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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 ...

Saturday, October 13, 2018

More physical activity may be needed to prevent HF than some other CVD events

 The title is a reworded version of the title of the article which is designated as reference 2 in the footnotes.

There are  2 (at least 2) epidemiologic studies that indicate a linear dose-response relationship between physical activity (PA) and the risk of heart failure. While one study ( Pandy et al see below) does demonstrate a "modest" reduction in HF risk at a lower levels of PA, both studies how a more robust reduction in HF at higher exercise levels.

Pandy et al (Circulation 2015,, see ref 1 below) did a meta-analysis involving about 370  thousand subjects , 20 thousand of which developed HF over a 13 years period.They compared the HF risk in 3 categories based on level of exercise, namely 500 MET-min per week ,1000 MET-min per week and 2000 MET-min per week.

500 MET-min per week is equivalent to 2.5 hours of "moderate" exercise per week or 1.25 hours of "vigorous" exercise per week.Moderate is defined a exercise requiring 3-5.9 MET and vigorous as about 7 METS. (It requires about7 METS to run a 15 minute mile or to finish Stage 2 on the Bruce protocol treadmill exercise tests. One should be able to walk a fifteen minute with a 02 consumption of 5 METS.)

1000 MET-hrs per week is 5 hours of moderate or 2.5 hours of vigorous exercise per week and 2000 as twice that or 10 hours of moderate exercise per week. Yes, that does seem like a lot,

Both the 2008 US exercise  guidelines and the 2018 guidelines recommend at least 500 but state that more benefits accrue with higher levels .

Pandy reported a linear,dose response with a "marked reduction in risk at very high doses of PA ( about 35%) at 2000 MET-min per week".

Their data:
exercise level                                HF RF

500 MET hrs per week                  0.9 (0.87-0.92)
1000 "  " " " " " " " "                       0.81(0.77-0.80
2000 "  "   "   "" """""                     0.65 (0.58-0.73)

Quoting the authors; "Only a moderate reduction ( about 10%) risk in HF noted at the minimal ( US guidelines) recommended level,"

The authors offer a mechanistic explanation namely that CAD event risk occurs at a lower level of exercise by reducing the usual suspect Risk factors (BP,Lipids,blood sugar control) while HF risk reduction occurs at a higher levels of exercise perhaps  by altering cardiac function and structure, i.e beneficial remodeling.

An earlier article Patel K, (Int J Cardiol 2013 see ref 2) had reached generally similar conclusions regarding the levels of exercise needed to decrease HR risk versus the amount adequate to  reduce general  CV risk, e m.gyocardial infarction.

Patel et al studied 5503 patients age 65 and older
During the 13 years of follow up incident HF developed in:
26% of those with little or no regular exercise
23% of those with "low"level of exercise
20% of those with "moderate"
19 % of those with high .

Low was defined a 1-499 Met-min per week
medium as 500-99
high as greater than 1000

The HRs for incident HF were:
low level exercise     0.87 (0.71-1.06)
medium                     0.68 (0.54-0.85) stat sig 
high                            0.60 (0.49-0.74) stat sig 

All exercise level groups had reduced HR for incident MI, stroke, and cardiovascular mortality but the lowest level group did not have a statistically significant  decrease in HR risk.

These 2 studies indicate that more exercise is associated with greater reduction in HF risk, although some HR HF decrease was noted in the lowest exercise group in the Pandy study.

Now for something completely different. A different type of study published by CR de Fillippi from the Cardiovascular Health study ( reference 3) provides an interesting  insight regarding possible mechanism(s) by which more exercise is better in terms of HF risk reduction. 

They studied 2, 9333 subject free of HF at the onset and  who had normal values for two biomarkers, NT-Pro BNP and cTnT (troponin).They then measured these markers every 2 to 3 years and compared incident increase in those markers in groups divided by their exercise levels.(They quantitatedle exercise using  a particular system and used numerical scores to define groups and I was not a to translate those values in to MET hrs to compare with the other 2 articles)

 They found compared with the participants with the lowest PA activity scores those with the highest (i.e. more exercise) had an low odds ratio of 0.50 (0.33-0.77) for a significant increase in NT proBNP and an OR of 0.3 for and increase in troponin.  Quoting  the authors "increased levels of NTProBNP and cTnT may reflect pathological precursors of hemodynamic stress and injury that are prevented by PA at some as yet more precisely defined level.

So how to put all this together.

An  appealing ( at least to me) mechanistic explanation is that an overall decrease in CV mortally and arguably a slight reduction in HF risk  can be brought about by modest exercise and even  perhaps slightly less  than modest levels  by reducing the usual suspect,traditional CVD risk factors.Modest here refers to about 500 MET hrs per week. but some studies have shown a decreased heart attack risk at even lower exercise levels.

A more robust risk reduction in HF risk (perhaps 20-35%) seems  to require higher levels of exercise  ( in the 1000 Met-hrs per week range and higher) by perhaps bringing about an advantageous remodeling of the heart or at least a mitigation of the deleterious remodeling of the heart than occurs with sedentary aging which in turn may predispose to the development of heart failure with preserved ejection fraction (HFpEF).

To the extent that CVD risk factor reduction can decrease heart attacks and the  accompanying reduction in   heart function some reduction in HF risk would be likely, i.e.some reduction in heart failure with reduced ejection fraction ( HFpEF). But at least half of cases of HF are not associated with decreased systolic function ( at least as measured by the ejection fraction  (EJ) but by the echocardiographic finding of decreased left ventricular compliance and distensibility which according to the work of Dr. Ben Levine and others at SW  Medical School in Dallas predispose to diastolic heart failure  (HFpEF) .That group suggests that at least 30 minutes of exercise 4 to five times a week might be sufficient to prevent that age related loss of cardiac compliance. ( see ref 4 below for more on this argument) and perhaps prevent at least some cases of HFpEF.


1)Pandy,A "Linear,dose dependent inverse association between PA(physical activity) and heart failure risk Circ. 115.132 p 1786-1794

2.Patel K. "Prevention of heart failure in older adults may require higher levels of physical activity than needed for other cardiovascular events." Int J Cardiol. 2013, Oct 168 (3) 1905-1909)

3)de Fillippi, CR "Physical activity, change in biomarkers of myocardial stress and injury, and subsequent heart failure risk in older adults. JAm Coll Cardiol.. 2012 Dec. 18;60 (24), 2539-47

4) Bhella, PS  "Impact of lifelong exercise "dose" on left ventricular compliance and distensibility"J Amer coll cardiology. 2014 , 64, no 12,p 1267  



Tuesday, October 09, 2018

2018 U.S. exercise guidelines-or how exercise is good for just about everything

The 2018 Physical Activity Guidelines Advisory Committee issued its report to the Secretary of HHS in February 2018.See here for link to full report.

Their prescription for exercise was unchanged from their 2008 recommendations.  They recommend 2.5 to 5 hours of moderate to vigorous exercise per week. This can also be expressed as 500 to 1000 Met-minutes per week. "Moderate" is defined as exercise requiring between 3 and 5.9 METS and "vigorous" as greater than 6 METS.

To put those numbers into perspective , consider than it would require about 7 METS to run a fifteen minute miles and about 5 METs to walk a fifteen minute mile and about 9 METS to run a 12 minute mile. It requires about 7 METS to complete Stage 2 on the Bruce treadmill protocol .A MET is 3.5 ml of oxygen per kilogram weight per minute. 

