with only  a few additions  because this topic is one I obviously feel strongly about .I used to really enjoy watching professional and college football on tv now I only occasionally watch  just to sample the action to notice obvious head trauma. Professional players increasingly are able to make some effort at an informed decision to play with considerations of the risk to their brains, high school kids and younger much less so. 

Grief Counseling-who benefits? hint- who get paid for it?

Bringing in grief counselors seems to be a fairly common occurrence. We hear about it when a tragedy, such a shooting at a school, occurs. We are told that such specialists are being brought in to do whatever they do to help the students cope with their loss.

There is even an organization through which one can be certified in grief counseling,the American Institute of Health Care Professionals. They also offer other certifications including "Health Care Life Coach".

Apparently the basis of grief counseling has been undermined in recent years by some published data. To add a veneer of fairness I mention this article which critically reviews articles that have claimed actual harm from the process focusing on two papers which they believe are flawed and have unduly damaged the reputation of grief counseling.

A 2007 Newsweek article quotes some research that demonstrated actual harm ( mainly prolonging of the symptoms for which they were treated) from grief counseling and claimed that solid proof on its efficacy is lacking.

Is the new professionalism and ACP's new ethics really just about following guidelines?

The Charter ( Medical Professionalism in the New Millennium.A Physician's Charter) did not deal with just the important relationship of the physician and the patients but presumed to define what the relationship of the physician  should be to society. The physician was to strive for social justice and was to act as the "steward of society's " finite medical resources.

Implicit in the stewardship of resources notion is the egalitarian concept of the collectivization of  privately owned resources i.e all of the assets and individual skills that constitute the medical resources. This is the view that resources as a whole should be considered as the common asset of everyone with each to have a right to their share or that the resources are "owned" by everyone.  This notion is antithetical of the notion of private property and seemingly ignoring the key role of  private property concepts as the basis for civilization, At least that is what David Hume,Adam Smith, John Locke and founding fathers thought about the importance of private property.

Owned is in scare quotes because the concept of ownership in a free society with rule of law entails the right of the owner to use his property,to exclude others from use of his property and the right to dispose of the property.If everyone owns the resource then no one owns it and no one could be excluded from use of the property.

All of the  medical resources of the United States cannot in any real sense or legal sense be owned by everyone. So the common ownership rhetoric must be metaphorical and physicians as stewards of the resources must be rhetorical as well. It is a poetic way of saying the physicians should rein in the ever increasing cost of medical care. Further they can do that  by ordering fewer tests and procedures and treatments,that they should abide by recommendations based on studies of cost effectiveness of various medical options, that they should not let their concern and duty to the individual patient override the collective good which will be brought about by doing what is best for the group and what will be best will be determined by the progressive medical elite.Just follow the guidelines,Doc.

The 4th of July, Pride and "How Can I help you/"

This blog is for the most part about medicine and the practice of medicine so quoting extensively from a economist's blog might seem off track and one may wonder what if any is the link to medicine. This recent posting by George Mason University's professor, Don Boudreaux is so congruent with my core beliefs and he expresses them so well  that I have to quote him.

Broudreaux's topic is why, on the 240 th anniversary of the United States, we should be proud to be an American. See here for the entire essay.

Quoting from his blog, Cafe Hayek:

"...I’m proud of the peaceful manner in which most Americans conduct their private affairs.  I’m proud of the widespread respect for private property that continues to govern people’s personal, private relations.  I’m proud of the entrepreneurial spirit that continues to exist among many of my fellow denizens of these United States.  I’m proud of – and deeply grateful for – the innovativeness and entrepreneurial creativity of many of my fellow Americans.  I’m proud that America continues to be a destination for people seeking better, freer lives.  I’m proud that many Americans continue to believe that the most ethical course in life is for each individual to be self-responsible, self-supporting, hard-working, honest, and upright.

