Lactate threshold and summer time running

Endurance exercise is traditionally considered to be a function of three factors.

1. Cardiac output which is , according to the Fick equation, the product of cardiac output and a-v oxygen difference. Cardiac output is  the product of stroke volume and heart rate.
2.Ability to perform at a high percentage of the O2 Max for prolonged periods.This can be measured or approximated by measurement of the lactate threshold.
3.Running efficiency.

 The lactate threshold is lowered during exercise in hot and humid conditions.

Pappadopoulos  et al (1) demonstrated in healthy young men that exercise at a temperature of 98 degrees  the lactate threshold was increased at a lower oxygen uptake ( from 2.86 +/- 0.13 to 2.38 +/- 0.09) while hypohydration was not shown to alter the lactate threshold.


Tanaka and Seals (2) state that there is evidence that the lactate threshold is lowered in older athletes but not when expressed relative to te percentage of 02 max.This suggests that decreases in lactate threshold may be secondary to decreases in 02 max. but however you look at it is lower.

)Pappadopoulos,c et al "Effect of hypohydration on the lactate threshold in a hot and humid environment." J Sports Med Phys Fitness. 2008 48 (3) 293-298

2)Tanaka,H and Seals,DR "Endurance exercise performance in Masters athletes:age associated changes and underlying physiological mechanisms. J Physiol 2008, 586 55-63

Ed Whitlock's marathon record for age 70 has been broken-well sort of

Gene Dykes, age 70, a retired computer programmer , ran a marathon time time of 2:54 23 at the 2018 Jacksonville Florida marathon . This  is faster than the previous accepted "record" of 2: 54 48 set by legendary Ed Whitlock for runners age 70 and over.

But the time may not be   "official" record time  according to the US Track and Field Association who said that the race was certified by them but was not "sanctioned"  which includes a fee paid by the race organizers to the USTFA  as well as a requirement to buy insurance from them .As of  July 10 2019 Wikipedia lists Dykes as holder of the age 70 record.

According to the USTFA a race must be sanctioned by them for any record setting times to be counted .

So far Whitlock still holds undisputed records for the marathon for ages 75,80 and 85 as well as numerous other age records.

Both  Whitlock and Dykes have had their maximal oxygen uptake measured.

Dykes had a 02 max that was surprisingly low for a very accomplished marathoner , 46.9 ml/kilo/min. But he could run at 93% of his 02 max before reaching his lactate threshold.

For comparison, Whitlock's 02 max at age 70 was 52.8 and 54 at age 82.

Pacemakers,ICD -too many too few? need newc guidelines?

About 200,000 pacemakers (PMs) are implanted annually for slow heart rate reasons  ("brady" indications) in the U.S. as are about 100,00 ICD (intracardiac defibrillators).A smaller number of PMs are implanted for CRT (cardiac resynchronization therapy). Data from 2012 quoted about 35,000 for that indication.

A big increase in ICD use occured after randomized trials showed a morality benefit for ICD in heart failure patients .There were two primary prevention trials- previously ICD were for secondary prevention , i.e patients who had survived a SCD event ( sudden cardiac death)

John Mandrola , writing in Medscape ,makes an interesting case for less use of ICD as does a series of excellent comments by his readers. See here.

Is the integrity of the doctor-patient relationship still a topic?

When I published the essay found below in 2015,there was considerable chatter in the medical blog space about the dangers posed to the traditional physician-patient relationship. Now little is written about that topic. The dogs bark and the caravan moves on.

The following was originally posted on 3/24/2015 and a lightly edited version appears below in the hope that there  may be some physicians who still care .

H.L. Mencken defined Puritanism as that haunting fear that someone,somewhere may be happy.

The Medical Progressive Elite's haunting fear is that someone,somewhere is making their own medical decisions with input from their private physician.This fear is shared by the third party payers. In recent years,there appears to be considerable progress in alleviating their fear.

The last thing that the third party payers and the medical progressive elite want is that medical decisions be made  a physician- patient "dyad".This situation is ripe for a classic Baptists and Bootleggers scenario,some of the  medical elite sincerely believing that medicine is too complex and expensive to be left to the judgment of patients with advice from their physicians and the third party payers striving to decrease the cost of doing business and increasing profits share holder value.