Now, about how exercise (physical activity or PA) is good for just about everything. 

The 2008 exercise guidelines reported that PA could lead to a reduction in risk of breast cancer and colon cancer . The 2018 reports adds the following cancers to those whose risk is reduced by PA :
bladder, lung, esophagus, endometrium and stomach.But reduction in heart disease risk is the major selling. point for an exercise program as well as decrease in diabetes and hypertension risk. 


The publication also offers evidence of a risk reduction for dementia and depression.

If the benefits of exercise could be achieved by a daily  pill, everyone would be taking it.








Thursday, September 13, 2018

The impressive and alarming success of the American Board of Internal Medicine Foundation

The American Board of Internal Medicine Foundation (ABIMF) is not the largest,most heavily endowed nor the best known of the many non-profit organizations who  function as advocates for various aspects of health care and medical practice. However, its success in promulgating concepts and influencing medical practice and health care seems disproportionately greater than one might expect based on its size. ABIMF's "greatest" achievement is the development and promulgation of the notion of Medical Professionalism and its major tenets: patient welfare,patient autonomy and social justice. The insertion of the later tenet into medical ethics is a major departure from traditional ethics and is destructive to the physician patient relationship

The first two tenets were long standing pillars of medical ethics and practice and dealt with the relationship between the physician and patient but in 1992, their efforts along with the ACP Foundation and a European Group proclaimed that part of medical professionalism included what they believed was the proper relationship between the physician and society

This  manifesto was published in the Annals of Internal Medicine in 1992 in a paper entitled Medical Professionalism in the New Millennium-A Physician Charter. The ABIF has continued after the 1992 paper to promote the primacy of patient welfare,patient autonomy and social justice and to advocate for "a just and cost effective distribution of finite resources".


 The notion of a co-duty,one to the patient and one to society,was not previously a part of western medical ethics.The 1991 edition of the AMA ethical code did not mention social justice or stewardship of society's resources. Cost effective care is the major thrust of the foundation's recent initiative called "choosing wisely" .  By 2012 over 100 other medical professional organizations had signed on to the Charter and education along those lines apparently is taking place in a number of medical school according to a 2012 article in the Annals of Internal Medicine.

It is the ABIM's MOC  ( Maintenance of Certification program ) that has caused the most angst for internists and reliable reports of its very questionable financial activities have triggered an unprecedented uprising  which surprisingly has had more than a little success.( Much credit for this is due to Dr. Wesby Fisher who on his blog has reported activities of the ABIM and the ABIMF that are  egregious and arguably illegal.)

Yet the sea change in the discussion about medical ethics and professional behavior importantly driven by the same folks who gave us MOC  may in the long run be even more damaging.

Thursday, September 06, 2018

Is the minimal level of recommended exercise sufficient to decrease the risk of heart failure?

In January 2017, I posted a blog commentary entitled " The minimum exercise levels of  the 2008 guidelines won't prevent heart failure". See here.

The gist of that commentary   was that the adherence to the minimal exercise levels indicated by the guidelines had been demonstrated by ample epidemiologic studies to reduce the incidence of cardiovascular disease (CVD) but  exercise at that level had not been demonstrated to reduce   heart failure (HF) incidence and that a higher amount of exercise was needed.

Since then I have more carefully studied a 2015 epidemiologic paper  by Pandy,which I had read before but obviously not with adequate attention , and a detailed physiologic comparison of cardiac function by Bella et al  in 4 groups of healthy subjects who varied  in their long term exercise levels to which I also had not paid appropriate attention. 

These considerations   resulted in a major revision my 2017 headline to " Adherence to the 2008 guideline will reduce HF incidence but more exercise will reduce HF risk significantly more"

Note: I have added an addendum to the 2017 posting  stating the headline is simply wrong 

So now to try and clean up the earlier erroneous  commentary .

First a review of some background:

The 2008 US and WHO guidelines recommend a minimum of 150 minutes of moderate exercise per week or 75 minutes of vigorous exercise. This corresponds to 500 MET minutes  per week or 8.3 MET hours .The US panel also said that further gain could be made by increasing that level to twice that amount. Moderate intensity was defined as requiring between 3 and 5.9 METS and vigorous greater than 6 METS.Note-the panel was addressing the risk of cardiovascular disease in general and not heart failure risk per se .


There is universal agreement that aerobic exercise will decrease heart disease risk ( and according to some studies-dementia,some cancers and type 2 diabetes) but there is disagreement as regards how little exercise  might be  sufficient to reduce cardiovascular risk  and how much exercise might be harmful. I leave those 2  questions  to another time.

In regard to HF:

Patel et (1) published a 2013 review of 5503 subjects age 65 and older from the Cardiovascular Health Study .They divided participants into inactive ,low level exercise ( 1-499 METS),Medium (500 to 999 METS )and high was defined as  greater than 1000 METS 

The hazard ratio (HR) for the low group was a non-statistically significant 0.87 (0.71-1.06,p=0.170.
The medium groups HR 0.68 (0.54-0.85)p=0.001
The high group HR 0.60(0.49-0.74, p=0.026<0 .001.="" p="">

Note that  the low and medium groups overlap the 500 level so  no conclusive verdict regarding HF risk reduction with 500 MET level can be made. You can say that the lowest exercise group enjoyed no reduction in HF risk but we do not know how many subjects were closer to the 1 than to the 500 level. We can say that the medium and high level  did demonstrate a HF  risk reduction but can conclude  nothing about the value of exercising at the 500 MET min level,which is the minimal level recommended by the 2008 panel. 

However, from Pandy's 2015 meta-analysis (2) that there demonstrable risk reduction  in HF in a group of subjects exercising at the 500 MET level. The authors examined data that included over 20 thousand HF events among 370 thousand participants in some 12 prospective cohort studies. 

The 500 MET-min  per week group had a reduction in HF risk ( HR-0.9 (0.81-0.92). However, a greater risk reduction was found in the 1000 MET Min per week group ) HR-.81 (0.77-0.86) and even greater reduction 0.65 (0.58 -0.73 ) in the group at the 2000MET min per week which corresponds to 10 hours of moderate exercise per week or 4 times the minimal amount suggested by the 2008 guidelines.

So the epidemiology  data indicate  that the lower level of recommended exercise will cause a measurable decrease in HF risk but in that regard more does seem to be better.Now to consider Bella's (3) physiological data which is consistent with Pandy's analysis.


 The following  2 paragraphs are copied from my earlier blog commentary.

" 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"

It appears that training at triathlon or marathon levels is not necessary to decrease long term risk of heart failure but the exercise has to be persistent. The term "lifelong "used by Bella may be an exaggeration but his subjects had a 25 year history of regular aerobic exercise.

Bella's data seems to confirm the notion that the 2/12 hours per week recommendation just might decrease the risk of HF with the caveat " if done over a long period of time". The same  group has subsequently published data showing that beginning a  more intense exercise program in a person's 60s or 70's will not result in improved left ventricular compliance but , of course, one would expect  health benefits.

I quote a key paragraph from Bella:

"This study's key finding is the novel observation that at least 30 minutes of dynamic exercise per session 4  to 5 days per week over a lifetime can sufficiently prevent most of the decrease in compliance and distensibility observed  with sedentary aging.This finding holds important implications for global health as ventricular stiffening has been implicated in the pathophysiology of many common CV conditions affecting the elderly.

