The major barrier to third party payers control of medical costs is being dismantled

A major barrier ( I argue the major barrier) to control health care costs by the third party payers has been and still is to a lesser degree medical ethics ; more specifically, the duty of the physician to act as a fiduciary for the patient. At one time not long ago when the physician and patient believed or had determined that test x or treatment y was in the best interests of the patient the physician would be the  advocate for the patient  not an agent or employee of the insurance company whose interest was to deny the tests or treatment.He was not tasked with working in some type of mythical society-physician alliance to conserve collective medical resources acting as the steward of those resources.

Not infrequently the physician's desire to be the advocate of the patient and the insurance company desire to limit costs were in opposition.The patient versus the company with the physician on the side of the patient was the common narrative.

What if the medical ethics were different? What if the physician felt an ethical obligation to conserve the " resources of the collective"? What if the impetus for that ethical transformer seemed to take place from within the medical profession?

Whereas once if the physician did not advocate for his patient he might be ashamed but now according to the new ethic a physician might feel guilty by failing to act  as would "stewards of finite resources".  Victor Fuchs in a commentary in the NEJM carried this  insult to logic to its limit in the following way.

In his closing paragraph, Fuchs tells us that when a physician works in a health care collective in which there is a fixed annual budget the physician resolves the dilemma ( between favoring the individual and the collective) by favoring the cost effective option. This according to Fuchs become "appropriate". So,the cost effective choice is the appropriate choice and also the ethical one. It is ethical in the moral calculus of Kant he claims "because if all physicians act the same way,all patients benefit" .It is hard to find statements any sillier in a major medical journal.

 A  major  barrier demolition  occurred in 2002 with the publication of "The Charter" ( Medical Professional in the New Millennium- A Physician Charter) authored by the ABIM  Foundation , the ACP foundation and a European Foundation of Internists.

A number of forays against the barrier had been made earlier including a multi part series in JAMA in which the author proposed a way to increase quality of care while decreasing cost by a egalitarian-utilitarian, cost effectiveness calculus in which the group benefited while a given individual patient might not.  Notable also was the publication  of "New Rules" by Troyen Brennan and Don Berwick in which they advocated elimination of the traditional doctor patient relationship and moving away from "decentralized individualized decision making".  

In The Charter, three major ethical principles were put forth; patient welfare,patient autonomy and social justice. Previously medical ethics was concerned with the relationship of the physician and the patient.Now the authors of the Charter presumed to define the relationship of the physician and society. Further, the relationship they claimed was one in which the physician was the steward of society's resources. This colossal, gratuitous assertion represented a sea change the implications of which might not have been immediately apparent. To many it was not apparent that implementation of the third principle was in conflict with the first while a number raised objections  the majority took little notice.The dogs barks and the caravan moves on.

 But all of the above really just relates to the intellectual smokescreen. The real elements that have fee for serve on life support and thereby strike a major victory for third party's payers cost saving and profit  enhancing initiatives are ACA,HITECH and now MACRA.

Is the athlete's slow heart rate really due to increased vagal tone as conventional wisdom suggests

An article from three British researchers makes a good case that vagal tone is not the reason for the athlete's bradycardia in a 2015 commentary in the Journal of Physiology.see footnotes

Traditionally, the slow heart rate of endurance athletes is attributed to increased vagal tone but the authors argue that this increased tone has never been demonstrated at least in part because it is not clear how that could even be measured as the vagus carries both afferent and efferent fibbers. Further experimental blockage of the autonomic nervous system has not lead to mitigation of the bradycardia.

They suggests that the slow heart rate is also not due to SA node fibrosis ( apparently a common explanation for SA node disease) as that also has never been demonstrated. They present evidence that the culprit is remodeling of the ion channels and related molecules in the sinus node-more specifically downregulation of the HCN4 channel  (also  strangely known as the "funny channel") . They reference a number of articles claiming there is remolding of  ion channels in aging and familial bradycardia and pulmonary hypertension.

Endurance exercise is known to cause heart remodeling leading to the features of the so called athletes heart ( so called eccentric hypertrophy). It is also know that cessation of exercise will lead to some degree of "re-remodeling" returning the athletes heart  to some degree of that of the sedentary person. Will a similar reversal happen in he electrical system in endurance athletes who quite exercise? or is this remodeling permanent? Baldesberger  et al published a long term followup  in retired professional cyclists who had stopped training for over thirty years and did report an unimpressive lower heart rate on Holter monitoring in 62 cyclists versus 62 golfers ( 66 +- 9 versus 70 +- 8 but 20% did have a HR less than 40 during the day. versus 6 % in the controls.So is the sinus nodes remodeling to some degree not reversible-these cyclists had not trained for 30 years. (There is more interesting data from this study which is a topic for another blog commentary,here the interest was in the bradycardia not other possible cardiac complications . and it did appear the cyclists had a bit more bradycardia.) 





footnotes

1) D'Souza, A et al . Cross talk opposing view:Bradycardia in the trained athlete is attributable to a downregulation of a pacemaker channel in the sinus node. Journal of Physiology 593 no. 8 1749-1751,April 2015

2) Francesco, D. The Role of the Funny Current in Pacemaker Activity. Circ. Research 2010;106, 434-446

3) Baldesberger, S et al Sinus Node  disease and arrhythmias in the long term follow-up of former professional cyclists. Eur hear journal 2008 29, 71-78

The minimum exercise levels of the 2008 guidelines won't prevent heart failure.