This medicine-is-too important-to-be left-patients-and-their- physicians view  is made crystal clear in the following quote from the book,"New Rules"  written by Drs. Don Berwick and Troyen Brennan:

"Today, this isolated relationship[ they are speaking of the physician patient relationship] is no longer tenable or possible… Traditional medical ethics, based on the doctor-patient dyad must be reformulated to fit the new mold of the delivery of health care...Regulation must evolve. Regulating for improved medical care involves designing appropriate rules with authority...Health care is being rationalized through critical pathways and guidelines. The primary function of regulation in health care, especially as it affects the quality of medical care, is to constrain decentralized individualized decision making."

Dr.Berwick went on the be the  head of CMS for a while and Dr. Brennan went on to be the chief medical office of Aetna insurance company and then CVS Caremark.Sometimes the line between the Baptists and the Bootleggers gets a bit blurry.

Destroying the physician patient "dyad" or relationship  has been a strategic goal of the progressive elite for years and a major initiative to that end was the 2002 publication "Medical Professionalism in the New Millennium:A physician charter".That was a joint effort by the ACP Foundation,the ABIM Foundation and the European Federation of Internal Medicine. The project chair was Troy Brennan and, in my opinion, importantly in terms of future funding and  promotion of the "charter" a member of the project was  Dr. Risa Lavizzo-Mourey of the Robert Wood Johnson Foundation.The RWJF has been a major source of funds for the ad campaign for the Professionalism project.   CEO and . Dr. Harry Kimball ,president of ABIM from 1991 to 2003, was also a project participant.

The Professionalism 's theme is to downplay the fiduciary role of the physician to the patient and insert a nebulous co-duty of  the physician to be a steward of society's limited medical resources and to work for social justice. A particular political agenda was inserted into medical ethics. For physicians who wondered how that role was to be played out, later the ABIMF clarified  things by explaining that one could be a steward of the [collectively owned] medical resources  and social justice would be achieved by providing efficient health care.In one document the authors changed the nature of traditional medical ethics and  also rewrote the meaning of social justice which was now efficient care as opposed to the widely accepted meaning of social justice as redistribution.  In a bait and switch move they have redefined social justice as efficient health care attempting to aggregate the values that individuals might place on a treatment with some collective metric allegedly representing the greatest good to the greatest number.They then further simplified things for the practicing internists (actually all physicians) by gratuitously asserting that following guidelines would be the road to social justice.

Disappointingly, the AMA went along with this flim flam sophistry of the physicians as stewards of society's collectively owned medical resources.See here.

In the ACP-ABIM world no longer would the patient and the physician  be the primary determiners of a test or treatment value but value would be designated as high or low  primarily on a cost effectiveness calculus.Rather than treating each patient as an independent moral agent an aggregate utilitarian metric would be imposed  in which "high value care" is not in the eye of the patient but rather defined by a third party and expressed in  quality adjusted life years per dollar spent The only or at least determinate value is economic efficiency.

Of course, the medical professional elite is a subset of the larger progressive community whose operational credo is that most things are too complex and complicated  to be left to average people and if they will not listen to the delivered wisdom they should be compelled  while the progressive's polar star and major talking point is  to fight against inequality. The poster child for the stick approach has be the comments of Dr. Robert Benson Jr.,the emeritus president of ABIMF,writing on the blog of the ABIMF:

" CMS, which has the ultimate negotiating position in the form of reimbursement for Medicare services, could only accept negotiated bundled charges. It could also refuse payment for non-compliance with the Choosing Wisely recommendations."...ABIM could require candidates to achieve a perfect score on questions related to costs and redundant care as a requirement for admission to secure exams for initial certification or MOC." (This would seem to be a rather severe penalty for not complying with a "recommendation" which Benson thinks should be an edict.)

Consider how important the Choosing Wisely rules would be if  Benson's wishes were enacted.Consider how much of a target the Choosing Wisely decisions would be to various lobbying groups.Third party payers would relish such a situation.

If you want to know what the ABIM and its foundation are about, just read  the ABIMF blog.

The combination of mega hubris and libido domini spells trouble in health care as it does pretty much everywhere.