Contrary to my earlier commentary the minimal levels of exercise may well be enough to decrease the risk of HF but exercise at about twice that levels is likely to bring about a more significant reduction. Note that Bella's comment of 30 minutes 4-5 days a week corresponds to the minimal recommendation of 150 minutes of moderate exercise per week.

1)Patel,K et al Prevention of heart failure in older adults may require higher levels of  physical activity than needed for other cardiovascular events.Int j Cardiol 2013 1905,-1909.

2)Pandy, A Dose Response relationship  between physical activity and risk of heart failure.A meta-analysis. Circulation 2015 132 1786-1794

3)Behlla,P Impact of lifelong exercise "dose"on left ventricular compliance and distensibility. JACC 64 1257-1267 2014  

Wednesday, September 05, 2018

Does the notion that people have a duty to be healthy shatter traditional medical ethics

First lets define what we mean by traditional medical ethics.This would include the medical ethical precepts that constituted medical ethics before the announcement of the "New Professionalism" by the ACP and others. Basically and stating it informally it is that the physician has a fiduciary duty to the patients, and he should place the patients interests before his and of course first do no harm.

Keeping those precepts in mind, consider the following statement which is typical of a growing trend in medical commentaries .

People ( patients) have a duty to be healthy ( practice "healthy behaviors" and eschew "unhealthy behaviors") and comply with medical advice for the good of healthy population.

Drs. JF Wharam and D. Salmasy, writing in the Jan. 14,2009 issue of JAMA. In their discussion of P4P arrangements they state:

...policy makers, health care executives,disease advocates, and scientists with clinical or epidemiological expertise effectively choose population-level goals and thus impose obligations in a manner that
might ( my italics) infringe on patient and physician autonomy. Without fair deliberation,such goals, however wise, cannot claim legitimacy

I suggest that the word "might" be deleted from the above quote. It will infringe. Further, it is not clear what would constitute "fair" deliberation.When someone begins to talk about being fair,watch out.So with "fair deliberation " such claims ( if wise) are , according to the authors therefore  legitimate.



When physicians get some of their income by meeting certain population based goals( e.g. have x% of patients with a hemoglobin A1c under some number) patients who might seem to eat too much or not always take their medicine or whatever else might  be perceived  by the physicians as getting in the way of the population based goals and keeping  the doc from her bonus.Again it is issue of serving two masters,the real life patient in the exam room  versus some insurance based collective construct.

Friday, August 10, 2018

Many Kudos for the anti-MOC warriors and glimmers of hope

Dr. Wes Fisher ,an EP Cardiologist from the Chicago area, has waged what was  for a long while a
one man crusade about the questionable activities of the American Board of Internal Medicine and its own foundation the ABIM foundation and the harmful effects of  their maintenance of certification  (MOC) program. I have blogged a bit about that before and now a number of other physicians have joined in the fray.

Now it seems his prodigious work in that area is beginning to pay off.He recently took part in a very instructive  podcast with Dr. Michel Accad. Fisher is now working with a law firm doing preliminary work hopefully leading to a law suit against the ABIM possibly involving anti trust  issues and fraud.

Money is need for the litigation to move forward.To aid in that effort , Dr. Accad has offered a copy of his brilliant book, "Moving Mountains" to folks who contribute to a fund for the litigation.

Go to the pod cast to learn in details about the antics of the ABIM that catalyzed Dr. Fisher's efforts. See  this link for episode no. 17 of the Accad and Koka Report and links are available there for a GoFundMe link for Fisher's law suit and to the organization he founded, Practicing Physicians of America.
https://practicingphysician.org/


Incidental note. For the last 2 days I have been unable to link to Dr. Fisher's website. I enter drwes.blogspot.com and am diverted to www.widgetserver.com .I was able to backdoor into his site from his Twitter feed.Has his web site been hacked? Coincidence? Addendum , two days later Dr. Fisher's web site was up .


Thursday, July 12, 2018

How well do the Echo guidelines work to estimate cardiac filling pressures ?

Elevated filling pressure is thought to define heart failure as it is thought to be the driver for exercise intolerance and shortness of breath.

Filling pressures can be invasively determined by catheters in either the pulmonary artery wedge position or in the left ventricle.

One of the major aims of echocardiography is to provide reliable estimate of filling pressures .It is generally accepted that echocardiographic indices are more effective in determining  filling pressures in patients with reduced ejection fraction (EF) and is more problematic in patients with preserved EF

The 2009 echo guides  for determination of diastolic function were revised in the 2016 guidelines and both  have been the target of some criticisms.

IMO a 2015 article ( 2) from the Cleveland Clinic offers data that raises reasonable concerns about the estimation of filling pressure in patient with preserved EF.It should be noted that the classification system of degrees of diastolic dysfunction (DD) used by the authors is not the exact system proposed by the 2016 guidelines. but rather those of the 2009 guidelines.(1) and the authors' criticism relate specifically to the 2009 system.However I believe their conclusion ( see below) regarding the basic underlying paradigm holds regardless of tweeks made to the 2009 guidelines.

The authors reviewed 460 consecutive patients who underwent echocardiography within 24 hours of elective left heart catheterization.

Their figure 5 plots left ventricular diastolic pressure (LVEDP) against normal and the 3 grades of DD in patients with EF greater than 50 % and those with EF less than 50%.In both groups there was no difference in LVEDP between normals and those with Grade 1 and Grade 2. The only statistically significant difference was that between normals and those with grade 3  DD who had EF less than 50%.

The authors conclude: "the findings of this study question the notion that DD is a predictable, progressive process beginning with impaired relaxation followed by reduced compliance and increased filling pressures. The prognostic value of echo graded DD may relate more to its reflection of intrinsic properties of the left ventricle, or to exercise hemodynamics  than to its correlation with resting hemodynamics alone. "A Mayo Clinic study  of 467 patients ( 3) by Kane et al found  no higher pulmonary artery systolic pressures at rest  or on  exercise in those patients with the echo diagnosis of impaired relaxation.



 1) Nagueh, SF Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echo 2009, 22, 107


2) Grant A, Grading diastolic function by echocardiography:hemodynamic validation of the existing guidelines. Cardio Vascular Ultrasound 2015.


3)Kane, GC et al Impact of age on pulmonary systolic pressure at rest and with exercise.Echo Research and Practice, 2016,3(2) 53-61


addendum 8/1/18 spelling errors corrected and several poorly worded sentences revised.

Sunday, July 08, 2018

The great social justice bait and switch courtesy of ACP,ABIM and RWJF

Certain members of the leadership of the American College of Physicians,the American Board of Internal Medicine and the Robert Wood Johnson Foundation authored a manuscript designed to permanently change the physician patient relationship.The paper is entitled "Medical Professionalism in the new millennium: A Physician Charter.",.which I will refer to in this commentary as "The Charter" .  It was a project of  the  foundations of the ABIM and ACP and the European Federation of Internal Medicine.See here for the document.

The documents simply asserted that physicians are the stewards of a [collectively owned] store of medical resources and that physicians have a professional obligation to work for social justice. While they did not explicitly deny the fiduciary role of the physician to the patients in effect  they declared that there was a co duty to conserve the "limited" medical resources as well as the duty  to the individual patient.Contrary to the biblical warning about serving two masters the Charter's authors urge a stewardship of medical resources which subsequent publications by ACP,ABIM and others  said will best be made operational by physicians  following guidelines.

In my opinion this publication is a poster child for the use of gratuitous assertions.