I’m proud, in short, of America’s bourgeoisness.  It’s this bourgeoisness that has made America great.  This greatness comes not from bellowing politicians, not from well-weaponed armies, not from arrogant judges, not from meddling bureaucrats, not from pompous Washington and New York and San Francisco pundits; it comes not from anything but the hundreds of millions of ordinary Americans who daily work hard, honor their contracts and other people’s property, cherish their families, friends, and neighbors, and think it perfectly natural to ask strangers in commercial settings “How can I help you?” "

 It has always seemed natural for a physician to ask that same question upon seeing a patient. In fact I recently saw an orthopedics for pain in my calf who asked that exact question.

As I read commentaries about the MACRA proposal and the nearly 1000 pages it takes to describe the process I wonder how long as the bureaucratic interference levels continues to increase and impede medical practice  will it be before that question will be merely perfunctory as more and more time and effort will be drained  away in an effort to go by the rules of " quality care" and properly document them so the reimbursement  will be 3 or 4 % more or less ( see here) and less available to do what is needed to help the patient.

Addendum; For an excellent  review of how MACRO will change just the "Meaningful Use" program (and there is much more to it than that) see here.

 h/t to Margalit Gur-Arie on her blog "On Heath Care Technology"

The last refuge arguments for central planning find a home in health care discourse

The economist and historian Dierdre McCloskey put it this way ( my paraphrasing). If some one glanced at what happened in the twentieth century and still believed in the value of central planning, they were not paying attention.

The Marxian dreams and even the subsequent efforts of the market socialists such as Oscar Lange ended badly or sometimes never really got off the ground. Things ended   badly in the case of the USSR and Communist China wherein the promises of greater prosperity and equality ended in mass starvation and mass murder.The 1917-1991 gigantic social experiment was a failure.

 The contrast between East and West Germany and North and South Korea could not be more striking and devastating to the devotees of socialist planning and their advocates  had to find arguments not based on economic success.

The economist Anthony de Jasay in his book Political Economy,Concisely  discusses what he considers to be   the two last refuges of the socialist central planner;the plea for social justice and the doctrine of unequal exchange.

We can find versions of both in the rhetoric of the defenders of the Affordable Care Act (ACA) and in the pronouncements of the medical progressives whose major premise is that medical care is too important and complex to be left to the individual physician and patient and that we must have wise leaders with ideas to replace the traditional "dyad" of the patient and physician as the deciders of medical care .


."The curious task of economics is to demonstrate to men how little they really know about what they imagine they can design." FA Hayek from The Fatal Conceit

Exercise associated collapse

The term exercise-Associated Collapse (EAC) as used by Dr. Tim Noakes of Cape Town South Africa refers to athletes collapsing after completing a marathon or longer event, though the term more generally could refer to anyone collapsing during or after an endurance event.

Noakes writing specifically about the endurance race event collapse is describing a runner who typically finishes the event and then feels lightheaded, possible nauseated and may indicate that he feels like he will faint. The blood pressure is low in the 100 to 110 range with a mild tachycardia in the 110 range. Noakes emphasizes that the appropriate intervention is to elevate the legs or low the head below leg level. This maneuver, in his vast experience will bring about recovery fairly quickly without the use of IV fluids. This approach received some documented support from a small randomized trial recently published by Noakes and co workers. See here for abstract.

Although the runner will be to varying degrees dehydrated, or volume depleted, Noakes indicates that the faint is not due to the volume status per se. Rather the mechanisms he postulates is as follows:

The post exercise collapse ( as opposed to the collapse that may occur while exercising which brings to mind a number of other more serious possible causes ) is due to postural hypotension related to several factors.

With exercise in the heat there is increased blood flow to vessels near the skin leading to a redistribution of blood to the peripheral veins ,more so as the ambient temperature increases.

Next the action of the calf muscles, while exercise continues, will reduce the volume of blood stored in the lower limbs and maintains an adequate venous return to the heart. When exercise stops, the calf muscle mechanism for venous return decreases and blood accumulates in the dilated venous system leading to decreased venous return and hypotension in the upright position.He also suggests that in the trained athlete there is a blunted compensatory increase in heart rate in response to a lowered blood pressure further increasing the likelihood of faint or near fainting.