Why a non-cardiologist thinks generally ablation is bettter than medication for rhythm control

Of course the teaser tittle is misleading.You should ask "better for what".Remember the old auto ad that claimed Fords (or some brand) are better,again better than what and for what.

A  better,more focused claim is that ablation is better than drugs to convert atrial fibrillation to normal sinus rhythm.That issue arises only after the decision of rate versus rhythm control has been made.There is convincing evidence to that point that ablation works better. There is also general agreement that patients feel better with a sinus rhythm than when their atria are fibrillating.Atrial fibrillation is a bad method of running a cardiac pump.

What has not been proven with randomized clinical trials is that ablation results in longer lives and fewer strokes.

The recently presented CABANA trial (https://www.acc.org/latest-in-cardiology/clinical-trials/2018/05/10/15/57/cabana) was long awaited and was hoped to answer that question

This was a large (n=2204),multicenter trial  with five year followup comparing standard AF ablation procedure with either rhythm or rate control medication.When the data were analyzed by the venerable,preferred, orthodox method of analysis ( intention-to-treat or ITT) there was no difference in the combined end points of death,disabling stroke,or cardiac arrest nor was there for each component of the combined end point.

ITT is also referred to as "once randomized always analyzed". If 1,000 were assigned to medication and another 1000 assigned to ablation, all of the Medication group would be analyzed according to the group to which they  were assigned even if they switched over to the ablation group. This method is ,according to standard epidemiologic-statistical dogma, is the only analytic approach which will preserved the "integrity of the randomization process." Randomization is done in the first place to control for the effect of known and unknown variables so that the two groups are balanced in regard to prognostic variables. ITT has been called the de facto standard and it is "conservative", i.e it minimizes Type I error,  it is less likely to show a difference when there is no difference. In criticism of ITT one could say it is too conservative and more susceptible to Type II .

Per protocol analysis (PPA) compares treatment groups that include only those who completed the treatment as originally allocated.Whereas ITT makes the two treatments look similar PPA is more able to how differences.

When PPA was applied to the CABANA data there was demonstrated a decrease in mortality in the ablation group.So there are dueling conclusions based on the method of analysis.(1)

My argument is that regardless of there being no difference in mortality (or maybe there is a difference favoring ablation depending of what analysis you prefer) ablation works better to decrease atrial fibrillation and people feel better without AF and the procedure is safe. It is safe according to either way  you analyze CABANA and we already knew it was safe. The extensive data from Cleveland Clinic  (2) makes that clear. So you do not have to believe that ablation save lives or decreases strokes to favor ablation over rhythm control medication, but of course ablation is not for everyone.

After the data were presented the predictable flurry of spin emerged touting the results  of the PPA and of the "as treated "data.But the EP folks did not really need an alternative analysis to continue with business as usual as ablation is safe,it works better and when successful in decreasing or eliminating the atrial fibrillation "burden" there is better quality of life.

This is certainty not a recommendation to treat everyone with af with ablation but rather an argument in favor of ablation over medication for rhythm control.For  many patients for various clinical reasons, rate control may be the better choice and  a trial of rhythm control meds before ablation is a reasonable and common approach.

1) "...a man hears what he wants to hear and disregards the rest".The Boxer, Simon  and Garfunkel.1982

2)Rehman,KA Life-threatening complications of atrial fibrillation ablation. 16 year experience in a large tertiary care cohort. JACC,March2019, vol 5 no. 3, p 284
(fifteen year period,10,278 patients, no deaths, 100 life threatening complications (mainly pericardial effusions and stroke),no aorto-esophageal fistulas,

Addendum: 10/30/19 This article from the Nov.2019, Journal of American College of Cardiology by Cheng et al presents data suggesting that the Cleveland Clinic experience may not be universal.
http://www.onlinejacc.org/content/74/18/2254?download=true

Does a high coronary calcium score in long time endurance athletes mean greater mortality

Another article (2)  has  been published regarding the proposed relationship between high level endurance exercise and coronary calcification.

 We get this comment from the chief science officer and CEO of the Cooper Institute , Dr. Laura DeFina :

" The key question addressed in the present study was whether the presence of a high CAC associated with high levels of exercise training as typically practiced by masters marathon runners is associated with greater mortality.For this question,the answer is clearly no"

During times when I am influenced by Lily Tomlin's observation (1) I tend to think - perhaps unfairly-of studies such as these as coarse-grain,multi-comparison, big "n" small "RRs" fishing trips.