Quoting from the Charter" essential to the contract [medicine's contract with society] is the public trust".


The Charter was published in the Annals of Internal Medicine  and Dr. Harold Sox, the then editor of the Annals of Internal Medicine, offered an introductory commentary. He said in part "the condition of Medical Practice are tempting physicians to abandon their commitment to the primary of patient welfare....the Charter call physicians to promote fair distribution of health care resources"

 I suggest that the choice of the words "primacy of patient welfare" is significant in the omission of the modifier "individual" in front of the word patient. Subsequent promotion of the Charter has made it clear that patient welfare will be defined in terms of the aggregate not in terms of the individual patient.  A subsequent publication ( JAMA: November 13,2013) by Dr. Sox advocating  "population Medicine " made it clear what type of patient welfare Dr Sox favored. See here.

A brief quote from Sox; "

"Perhaps the de facto organizing principle for US health care,approaching each patient strictly as an individual is obsolete.The population health approach is an alternative." (I have added the bolding)

Dr. Sox makes explicit what is hinted at and glossed over in the charter,namely the sacrifice of the individual to the group, the individual patient to the aggregate, or at least  to some aggregate metric claimed to represent the good of the group.

 The charter promised social justice and operationally that has been translated to following guide lines based on alleged aggregate benefit.







Friday, July 06, 2018

Medicine is increasingly dominated by collectivist ideology.

This commentary title is an truncated and slightly altered version  of the following quote from the brilliant essay by Dr. Michel Accad. "Medicine today is dominated by the collectivist ideology" . See here for the reference to his 2009 contribution. 

This is a theme I have thought and fretted about far too much.Many of the thoughts I have mulled over and occasionally expressed in this blog are far better expressed in Dr. Accad's essay. Here is a sample;

"In the broadest sense, medical collectivism is the belief that medicine cannot be left to voluntary and unrestricted transactions between individual patients and individual healers but must be improved, directly or indirectly, by the hand of government."

and another.

" Individuals and populations ,patients and society are conveniently conflated as a matter of fact."

And here is the real money quote.

"..hoodwinking physicians into practicing population medicine is of course the essential means to confuse practitioners into thoughtlessly carry out sweeping interventions whose primary benefit is the profit of third parties."

Docs who were trained in my era ( I know that was a long time now-MD-64) learned that the principle ethical precept was do what was right for the patient and there was ,with few exception.s no other obligations.  What was definitely not on the table was the notion that physicians had an obligation to conserve the nation's medical resources. Social justice was not on the table.


I believe the metaphor of the Bootlegger and the Baptist captures an important aspect of what is happening in  medical practice in the United States.

I do not envision a wide spread plot or conspiracy of third party payers and academic physicians and leaders of major medical professional organizations meeting regularly to further their long term dream of finally taming the physicians and disabusing them of their traditional role as a fiduciary of their patients. However, the third party payers certainty welcome the efforts of the academic medical elite in that regard and some times welcome them into their ranks .

The Baptists in this conception are those physicians who sincerely believe that in the age old conflict between the interests of the individual and those of society as a whole that the trump card would be held by society.The Bootleggers are the third party payers whose bottom line increases in proportion to the acceptance of those views.

Thursday, July 05, 2018

Is the Choosing Wisely campaign a giant flim flam benefitting the thrid party payers?

Is the choosing wisely initiative (CW) just a clever ploy to save money for the third party payer?
 or Is it just about a sincere effort by physicians who really care to eliminate to the extent feasible fraud and waste?

Is CW an extension of the New Professionalism movement?

I  argue that CW is a flim flam and a power grab jointly shared by the third party payers and the medical progressive elite who provide the academic cover and propaganda. I  argue that it is in fact about much more that elimination of fraud and waste and that it is a logical outgrow of a major element of the change in medical ethics that the New Professionalism movement is attempting to bring about.

It is a story about the ACP the ABIM and a foundation ( the ABIMF) established with money obtained from internists taking certifying exams whose fees greatly exceeded any reasonable cost of providing those examinations and about  another foundation  , the Robert Wood Johnson Foundation (RWJF)

I  argue that it is not just the CW ad campaign funded by ABIMF and RWJF but it is larger namely The New Professionalism-Choosing wisely-high value care flim flam.

The New Professionalism authored by folks from ACP,ABIM and the RWJF  provided the cover or alleged philosophical foundation for CW and the push for high value care.The follow the money rule continues to have great explanatory value.


Wednesday, June 27, 2018

Why did the greatest "ancient marathoner" slow down signficantly in his 70s?

Why did the greatest ancient marathoner of all time slow down so much in the decade of his 70s?

At age 73 Ed Whitlock finished a marathon in 2:54:48. Twenty-five years earlier he ran a marathon in 2:31:23. In a quarter of a century his marathon time decreased by only 23 minutes. See here for the blog Cannute's Efficient Running Site 's tribute to Whitlock.

Whitlock's 02 max was measure at 52.8 ml/kilo/min when he was aged 70 and 11 years later at age 82 a measured Ox max was essentially unchanged ( 54 ml/kilo/min).

A person's maximal oxygen consumption ( 02 Max) decreases with age. The per decade decrement is generally said to be between 5 and 10 Percent. The jury is still out regarding if the rate of decline in endurance athletes is more,less or the same as more sedentary humans. There is good evidence indicating that the rate of decline increases around age 70 and values as high as 15 % percent per year or more have been reported. Assuming the 02 Max measurements are correct, Whitlock's 02 max was essentially unchanged during his running trek through his  70s but his marathon times decreased significantly.

As commented on by Cannute, Whitlock in his 40s was a very good marathoner but was not setting world age marathon records . At age 48 he ran a marathon in 2:31:23- a very good time for age-actually any age- but not the record.  Ye,t by age 70 he was setting marathon records for age and continuing setting records until a few months before his death at age 86.He set the age 85plus marathon record in Toronto clocking in a 3:56:33

So what was his secret? Obviously his genetic endowment included a high 02 max. His marathon times did decrease between age 70 and age 80. He was running sub four hour marathon at 80 plus while running sub 3 hour at 70 plus while his measured 02 max seemed constant over that time period.

Of course there is more to running marathon than 02 max.

Whitlock's training in his 70s and 80 did not follow the current generally accepted marathon training  principles. He did no speed work except in races. In his 70s he is said to  have run up to 3 hours a day , almost every day at a very slow pace, described as a slow shuffle. He carried the LSD (long slow distances) program to a extreme.

Tim Noakes, noted exercise physiologists and long time endurance athlete, believes that a major reason than marathon times decrease markedly in the decade of their 70s is that most older runners cannot maintain the hours of training necessary to perform well in the marathon  in part because  there are too manyminor ( and major injuries), too many aches and pains. The muscles endure better than the "connectors", i.e the structures and tissue connecting the bones to the muscles and joints.

Yet it may be that even in the absence of significant injury or a nagging series of minor injuries a human's running speed for distance decreased significantly during the 8th decade of life. (about 25% decrease in marathon running speed for the world's greater old timer marathoner.) One suspect to consider is  muscle loss of "spring function" and the spring function of tendons and the arch of the foot. You figuratively and maybe literally loose the "spring in your step".









Monday, June 25, 2018

Bundle of His Pacing an overnight game changer fifty years in the making may have reached tipping point

Benjamin J. Scherlag,PhD, is credited as the first person to demonstrate an intra cardiac tracing of  His Bundle (HB) electrical activity In1967 he demonstrated ventricular pacing from the bundle of His.