So the treatment is the standard treatment for what used to be called vaso-vagal faint namely the Trendellenberg position. He believes that dehydration is not the cause and volume repletion is not the treatment, although obviously volume replacement is appropriate but can be done orally.

Noakes in his book ,Lore of Running, 4th edition, says that approach has worked well in his vast experience in the medical tent after the Comrades ultramarathon in South Africa.

Key information to management of the collapsed athlete is the following;

Location of collapse (i.e. while running versus after the race)
Level of consciousness and cognition (altered states suggest something more ominous that benign post exercise hypotension-particularly exercise associated hyponatremia )
Rectal temperature greater than 40C ( 104 F) means heat stroke.

Noakes and others have emphasized the importance of prompt measurement of serum sodium and blood sugar. Serum sodium less than 120 plus altered mental status should lead to administration of 3 % NaCl.

This preventive medicine stuff is not easy

Case in point  is in regard to hormone replacement therapy (HRT) for menopausal women.It has not been easy to get that right.

The stylized facts of the history of that effort briefly are:

Use HRT widely as heart disease will be prevented plus the usual listing of such things as better skin,lessened hot flashes,improved mentation and all of the advantages of being younger rather than older.

Give HRT to almost no one as actually it increases not decreases incidence of heart disease.Yeah we got the sign wrong.And then there was the issue of increased blood clots and cancer risk.

Then  a study demonstrates decreased incidence of clinical heart disease if the HRT is given early after the onset of menopause.The earlier data that demonstrated increased heart disease was derived from a study of older women who received HRT later after the onset of menopause. This suggests that a major determinant of outcome is timing.

See here for the more recent study on HRT in which women received HRT soon after the onset of menopause which demonstrated a decrease in the incidence of clinical heart disease.

Preventive medicine is not rocket science. The rocket scientists know with impressive accuracy where the rocket will come down as the law of physics applicable to that application are pretty well worked out. Preventive medicine is much harder.

addendum: See this essay on the arrogance of preventive medicine by Dr. David Sackett. Preventative ( the once incorrect term is now acceptable) medicine, of course, is a cornerstone of "population medicine" with its arrogance magnified.

Information voltage drop-not just a hospitalist issue

I recently read that hospitalists have a term for one type of failure to communicate namely "information voltage drop"

This refers to the information relevant to the patients discharged from the hospital not reaching the outpatient "health care entities", eg the nurses at the nursing home and/or the doctors who don't go to hospitals i.e. doctors doing the primary care. This would obviously would not be a problem if the physician in the hospital and the physician in the office were the same person as it was typically in the heyday of the general internist.

It is , of course, a multi-two way street, information from the primary care docs do not always get to the hospitalists in a complete accurate form. reports from tests in the hospital may not get to the chart in time for discharge, etc etc.

 A google search yielded 131,000 hits for that term in quotes. The blog "notes form dr.rw" recently discussed the important issue of the drop of key information from the hospital setting to the post hospital care. I has seen it repeatedly in my mother-in-law as she veered  from nursing home  to the ER and then hospitalization.On one occasion her dose of  Remeron (mitazapine) was not given for weeks in the nursing home due to nursing oversight and then started back in the hospital at the dose the docs thought she was taken resulting in near coma and a neuro consult.

Voltage drops can occurs in very short times and distances. I informed at least 6 different medical personnel prior to a invasive cardiac procedure , one not fifteen feet and four minutes before an IV bag was hung containing the same mediation regarding which  I had repeatedly mentioned a personal  allergy.Fortunately the dose of Versed I had received  was low and I  could protect myself.

Does the Conflict of Interest statement in medical journal articles really mean anything?

 I am beginning to think that the answer to the question in the heading is no.Thinking about a article in the NEJM published at the time of the run up to the passage of Obamacare and who the authors are probably shaped my opinion.