IMPORTANT CORRECTION:Since this commentary was posted I  realized I misinterpreted the two articles I quoted leading to the title conclusion which is incorrect.That has been corrected on 9/6/18 by the posting entitled " Is the minimal level of recommended exercise sufficient to decrease the risk of heart failure?"


The 2008 U.S. and WHO  exercise guidelines recommend a minimum of 2.5 hours of moderate intensity exercise per week or 1.25 hours of vigorous exercise per  week. This can be expressed as 500 METS Min per week or 8.3 MET hours per week.

This minimum value is widely quoted but often unnoticed is that  the panel also suggested that further gains could be made by increasing those exercise levels to twice those values, i.e 5 hours of moderate or 2.5 hours of vigorous exercise.

 Moderate intensity was defined as between 3 and 5.9 METS and vigorous as over 6 METS.For example running at a 15 min per mile pace is about 7 METS which would be the lower end of what the panel meant by vigorous.(This does not address the problem of relating exercise levels to a person's exercise capacity. For example, to  a person with a 02 max of 60 a fifteen minute mile is  mild exercise while the same pace for someone with a 02 max of  25 the term vigorous is  appropriate. Since age strongly correlates with 02 max should  the guidelines somehow take age into consideration in the recommendations.How to do that is not clear.

Cardiovascular disease (CVD) risk reduction has been shown in a number of epidemiological studies for people exercising at those  minimum levels and arguably at even lower level. Lee et al (1) showed that running at little as 5 to 10 minutes per day would significantly  reduce CVD mortality.This would make a little running seem very effective  while others (Pandy et al see below) did not show that degree of risk reduction with that low  level of exercise but the minimal recommended  level will likely reduce CVD risk according to several epidemiologic studies.

Eijsvogels (2) reported that the maximal risk reduction was found at a volume of 41 MET-hrs/week, which is 3-4 times the minimal recommended level.However, only 3.5% of the subjects exercised at that level or above and therefor the confidence interval for  hazard ratio (HR) estimation was wide and not statistically significant. The authors emphasized that they found no evidence of harm or adverse cardiovascular outcomes at this level but the relatively small number  of people in that category raises the possibility of a type11 error.

While rather low levels of exercise seem to decease CVD risk, heart failure  risk  reduction may require higher levels of exercise. Pandy et al (3) and coworkers from Southwestern Medical School reported that heart failure (HF) risk reduction occurred only at levels  significantly higher than the minimum guideline recommended values. "We observed a linear dose response for HF risk with a marked reduction in risk at very high doses of PA (physical activity  ) ( 35% risk reduction in HF risk at 2000 MET-min per week)".. This would be 4 times the minimal recommended value or 10 hours of moderate or 5 hours of vigorous exercise per week.

Schnohr et al (4) reported that their analysis of a data set from the Copenhagen City Heart Study demonstrated a U shaped association between all cause mortality and dose of jogging. A number of other articles cited by Schnohr  in that publication actually report a inverse relationship  showing no U or J shape. Accepting the thesis of  the existence of a U shape curve, he goes to comment on results from several large studies and speculates where the curve might ascend.The studies found that running  about 35 miles per week was the upper limit of incremental health benefits and "these studies found that a weekly cumulative dose of approximately 30 miles of running per week or 46 miles of walking is approximately the "safe" ( my quotes) upper limit for optimizing long term CV health and life expectancy", So if the curve turns upward  it does not seem to do so at running volumes in the 30 miles per week range. This volume of running would seem  satisfy the running volume "requirement" sufficient to decrease HF risk. suggested by Pandy's work..

So the epidemiological data would tend to confirm that the 2008 minimum guidelines would decrease CVD and all cause mortality but not the risk of heart failure which seems to  require at least twice that level of exercise.

Several publications from a group in Dallas (5) provide useful insights regarding the mechanism by which a higher level of exercise might  lessen heart failure risk, that is diastolic heart failure ( i.e  heart failure with preserved resting ejection fraction frequently abbreviated as HFpEF).