In 1970 OS Narula and Scherlag demonstrated the feasibility of temporary HB pacing in humans.

 In a 1978  article in Circulation, Scherlag,El-Sherif,Lazzara and others presented clinical and experimental data demonstrating the normalization of bundle branch blocks  ( right and left) with HB pacing.

Thirty years after Narula's work, Deshmukh's 2000 publication reported his experience in placing    permanent His Bundle pacing leads in   18 patients with dilated cardiomyopathy,poorly rate controlled atrial fibrillation and narrow QRS complexes who  underwent AV node  ablation. He  later published a larger series with 3 1/2 year follow-up on patients with supra-Hisian AV block.Although results were encouraging, the time for more widespread use of HB pacing has not yet quite arrived. The procedure was thought  to be  too challenging and  commercially designed equipment which would facilitate the procedure was not yet available . It required   a separate mapping catheter and higher pacing thresholds and it was not clear  exactly what subset of patients would be benefited by this method to a degree greater than obtained by the simpler apical right ventricular pacing in regard to which data suggesting the harmful effect of RV pacing were not yet fully appreciated. So HB pacing was not perceived as being ready for prime time.

From 2006 through 2012 work from Kronborg from Denmark and Zanon and others from Italy   strengthened the case for more widespread application of HB pacing.In 2011 Zanon reported the experience from  multi-institutional data using the Medtronic Select Secure system describing 307 patients implanted in the His zone with 87 having direct HB pacing and 220 with indirect or "Para-Hissian" pacing.

Two important papers from the United States were published in 2015:

A series of 98 HB paced  patients was reported by electrophysiologists from the Geisinger Clinic.
 with a longer follow reported by the same group in 2017.Also Lustgarten reported on a cross over trial comparing Bi-ventricular pacing with HB pacing in patients  receiving Cardiac Resynchronization Therapy (CRT).

Both papers indicated that the procedure was less difficult than previously thought due in part to newer specially designed sheath and leads,required lower pacing thresholds than earlier reports and follow-up data regarding stability of leads was encouraging and left ventricular function improved at least as much brought about by Bi-V pacing. Further the Geisinger data , while not a randomized trial,indicated that long term follow-up showed no decrease in left ventricular function while a parallel group who had the standard right ventricular apical pacing did  decrease left ventricular function  and a 22% incidence of pacing induced cardiomyopathy was reported.

In EP cardiology, as in most things, there are tradeoffs. The HB paced patients had , in the Geisinger data, twice as many lead revisions after five years( 6.7% vs 3%) and significantly more generator changes when compared with the RV paced group ( 9% vs 1%) . In additional the procedure time was slightly longer as were  fluoroscopy times.

The Geisinger HB registry data was updated and published in 2018.This article was one of  several recent articles describing experiences with HB pacing in a variety of clinical settings and we may have reached a "tipping point" in terms of EP Cardiologist's attitudes re HB pacing.

Francesco Zanon from Rovigo Italy ,an early adaptor of HB pacing, published data on 147 patients referred with a variety of PM indications and various types of bundle branch block. 80 % of patients experienced disappearance of the BBB . 90% of the  patients had effective HB pacing with a mean follow up of five years. He spoke of a "new philosophy of how we pace".

 One of the fathers of electrophysiology, Benjamin Scherlag,has called for a randomized trial comparing HB with BiV pacing for CRT and Dr. Kenneth Ellenbogen has also commented on the need for  RCTs and wrote an editorial suggesting that possibly HB pacing was the Holy Grail of  pacemaker therapy .









Tuesday, June 12, 2018

age related decline in exercise capacity is not just decrease in 02 max

It has been suggested that the study of the physiology (pathophysiology?) of aging might be informed by the study of aging athletes.

Analyzing information about Ed Whitlock,thought by some to be the greatest "ancient marathoner" ever, may offer some interesting insights.See here for more regarding Whitlock.

02 max measurements were made on Whitlock at age 70 (52.8 ml,/kilo/min)) and age 81 (54ml/kilo/min).

At age 72 he ran a 2:54 marathon and at age 82 his marathon time was 3:41.So his running time decreased significantly from 6.62 minutes per mile to 8.4 minutes per mile.His speed decreased from 9 miles per hour to 7.11 miles per hour, a 20% decrease.  Yet during that same time period his measured maximal oxygen uptake was unchanged. We also know from  published interviews  that his training did not significantly diminish. So what was the cause(s) of his decreased running speed?

The decade of the the 70s is generally said to be one in which the age associated decrease exercise capacity seems to accelerate. and 15 to 20% decrement per ten years have been reported.A reasonable assumption is that a major factor in that decrease is decrease in 02 max. Yet Whitlock's 02 max was unchanged while his running speed decreased in the range typically said to occur in normal humans.

Similar data on other runners have demonstrated that running speed for distance running decreases proportionally greater than the temporal decrease in 02 max.However, in cyclists a different pattern is seen with the 02 max and speed decreasing more proportionately .

It is tempting  to evoke the role of the pounding of the legs in running versus cycling. The long time distance runner and exercise physiologist, Tim Noakes ,has opined about the long term effect of "pounding" on decline in exercise capacity.The constancy of Whitlock's 02 max and the 20% decrease in marathon times from early 70s to early 80 reminds one of the high school coach's aphorism "you are  only as young as your legs".

Could some answers be found in study of titin and its isoforms?Titin (aka connection) is the body's largest protein and is said to act like a spring for muscles, recoiling the sarcomere after it is stretched.

There is a short,stiff isoform ( N2B) as well as other more elastic isofroms ( e.g. N2BA ) . The phosphorylation of titn results in a post translational modification of titin with production of more elastic isoforms. Beta adrenergic stimulation may increase the phosphorylation of titin.

The stiffer ventricular muscles of patients with diastolic heart failure have less of the more elastic titin isoform and more of the shorter stiffer titin isoform.

Titin may or may not play a role -probably more than one factor conspire by a number of mechanisms to cause runners in their seventies to loose much of the "spring in their steps."even if their cardiac output changes little  even though a constant cardiac output over that 10 years period is likely very far out on the curve.






Friday, May 11, 2018

Is ablation better than drugs for A FIb? What did CABANA trial show?

The results of the Cabana trial were presented at the Heart Rhythm Society meeting in May 2018. The full results will be published later. Here is Larry Husten's reporting in Forbes.

The intention-to-treat (ITT) analyses indicated there was no statistically significant difference between ablation and drug treatment in regard to the primary outcome which was the total of death,disabling stroke, serious bleeding and cardiac arrest.

On the other hand the per-protocol analysis (PPA) gave different results indicating  an advantage to the ablation group.

It got down to a battle of the Packers. Dr Doug Packer,who presented the data,said that the per protocol analysis should trump the ITT, while Dr. Milton Packer seemed to think that venerable epidemiologic principles would be violated if one did not follow the ITT analysis.

There is already talk of the need for a sham trial  and EP cardiologists talking about sub-group analysis (ablation maybe better in those under 65 years of age and in those with heart failure) and touting the quality of life benefits of ablation .

One obvious problem (many more will likely be talked about) was the drug treatment group was not homogenous-it  included both rate and various rhythm  control strategies.  

Since there seems to be a battle between the ITT folks and the PPA supporters ,for those who might want to drive deeper into the issue , here is a place to start.

Thursday, May 03, 2018

Argument for aerobic exercise in patients with Parkinson's disease.