In the August 1,2013 NEJM a special report is published entitled "Prescription for Patient-Centered Care and Cost Containment" The authors are Thomas Daschle, Pete Domenici,William Frist and Alice Rivlin.The article predictably is in favor of the Accountable Care Organization and opposes fee for service in medicine. The article is not remarkable  for its content.That could have been predicted from the names of the authors. What I find remarkable- but not unusual or atypical- is that one of the authors who is a principle in a venture capital firm that invests  in health care businesses states that he has no conflicts of interest and that his business interest would not even possibly be conceived as such.

Dr. Frist's credentials are well known as he is an accomplished cardiac and transplant surgeon and former US Senator.His family's association with Hospital Corporation of America is also well known and Dr. Frist is not now associated with that organization. A few minutes of effort on the web yields considerable information about his current business interests at the time of the article's publication.

He is a partner in a venture capital firm, Cressey and Company,which specializes in health care related investments.These following are listed under partnerships on their website: 1)equity partnership in US Renal Care,a large private dialysis enterprise,2)Encompass Home Health,a provider of hospice  and home health care with over 100 locations in 12 states 3)Jazz Pharmaceuticals 4)Select Medical which owns rehab and long care facilities, 5) Spine Wave Inc  6)Strategic Heath Care Program 7) Wound Care Specialists.

Section 5 of the ICMJE form , which authors of articles are obliged to complete and  which can be accessed for all of the authors on the NEJM website states:

"Are there other relationships or activities that readers could perceive to have influenced or that give the impression of potential influencing what you write in the submitted paper?" (my underlining)

Dr. Frist and the others all answered no to each of the questions.

At the very slight risk of appearing cynical I suggest that his relationship with Cressey just might " give the impression of potential influencing" to some readers.  The words potential and impression seems to make that question one that would be hard to answer in the negative if someone were involved in just about any aspect of health care.

 I wonder how many readers might consider the article in a different light if following the article there was a statement that Dr. Frist was a partner in a firm whose income stream is dependent  on various health care entities. I'll bet more than a few readers might just think about the potential of influencing even though Dr. Frist is not on the actual boards of the companies in which he invests nor is he likely to be involved in anyway with the day to day operations of these businesses.Is the ICMJE form and the manner if which the form is answered really provide any useful information to journal readers ?  Do the editors of medical journals need to have any oversight over the ICMJE form answers?Does the COI statements appearing regularly in medical journal mean anything at all?

I am not suggesting that Dr.Frist's views on the various topics covered in the NEJM article were determined or even influenced by considerations of what the author's  recommendations would have on the income streams of the various health care business entities in which he is invested.But it is certainty possible that readers of the article just might get the impression of potential influence if they were informed about them in the COI statement.

Managed Care and "learned helplessness" and medical professionalism

Health Care Renewal in the Sept.22,2006 posting referenced comments by the editor of The British Medical Journal,Leona Godlee, suggesting that physicians in the British NHS may have been so beaten down by their increasingly dysfunctional system that they seem unable to stand up and fight back as their medical professionalism demands. Roy Poses then links their behavior and some he has witnessed in physician's seeming inability to push back at the administrative forces that are squeezing the life out of American medical case to the concept of "learned helplessness."

From that reference and Google I learned that "Learned helplessness" is a term born in the 1960 psychology experiments in which animals "learned" that they had no control over a given experimental situation. Later, when the animals were placed in a different situation in which they had control, they remained passive and were unable to act . Actually only about 2/3 of the animals learned helplessness in that way, the others were able to solve a simple problem to escape a electric shock.(About 5 % of animals seemed to be rather helpless even before the conditioning.) That work by Martin Seligman lead to a theory of depression.

I have written before about some of the ways that Managed Care has damaged medical professionalism in this country. Examples abound. No longer are consultations routinely arranged by physicians based on their personal knowledge of the clinical expertise of the consultant but rather to someone on the patient's insurance plan. Medications sometimes are chosen more on the basis on the insurance company's pharmacy management's arm formulary than on the basis of the physician's judgment. Time pressures directly or indirectly shaped by HMO and Managed Care have placed physicians in the untenable situation of not having time to deal with the patient's problem(s). Approval for testing and procedures have to be pleaded for.More and more time is wasted checking off boxes purported to capture the "quality" of care that the health care professional delivers that is the future will be more determinative  of the physician's compensation.