 Dr Paul Bhella and his  associates  did extensive physiological studies on four groups of healthy volunteers over the age of 64. Four groups were designated   on the basis of their exercise history for the preceding 25 years. (not a typo) 1) sedentary-no more than one exercise session per week  2) casual exerciser-2-3 session per week 3) "committed" exercisers-4-5 session per week and 4)competitive master level athletes -6-7 session per week and competed regularly.  All had normal systolic function ( as defined by a normal resting ejection fraction) but groups one and two has decreased left ventricular compliance while the committed and competitive groups had left ventricular pressure volume curves and left ventricular masses similar to young healthy controls. ( see here for my  further comments and a few caveats regarding this paper including reference to Tanaka's work that challenges the notion that long term endurance exercise  does in fact preserve  ventricular compliance)

Quoting Bhella ". . at least 30 minutes of dynamic exercise per session for 4-5 days per week over a lifetime can  sufficiently prevent most of the decreases in LV compliance and distensibility observed with sedentary aging" So the idea is that sedentary aging leads to stiff left ventricle and life long running may mitigate that process.

 In other words 2.5 hours of vigorous exercise per week which was the higher level of exercise ( i.e. twice the minimum  recommenced by the 2008 panel) might beneficially reduce the age related increase in ventricular stiffness. It does not take that much exercise per week but you have to put in a lot of weeks- and it was vigorous. Remember  Bhella's groups activity levels were for the 25 years before the testing. The authors speak of Lifelong exercise. 


 This exercise level is far below the typical exercise histories that one typically  finds in the cases of athletes with atrial fibrillation or the athletes in whom an abnormal gadolinium uptake was reported and whose cases are  sometimes emphasized by various writers warning the public about the dangers of "excessive exercise". I suggest that  2 to 3 times the  2008 Panel's minimal recommendation should not be considered excessive.

1)Lee, D  Leisure-time Running Reduces All-cause and cardiovascular mortality risk. JACC 64. 472-481.2014

2) Eijsvogels, T, Exercise at the extremes-The amount of exercise to reduce cardiovascular event
JACC, 67, 316-329, 2016

3)Pandey,A Dose-Response Relationship between Physical Activit and Risk of Heart Failure.A meta-Analysis, Circulation 2015, 132 1786-1794

 4) Schnohr,P Dose of Jogging and Long term Mortality. JACC, 65, 311-410,2015

 5)Bhella, P Impact of Lifelong Exercise "dose" on left ventricular compliance and Distensibility.
JACC 64, 1257-1267 2014

John VonNeumann " There's no sense in being precise when you don't even know what your're talking about"

addendum: 5/22/17 Several editorial flourishes made  and spelling errors corrected and more were made on 9/3/18. 9/6/18 Notification posted on this commentary referencing the correction made on 9/6/18.
 

High school and college football deaths average about 3 per year

A recent report by KL Kucera et al give details on high school and college fatalities related to head and/or spinal injuries .

From 2004 through 2015 there were 28 deaths reported related to head or spinal injuries,24 in high school players and 4 in college. 1.1 million play high school football while there are 75,000 collegiate football players.

Four of the 22 high school players had suffered a concussion in the four weeks  preceding the fatal injury and in three cases the second impact syndrome was implicated .Running backs and linebackers were the two most common positions.The head down-head first position was frequently implicated.

 I wonder what  parents and grand parents of high school footballers think about the ambulances frequently parked off to the side of the playing field.

two studies reassuring endurance athletes re long term heart damage

Two, articles, one from Germany and one from Italy might provide some reassurance to long time endurance athletes worried about too much of a good thing damaging the heart.

Bohn et al from Germany reported  a group  of long term endurance athletes with many years of endurance exercise history whose extensive cardiac evaluation showed nothing to suggest that ARVC is a problem.

Pelliccia and co workers studied 1777 active competitive athletes and described echo findings and concluded their tendency to have somewhat larger left atria represented physiological adaptation which is largely without adverse clinical consequences and found a fib to be uncommon, less than 1% and similar   to that of the general  population. He also concluded that left and right ventricular exercise induced remodeling were basically balanced.This conflicts with some of the work of La Gerche  and Heidbuchel who postulate that the right ventricle is less well designed that is the left ventricle  for endurance exercise and and predisposes it to arrhythmias arising from right ventricular  remodeling . But finding a bunch of white swans does not preclude the existence of black ones.

The often quoted , case control studies  reporting hazard ratios of 4 and five in regard to atrial fibrillation in long time endurance athletes ( and the meta analysis that summed them up with some statistical trappings) just might be vulnerable to selection  bias while these two studies cited above just might be vulnerable to survivor bias.

Can "too much" exercise increase risk of atrial fibrillation in men but not women?

Can "excessive " exercise increase the risk of atrial fibrillation in men but somehow spare women hyper-endurance exercisers from that risk? That seems to be what the data show in a 2016 Meta analysis by Mohanty et al published in the June issue of the Journal of Cardiovascular Electrophysiology . See here.

The really fun thing about meta analyses is the frequency with which one can cite conflicting results from various studies. In  another meta analysis Kwok et al found no association with increasing exercise and risk of AF in either sex.  In spite of these conflicting data sets a quasi consensus seems to be that at some level "too much"  exercise predisposes to atrial fibrillation.- determining the level of too much is another matter.  As in  many biological and medical issues it is easier to get a pretty good idea of the direction of the vector than is  ascertaining the magnitude but  sometimes the direction is in dispute as well.