There ae no randomized clinical trials that demonstrate the benefit of regular aerobic exercise in delaying the progression of Parkinson's disease  (PD) nor in the decrease in the risk of development of dementia.However the Mayo Clinic has published an excellent review of the literature regarding  the beneficial effect of exercise on various brain areas and functions. See here.

Quoting the authors : "This aggregate literature provides a compelling argument for regular aerobic exercise and cardiovascular fitness attenuating PD progression."


h/t to Dr. Robert Donnell at his blog "Notes from Dr. RW" .


Monday, April 09, 2018

People who are more fit have less atrial fibrillation and less strokes if they develop AF


Individuals who are more fit ( have a higher functional aerobic capacity) are less likely to develop atrial fibrillation (AF) and if they do develop AF they are less likely to have a stroke or die.

These are the conclusions from a long , large study from Mayo Clinic.See https://www.ncbi.nlm.nih.gov/pubmed/29221502. ref 1

The final study cohort included 12,043 patients referred for a treadmill exercise test and were followed for a median time of 14 years (9-17).They were classified into four groups based on functional aerobic capacity (FAC) .Each 10% increase in FAC was associated with an decreased risk of incident AF ,stroke and mortality by 7 %.

Was the decreased risk observed in the more fit due to a direct physiological effect of exercise or a result of the reduction in the standard risk factors observed in the more fit individuals  or is that a distinction without a difference?

Folks who may be accused of exercising too much may find some satisfaction in the data revealing no level of fitness above which there was an increased risk of A demonstrated in this study.In other words they found no "U-shaped curve" regarding level of exercise ( or more properly of fitness as this study did not measure exercise level) and AF risk.




1)Hussain, N, Impact of cardiorespiratory fitness on frequency of atrial fibrillation,stroke and all cause mortality. Am J Cardiol 2018, Jan 1, 121 41-49

Thursday, April 05, 2018

More on the "lying"or at best really stupid electronic medical record

My medical record at a well known medical center -which shall remain nameless-has labelled me as having atrial fibrillation and it seems to be written in indelible electronic ink refractory to my attempts to erase it.

It came about because of two computers conspiring  together. The first was the computer inside of my pace maker.Its algorithm to detect atrial fibrillation detected signals which were interpreted at "AT/AF", meaning atrial tachycardia/ atrial fibrillation. It was a false positive call , tricked by a Pacemaker phenomenon called far field sensing. This occur when the sensing lead in one cardiac chamber senses activity in the other chamber and miscounts it. Ultimately the Medtronic tech recognized it and adjusted the atrial lead sensitivity so that the double counting would not occur. Problem fixed but..

The second computer, my electronic medical record (EMR) latched on to the "diagnosis of atrial fibrillation and will not let go. I have written my "patient portal" with a full explanation indicating that my EP cardiologist concurred.

Recently, I met with my new primary care internist and we discussed my Blood pressure, my pacemaker and no mention was made of AF.He never said the words atrial fibrillation.I gave him two of my old EKGs which did not show atrial fibrillation . Yet when he gave me a copy of my patient visit summary my current health issues were said to be 1.pacemaker 2.atrial fibrillation.

Did the computer write the second diagnosis on its own. Did the doc see it, did he even read what was printed out? I cannot believe he even saw it. I cannot believe a board certified internist of over 25 years experience would not have asked why was I not taking an anticoagulant as my CHADS2-VASc score of 3 would warrant anticoagulation according to all guidelines.In the days of the paper medical record can one imagine an internist handing a patient a report that said he had atrial fibrillation when he was aware of no evidence that he in fact had AF?

Of perhaps less significance, my printout also listed a physician who I had never seen, never heard of before and apparently is a pediatrician not even affiliated with the hospital.

The computer systems with which physicians try to make "meaningful use" were  designed to assist coding and quality reporting and have little to do with really improving patient care and often have the opposite effect and not infrequently are harmful.




Tuesday, March 20, 2018

If endurance exercise is the fountain of youth how much do you have to drink?

The arc (s?) of the normal aging heart -

One of the stories told  by physiologists and cardiologists regarding the age related downhill course of cardiac function is something like this.

One way to simplify  cardiac function is to consider the two parts of the cardiac cycle,1) contraction and ejection of blood and 2) relaxation and the refilling of the ventricle.

There are data indicating that the first signs of an impending problems are seen in the filling phase ie. diastole.From extensive echocardiographic and invasive physiologic measurements in humans the following sequence can be sketched out.

First there is impaired relaxation following by decreased elastic recoil and later diminished  compliance ( which is to say increased stiffness) and then -at least according to work from the EEM group- remodeling of hearts with thicker walls and smaller ventricular volumes).Simply put a sedentary ageing  lifestyle leads to a small stiff heart and long time endurance exercise leads to a larger more easily filled heart.The contractile function of the heart is well preserved with ageing , at least as indicated by measurement  of the ejection fraction.

This is largely consistent with the mainstream echocardiographic model which proposes a predictable,progressive process beginning with impaired relaxation,followed by decreased compliance and ultimately- as a compensation- elevated filling pressures.This model describes three phases of diastolic dysfunction indentifiable by combination of echo findings believed to reflect  how well or poorly blood flows into the ventricles from the atrium. This model recognizes that the various indices ( e.g E/A ratio, IVRT,maximal E wave velocity and the time constant of isovolumic pressure decay (Tau) change with age so that what would be abnormal in a 20 year old is normal in a 75 year old.It is thought that that filling pressure can be estimated by use of this model. NOTE-see end note 1 for reference to data that challenges the mainstream model by in part  providing data that cardiac cath measurements of left sided pressures do not regularly correspond with the three echo defined stages of diastolic dysfunction)

Now we look at what I have labelled as the "Dallas or EEM theory" of cardiac ageing. see end note 2

A series of articles from the University of Texas Southwestern Medical School and the EEM have provided extensive invasive and noninvasive data regarding cardiac function at various ages and the effect of longtime endurance exercise versus sedentary ageing on  cardiac structure and function.

Levine et al first demonstrated that lifelong endurance athletes ( 25 years or more of running a lot) had left ventricular compliance virtually identical to those of sedentary 20-30 years olds. Then they compared ventricular compliance in four groups of 25 each of people who exercised at various levels over a 25 years period. These were all subjects over the age of 64 and were screened to excluded pre-existing heart disease.Group 1 was sedentary people who exercised no more than one session per week. Group 2 were labelled "causal exercisers" and exercised 2-3 times per week. Group 3 (Labelled as committed exercisers}worked out 4-5 times per week and the "competitive" group trained 6-7 times per week and regularly raced.The racers had the most elastic ventricles while group 3 was "very close" in terms of ventricular compliance while groups 1 and 2 has significantly stiffer hearts.

Next Levine studied a group of 70 year old subjects  and an exercise program was unsuccessful in improving the reduced compliance observed in that group. Next a study was able to show that middle aged subjects with a year long exercise program ( that involved in part high intensity interval training) were able to increase their ventricular compliance.


My main question in this regard is "how much exercise "is sufficient to maintain a healthy compliant left ventricle." Levine's amazingly compliant  (pun intended) subjects not only stuck with program for a full year but after the first 6 months participated in a hig intensity interval program using the 4X4 workout program that involves 4 minutes of exercise at 95% of maximal heart rate followed by 4 minutes of rest done four times.