In an earlier posting, I considered the notion that not only have the practices of managed care-which would not have occurred if we had not agreed to go along with them-seriously eroded the physician-patient relationship but also the relationship between physicians.

Dr. Godlee's editorial was aimed at the British physicians but are U.S. physicians far behind in the areas of learned helplessness and diminishing professionalism? To not speak out against the practices and structures of managed care that clearly are detrimental to patient care, and to go along to get along would be about as antithetical to medical professionalism as anything I can think of. Some of the current behavior of physicians may well be characterized as learned helplessness but in the early days of managed care our failure to act must have had other origins as we had not yet had time to learn to be helpless Moreover  the new Professionalism, as envisioned by the ACP and the ABIM and the Robert Wood Johnson Foundation  meshes neatly with the learned helplessness . By following guidelines physicians can work for the common good and further social justice all the while not feeling helpless at all. 

Note: Obviously the reference to the BMJ article is not breaking news. In reviewing drafts of earlier blog commentaries I realized I had neglected to post this one.

Worried about your health care?Do not fear, the Medical Platonic guardians are gearing up

Plato envisioned a utopian society ruled by philosopher kings,leaders with ideas. Brilliant and knowledgeable, logical and devoted to the good of the crowd. Even back then the question was raised, "who will guard the guardians?" or "Quis custodiet ipsos custodes?"

The platonic ideal has persisted through the years since Plato pontificated.Currently those whose world view echos Plato are called progressives or [modern day]liberals as opposed to the classical liberals who hold the opposite view.Also, from what I've read the neo-conservative Leo Straus was a bit enamored with some of Plato views on government.

A apparent modern Plato fan is H.J.Aaron who has had three commentaries in the Perspective sections of the NEJM in the last year. He seems to be their go-to guy for his Platonic mindset and particular for  IPAB issues.Here is a link to  a sample of his views.


He praises Congress for their willingness to "abstain from meddling in matters they are poorly equipped to handle." ( Well, that would be a first) He seems to be aware of Public Choice theory (he has a PhD in Economics from Harvard) when he talks about the temptation of Congress to spend money for political ends but seems to have missed the point when he apparently assumes that the IPAB panelists would be immune to lobbying efforts.Clearly, he believes it is a good and desirable thing for Congress to delegate its powers to agencies and other bodies- a view somewhat in opposition  to what James Madison envisioned but a major feature of the administrative state.

He likens the creation of IPAB to the creation of the Fed Reserve which was to be an entity not subject to congressional control set up a governmental entities largely not controlled by Congress.

IPAB is not much in the news currently as the legislative trigger for its activation has not been pulled  but be aware it is still on the books and is available to be the mechanism by which selfless, wise leaders will direct health care miraculously immune to pressure from  lobbyists representing interests that Madison referred to as factions.

Politicalization of medical ethics-you have to ask why and by whom

The politicization of medicine is cogently  discussed  by Dr. Thomas Huddle. See here for an abstract of his article.

First, with the publication of the Charter, Professionalism in the New Millennium in 2002 the notion of social justice was injected into the listing of attributes and behaviors that physicians should exhibit to act professionally.Rather than a well reasoned and documented  argument for such action being presented by the authors, we saw a series of gratuitous assertions.

Subsequently a commitment to social justice was declared to be an ethical imperative in the American College of Physicians'  (ACP) ethics manual. Other professional organizations followed suit pledging at least rhetorical support of the inclusion of social justice into their ethical propositions.

 Dr Huddle, who teaches at University of Alabama Medical School at Birmingham, says in part:

1) civic virtues are outside the professional realm, (2) even if civic virtues were professionally obligatory, it is unclear that civic participation is necessary for such virtue, and (3) the profession of medicine ought not to require any particular political stance of its members.