End note 1. Grant et al (Grant A, Grading diastolic function by echocardiography:hemodynamic validation of existing guidelines.Cardiovascular Ultrasound 2015 513 :28) compared echocardiography results with  left heart catherization data in 460 patients.The data demonstrated that there were no differences in regard to left ventricular pressures between patients with normal diastolic function and those with grade 1 or 2 diastolic dysfunction but there were differences between normal and grade 3 diastolic dysfunction in patients with reduced ejection fraction.In those patients with preserved EF, there is no statistical difference between normal and any grade of diastolic dysfunction. (see figure 5 of their article which graphically illustrates the lack of the "predictable, progressive process "which characterizes the  current paradigm.)If the detection of elevated LV pressures which generally correlates with exertional shortness of breath is in part the goal of echo studies of diastolic function it appears to not be reached based on Grant's data.

end note 2. Dr Ben Levine is the founder and director of the Institute for Exercise and Enviromental Medicine (EEM) housed at the Texas Health Presbyterian Hospital Dallas and professor at University of Medicine Southwestern. His group have done a series of comprehensive physiological studies on subjects recruited from the Dallas Heart Study, a population based sample of 6100 subjects in Dallas .
In a nut shell the concept is that everyone with aging develops some degree of diastolic dysfunction related to impaired relaxation and loss of diastolic suction,Later aging (particularly sedentary ageing) is associated with loss of ventricular compliance ( AKA increased stiffness). A long term endurance exercise program is capable of mitigating the changes in compliance but not the decrement in relaxation and diastolic suction. EEM's studies  further indicate that a sedentary lifestyle may lead to a small stiff heart which may be the precursor to heart failure with preserved ejection fraction (HFpEF) ) and the Dallas group suggest that an appropriate amount of endurance type exercise begun no later than early middle age may play an important role in the prevention of HFpEF.

"Humans are pattern-seeking story -telling animals and we are quite adept at telling stories about patterns, whether they exist or not".Michael Shermer.

In 2008, Shermer coined the term "patternicity" -the tendency to find meaningful patterns in meaningless noise. I am not suggesting that the extensive,very carefully done research referenced above is meaningless noise.I just really like the quote but I certainty hope the "Dallas hypothesis" ( my term) is a reasonably accurate approximation of the ways things  really are- having spent a lot of time running a lot over the years.

Sunday, March 18, 2018

Mitochondrial function in octogenarian endurance athletes

Scott Trappe from Ball State University and colleagues from the Karolinska Institute studied 9 lifelong endurance athletes 80 years of age or older  with 6 healthy 80 years olds who did no regular exercise. Aerobic capacity and muscles biopsies -done to measure levels of oxidative enzymes- were compared between the two groups.

The muscle biopsies showed high levels of citrate synthase and beta hydoxyacyl-Co A dehydrogenase in the athletes said to reflect the oxidative potential of the mitochondria. These values were similar to those from untrained young subjects.Quoting the authors: " It is important to note that mitochondrial function normally declines with age and this decline does not appear to be reversible with endurance training in sedentary adults greater than 80 yr old or very old animals." This implies that one has to start earlier and maintain some level of regular aerobic exercise to keep your muscle mitochondrial young.

I have commented  before on the impressive aerobic capacity of select elite older athletes.see here.Trappe'sathletes had measured maximal oxygen uptakes of 38 +/- 1 while the healthy controls averaged 21+/1/ .(O2 max in the range seen in the athletes would roughly correlate to the levels seen in someone able to run a 26.2 marathon in 4 to 4/1/4 hours,A 21 02 Max should allow someone to finish stage 1 of the Bruce treadmill protocol and into the second stage but likely not to completion of Stage 2.)Stage 1 Bruce protocol corresponds to 5 Mets roughly equivalent to walking a 15-16 minute mile and  to be able to finish Stage 2 corresponds to 7 Mets roughly equivalent to jogging a 15 minute mile.

Trappe's article is entitled "New Records" but as amazing as these guys were aerobic wise an Englishman transposed to Canada is one rung above on the aerobic scale. Ed Whitlock at age 80 finished the Toronto Marathon in 3 hours and 15 minutes.Using table 2.3 from Tim Noakes's book ,4 th edition The Lore of Running this time would correspond to an estimated  V02 Max of 50-55! See end note 1





1) Trappe S Et al New Records in aerobic power among octogenarian lifelong endurance athletes.J. Applied Physiology 114.3-10 2013.

End note 1.Rather than considering estimated 02 max from a table we can see actual measured values done on Ed Whitlock on two occasions. From the excellent blog entitled "Canute's efficient Running Site" we learn that just before his 70th birthday Whitlock's measured V02 max was 52.8 and at age 81 it was measured at a physiology lab at McGill to be 54!. Assuming that the difference between 52.8 and 54 was just normal test-retest variation, Whitlock seemed to loose no aerobic capacity over a ten year period. Conventional   wisdom and more than a little data indicate that the 70-80 decade is typically a time period in which there is an accelerated decline in 02 max,perhaps twice that of the 10 % per decade decline than is widely quoted. Whitlock did not get the memo.The VDOTvalues that are referenced on Canute's website and found in detail on Jack Daniel's VDOT Running Calculation web site appear to give more realistic estimates of running times that those that I have been using for comparison with exercise testing comparison that those  found on Noake's table.


addendum: End note 1 was completely redone after discovering Canute's web site.

Tuesday, March 06, 2018

What does reduced ejection fraction in elete athletes mean?

Some NBA players  and  professional European cyclists (1) have been shown to have reduced cardiac ejection fractions (EF) and some NFL players(2 )have EFs in the lower range of normal.

 In regard to the cyclists this observation has , at least in one review, been used to bolster the argument that "too much exercise" is harmful , i.e. support for the  "U-Shaped" curve theory."Too much " exercise certainty can be harmful  (maybe that is what "too much" means) but reduced resting EF in elite athletes is not proof of that contention.

The "wisdom of the body "may dictate that maintenance  of stroke volume a priority and not EF. These athlete have large preloads ( aka end diastolic volumes) so that a smaller percentage can be ejected to maintain the resting stroke volume. These basketball players had a normal increase in stroke volume  and EF with exercise as did the NFL players.I believe the exercise EF was not measured in the cyclists.



1.Abergel, E. Serial left ventricular adaptations in world -class professional cyclists.J AM Coll Cardiology July 2004.
2. Abernethy,WB Echocardiographic characteristics of professional football players.JACC Jan 2003 p 280
3)Engel,D Athletic cardiac remodeling in U.S. professional basket ball players. JAMA Cardiol 2016, (1) 80-87 

Monday, March 05, 2018

Reversing cardiac aging-maybe some but it isn't easy

More about cardiac aging and aerobic exercise  from the Institute for Exercise and  Environmental Medicine  is found  the January 2018 issue of Circulation. Howden et al(1) report the results of a two year trial of a vigorous exercise program on various physiological measurements.

They were able to show some improvement in cardiac compliance ( i.e. a decrease in myocardial stiffness) in a group of middle aged,otherwise healthy subjects over a 2 year period but the exercise required was considerably more than frequent brisk walks or slow jogs around the park.Rather , part of the exercise program involved a vigorous high intensity interval program using the "4 by 4 " Norwegian Skier technique twice a week and later in program only once a week.

Dr. Ben Levine, the Director of the Institute, and his team seemed to be able to recruit subjects who would persevere in a demanding exercise program over a 2 year program  and   to also permit right heart catheterizations which were done to give the investigators a index of compliance of the left ventricle.The bottom line is that they were able to demonstrate a reduction in cardiac stiffness with their exercise program .