"Advocacy on behalf of societal goals... is inevitably political".

" civil virtues are outside of the professional realm" and " the profession of medicine ought not to require any political stance".

Requiring a commitment to social justice is clearly  political and requires physicians to take a particular political stance and a particular philosophical position..Advocacy for social justice is one feature of the modern liberal or progressive political stance.Such advocacy is not typically part of the conservative political viewpoint or the libertarian ( aka classical liberal) position.

The notion of justice upon which which the country was founded  was that of the justice embodied in the rule of law,i.e. treating everyone equally under the law. The foundational notion of the social justice line of thinking is essentially that treating folks who are unequal equally is unfair and unjust and therefor there must be societal ( i.e governmental)  effort to mitigate inequality by  re-distributional  and other coercive  efforts of the state.

The physicians who authored the Charter and the ACP's new ethics would appear to be of the progressive belief system  while there are many physicians in the country who are not. A small group of what I have labeled as the "medical progressive elite" have seemingly captured the conversation and are attempting to  profoundly alter traditional medical ethics.To the extent that they and similar minded individuals set the agenda of major medical professional organizations and medical students education they may have succeed. but I wonder how many practicing physicians are even aware of the views that they pretend to be a settled issue.

Why would such an effort be launched and well funded ? Who gains from efforts  to bring about a sea change in traditional medical ethics? The answer to that may be found in the plan that the elite medical progressives later introduced to enable practicing physicians to on  a day by day basis practice social justice.Simple they just had  to follow guidelines .In that way there would be an alleged greater benefit to the collective -although sometimes at the expense of the individual patient-and presto we have a utilitarian form of social justice with the collective and of course third party payers benefiting.Is this the "why"?


Note: An shorter version of this essay had been published previously. I redo it now because sadly a version of social justice seems to be firmly appended to medical ethics,on paper if not in practice and few voices are heard in opposition.I find physicians believing that they should work for the good of the group or the collective or society a very frightening notion, one with a slippery slope  as evidenced by what went on in collectivist societies in the last century.

Presidential Election 2016-the wisdom to choose.

Thomas Sowell laments the choice that we are likely to have in the upcoming presidential election.In a recent commentary entitled "Grim Choice" ,he writes that the November election will offer a choice between a "thoroughly corrupt liar and an utterly irresponsible egomaniac".“



"More than any other time in history, mankind faces a crossroads. One path leads to despair and utter hopelessness. The other, to total extinction. Let us pray we have the wisdom to choose correctly.” 

 Woody Allen

More thoughts on correction of severe hyponatremia

In adults electrolyte issues have traditionally been the arena in which internists ( and I guess now mainly hospitalists) earn their fees. Here is an interesting take on the correction of severe hyponatremia.

Severe ( often defined as less than 120) hyponatremia is typically considered as an medical emergency. Discussions regarding it usually consider acute hyponatremia ( as in runner's hyponatremia) and chronic. In the former some urgency exists in regard to treatment as the concern is brain swelling and catastrophic brain herniation. In chronic, too rapid correction runs the risk of osmotic demyelination.

Beer potomania is part of the differential diagnosis of hyponatremia. This article provides gives data on alcoholic patients with hyponatremia and explains several mechanisms for the low sodium other than what is usually thought to occur in beer potomania syndrome.

At least one labor union fails to recognize the social justice of Obamacare

Apparently the roofers union believed the administration's claim that if you like your health care insurance plan you can keep it. Now they finally seem to have realize the bogus nature of that pre ACA passage ploy.

See here for the union leaders statement asking for repeal of at least some of ACA.