This study is the most recent in a series of publications which have demonstrated that there is some level of prolonged endurance exercise that can at least to some degree mitigate the age related loss of cardiac compliance . Previously they had attempted to improve cardiac compliance in older subjects (in their 70's) and were unsuccessful. In this study they hoped they could find a "sweet spot", a time frame in which it was not loo late to reverse the age driven stiffness and they seemed to have , at least to some measurable degree, succeeded .

Levine characterizes the sedentary heart as a "small, stiff heart" versus the endurance athlete's heart as larger,slightly thicker and more compliant.

Levine describes the stages in the aging of the heart :1) loss of relaxation ,2) stiffening ( beginning in middle age), and finally 3) remodeling. The hope is that adequate exercise might mitigate  or significantly delay stage 2 which may be the precursor or  a prerequisite for heart failure with preserved diastolic function. Years of endurance exercise does not seem to prevent the first phase but Levine's data suggest that exercise may counteract the stiffening and remodeling.




1) Howden EJ et al Reversing the cardiac effects of sedentary aging.A randomized trial.Circulation,2018 137; (full text available on line without firewall)

Wednesday, February 21, 2018

diastolic heart failure-do we need a two (or more) hit theory?

Warning The following represents the musings of a non-cardiologist,clearly unqualified by training to speak with much credibility on this subject.

The earliest recognizable phase (s) of diastolic dysfunction seems to happen to everyone if they live long enough and late middle age may be long enough. This phase is labelled, in the jargon of echocardiography, as "impaired relaxation" and  according to the latest expert guidelines technically as " E/A ratio less than or equal to 0.8 and E  wave velocity less than or equal to 50 cm/sec."These values are obtained by measuring blood flow with Doppler technique across the mitral valve. Relaxation occurs simultaneously with elastic recoil (aka restoring forces) from which there is no current method to distinquish it.Authors addressing this topic seem fond of the spring analogy and it has been suggested that the world's largest protein molecule,titin,functions like a spring.

 To perhaps overly simplify a complex process,let us consider diastole or ventricular filling as a three phase event, pre-early, early and late.See end note 1 Pre-early is the phase after the aortic valve closes and before the mitral valve opens (the isovolumic relaxation phase),early is the phase when blood flow rapidly into the ventricle ( as  depicted by Doppler technique as the E wave) ,late is when blood is pushed from the atrium by contraction and represented a the A wave. In the young E is greater than A and remains so probably until about late middle age.when the E wave is no longer higher than A, the echocardiographer  now usually says "impaired relaxation"

The party line current theory describes the early phase of diastole as being driven by relaxation and diastolic suction. Extensive data show that several indices of  diastolic function change in the process of healthy aging. The ventricle takes longer to relax which is signaled   by a prolonged isovolumic relaxation time or IVRT. There is also slowing of the early flow across the mitral valve  depicted by a lower E wave velocity and a lower E/A ratio.

The early mitral velocity of blood flow decreases and the IVRT lengthens- changes believed to represent impaired relaxation and is reported as such on echo reports. (Even though it is generally agreed that there is no way to partition the relative effects of relaxation and diastolic suction as they occur at the same time.)  Simplistically diastolic suction function can be thought of elastic recoil,the release of the stored energy created by contraction. This is also referred to as restoring forces.  The late phase of diastole is influenced by the stiffness or compliance of the ventricle and the contractility of the atrium.

One of the missions of echocardiography is non-invasively estimate the "filling pressure" of the left side of the heart. Filling pressure is the  pressure at the end of diastole also referred to as preload.
Elevated filling pressure can be used to confirm or support the diagnosis of heart failure (HF) and is believed to correlate strongly with shortness of breath on exercise.

Since every one is thought to develop  a decrease early diastolic function but everyone does not develop diastolic heart failure ,could those patients with decreased ( or more decreased) ventricular compliance-which exerts its effect in late diastole- be the HFpEF candidates?

The story of the changes detected in the aging heart as depicted by the Group from Southwestern (1) goes like this:

Early on there is impaired relaxation.Left ventricular stiffening occurs during the transition period between youth and middle-age and "become manifest between the  ages of 50 to 64", This is followed by left ventricular volume shrinkage and remodeling ( wall thickening) after age of 65. So the sequence is impaired relaxation, stiffening and then remodeling.

There are data indicating that about 1/4 patients with stage 2 or 3 diastolic function    progress  to HF.(Impaired relaxation is stage 1, as ventricular stiffness builds up so does the pressure in the atrium and this is reflected with an increase in E ,and E/A increases , a pattern often referred to as pseudonormal (although the most recent ASC guidelines no longer use that term) , as things get worse the LA pressure increases more and values change appropriately earning the designation of restrictive pattern (again this is the older terminology banished by the 2016 revised guidelines)

So maybe a second hit is needed. One such hit could well be prolonged hypertension and the resultant concentric hypertrophy of the heart leading  to decreased ventricular compliance, or at least "ventricular chamber compliance".Left ventricular myocardial changes seen in obesity and diabetes could also represent a second hit and could contribute to both diastolic dysfunction and systolic dysfunction.

Myocyte apoptosis occurs with aging is accompanied by hypertrophy of the surviving myocytes and increase in fibrosis, all of which could conspire to stiffen the ventricle  as well as impairing relaxation.

The group from  Dallas (2) has presented data that a sedentary lifestyle can cause concentric cardiac hypertrophy and that prolonged aerobic exercise  ( at levels as least twice that of the standard exercise prescription which would be about 5 hours of moderate exercise per week) if started by early middle age may prevent the age related loss of ventricular compliance It should be noted that there are data and interpretation of data that contradict that hypothesis. See here  and here for commentary regarding the observations that more aerobic exercise is required to prevent diastolic heart failure that is sufficient to decrease the risk of coronary artery disease.

Diastolic heart failure is a well recognized companion of diabetes .Several possible second hit suspect mechanisms  have been described  in diabetes including deposition of glycation products and increase in myocardial cell tension.

Of course there is much more to it than that. Normal healthy aging per se has been associated with apoptotic loss of heart muscle cell,compensatory hypertrophy of remaining muscles cells and fibrosis leading to some stiffening of the ventricles with the only apparent "hit" being aging. But again that seems to happen to everyone and everyone does not develop diastolic heart failure.Maybe a second hit is needed and again according to the Dallas group a sedentary lifestyle may be one such second hit second hit.See here for commentary on effect of sedentary lifestyle on cardiac remodeling .

In broad, non specific terms the "second hit" is anything that increases cardiac stiffness.





1) Fujimoto,N. Effect of ageing on left ventricular compliance and distensibility in healthy sedentary humansThe Journal of Physiology2012 590 (pt 8)1871 (see end note 2)

2) Dr Benjamin D Levine N Fujimoto Paul Bhella and others have published extensively examining the effect of ageing,exercise and the lack of exercise on various aspects of cardiac function and age related impairment. They posit that long term endurance exercise begun at lest by middle age may prevent the loss of compliance that is common in sedentary human evens in the absence of the usual suspect heart problems (HBP,diabetes,obesity)


end note 1.I know there are "really 4 stages" I left out "diastasis"
end note 2. If anyone can explain to me the difference between compliance and distensiblity please comment.

Addendum 3/16/18 A few more additions to try and get this thing right.