" I am therefore calling for repeal or complete reform of the Affordable Care Act to protect our employers, our industry, and our most important asset: our members and their families.”
 

addendum: My apology. This post clearly is old news .In reviewing my store of unfinished drafts of posting I must have hit the publish button my mistake.5/31/16

The determinates of the stiff aging heart and what if anything can be done

Diastolic heart failure had been for the most part a diagnosis of exclusion.Symptoms and physical signs of heart failure (Hf) and an elevated natriuretic  hormone level in the face of a normal ejection fraction (EF) as determined by echocardiography or  gated myocardial perfusion imaging are the elements of the diagnosis.More recently echo studies of flow through the mitral valve opening have allowed a diagnosis of inclusion based on various indicators of diastolic flow and ventricular filling but evidence of diastolic dysfunction is not sufficient to make the diagnosis of diastolic heart failure with preserved systolic function abbreviated as HFpEF.

In the classic physiology text book's 70 kilogram man the stroke volume is 70 ml and the volume of  blood poised  in the left ventricle at the end of diastole is 120 ml, and the volume at the end of systole is 50 ml giving a EF ( 70/120) of 0.58 ( 58%)) where EF = EDV-ESV/EDV, Clinicians like to use the term pre load. Pre load is the end diastolic volume.

But the percentage ejected per beat is not even close to whole story of cardiac pump function  because first the ventricle has to fill and it has become apparent than at least as many patients have filling problems as have lower ejection fractions. The HF from filling problems is known as diastolic failure or in the jargon HFpEF ( heart failure with preserved ejection fraction) as opposed to HFrEF (heart failure with reduced ejection fraction)

Of course all patients with HFrEF also have diastolic dysfunction., i.e.failure of normal filling of the ventricles.

Echocardiography has become the major tool to diagnose  diastolic dysfunction. Doppler techniques measure blood flow early and late in diastole.In the healthy compliant  heart most the flow occurs early and that phase is is designated the A phase and the second phase is the E phase and the E.A ratio has become a useful indicator of diastolic dysfunction. As the ventricle become more stiff , for whatever reasons,the ratio of  E to A decreases and diastolic filling relies more on the atrial kick phase.

A model or  stylized working hypothesis concerning the heart stiffness has been proposed in which  two major elements. are considered: 1) reduced compliance which is defined a change in volume/change in pressure in the left ventricle The relevant pressure is the difference between the left atrial and left ventricular pressure and 2)  ventricular muscle relaxation.

Compliance is assessed to some degree and imperfectly  by the E and A and E/A ratio and the E/E prime ratio while the relaxation is measured by the isovolumic  relaxation  time of the left ventricle (IVRT) This is the  period after the closing of the aortic value and before the opening of the  mitral valve.An increased value denotes poor relaxation.The E/A ratio can be deceptive because as diastolic function decreases,the left atrial pressure may rise to help push the blood into the ventricle which tends to increase the E/A ratio that may have become depressed in an earlier phase of filling problems resulting in a "pseudo-normal" pattern.

To help sort out normal and pseudo normal ratios, tissue Doppler Imaging (TDI) can be helpful. TDI measures the movement of the mitral annulus as it move upwards as the ventricle fills and is designated  as E prime.

It has been recognized that the e/a ratio decreases with aging and some cardiologists recommend using an age adjusted set of value to determine if a value is abnormal just as values for lung function test indices are age adjusted. So is it  normal or is it the case that everyone get a bit of diastolic failure as they get older or for that matter a little bit of lung impairment.It has been suggested than the aging lung is a bit like early COPD.

Several groups of researchers have taken the optimistic view that regular endurance type exercise over the years can help prevent at least some of the age related  stiffness of the heart. There are data that suggest that is the case as at least some groups of older long time endurance athletes have better e/a ratios than their otherwise apparently healthy more sedentary cohorts. However the IVRT does not differ between the two groups, so the impaired relaxation of the myocardium that accompanies aging   does not seem to be mitigated by regular endurance exercise.

The putative underlying cellular mechanisms for increased  stiffness  and the sluggish myocardial relaxation are topics for  another day.Basically the narrative is that myocardial cells die with aging (apoptosis) and the surviving cells hypertrophy plus subendocardial fibrosis develops and maybe long time regular aerobic exercise might mitigate that process a bit.


addendum:5/30/16 Hitting the wrong key lead to publishing a uncorrected version. I think I fixed most of the typos ,etc now .
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