It is big n  study with 21,758 men followed for about ten years. The significance of n size is that with large numbers,small differences may be statistically significant but not clinically important. The point of saying multi-comparison is that sometimes researchers will do many regressions that may or may not be mentioned in the article searching for a p value of statistical significance. ( I ,of course, am not accusing authors of this article with that practice.)This article cannot be considered fishing as earlier work has suggested that high or very high levels of endurance exercise are associated with more coronary calcification but no increase and possibly a decrease in cardiac disease mortality.This article seems consistent with that notion.

We also get this quote from Dr. Carl Lavie : " Despite the fact that this type of high volume physical activity and exercise may promote calcific coronary atherosclerosis, it appears to still be associated with safety and possible lower mortality risks" Dr. Lavie has written several articles with Dr. James O'Keefe arguing that some relatively low level of exercise described as "excessive" would increase one's risk of death but has subsequently softened views what is excessive.

The analogy with the more potent statins and more coronary artery calcifications and lower C-V mortality seems obvious



1) Lilly Tomlin: No matter how cynical you become its never enough.


2)DeFina, LF et al ,"Association of all cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiol 2019 4 (2)174

Is it possible for experts to determine objective high value health care

Is value objective or subjective?

A common, though oversimplified and exaggerated view,  is that Adam Smith was the father of economics. His views were published in 1776 in his Wealth of Nations.He along with several other early giants of classical economists,David Ricardo,John S. Mill, promoted the Labor theory of value. Karl Marx continued that line of thinking in 1867 in his magnum opus Capital  in which he said " If a pair of shoes usually takes twice as long to produce as a pair of pants,for example then..the competitive price of shoes will be twice the price of pants."

Lawrence H, White , in his book The Clash of Economic Ideas talks about what he describes as the fundamental flaw in the labor theory of value is "its supposition that the price of a good reflects an intrinsic feature of the good,...rather than something in the minds of its buyers". The belief was that input costs determines the selling price rather than the reverse.

It was not until 1871 that the labor theory  of value was displaced by what is known as the subjective or marginal utility theory of value. Karl Menger one of the three co-founders of this idea,who worked independently, said in his Principles of Economics , "Goods always have value to certain economizing individuals and this value is also determined only by those individuals."

Simply put the value of a good or service is the subjective evaluation of the buyer.

In fact,it is this subjective value that underlies exchange-Fred values the apple more than dollar he give the grocer who in turn value the dollar more than the apple.Both  typically thank each other as exchange is mutually beneficial.


So since the late 19th century economists of almost all stripes have agreed that value is subjective.
If this is the overwhelming consensus views of economists what is the rationale or justification for organizations such as the American College of Physicians and others to  claim to be able to determine which medical procedures and treatments are "high value". Are they claiming that value is objective,that they can determine scientifically the real value,and further determine which values are high enough to merit the designation "High value"

First how is value determined by health outcome experts and how is a value determination judged to be "high". Is the process objective and scientific all the way down or is it the case that at some point someone's subjective value is inserted .

Through clinical research it is possible to determine if the outcome of treatment X versus treatment Y is better in terms of survival.So one could talk about life years saved by treatment X versus treatment Y-this is clinical effectiveness research.X is better-more effective than Y in terms of simple survival. But to determine value cost has to be injected into the analysis.How much did X cost versus how much did Y cost.,then one could look at life years saved per dollars and compare X  and Y in that way.

Obviously  years lived  per se is not the only relevant outcome to consider.How one lives (pain,mobility,level of cognition etc) are all important and those and other elements are lumped under the heading "quality of life" (QOL). Measuring quality to transform life years into quality adjusted life years is a difficult and ambiguous slippery  area and we will defer a discussion about whether than can ever be done for later but for discussion we'll assume that something called quality adjusted life years(QALY) can measured. (I seriously doubt that it can be measured  because in part I do not believe you can aggregate quality of life.I doubt that it is meaningful to add Frank and Fred's  quality of life and transform that some aggregate of quality years.)

After the QALY are determined for procedure X and Y then in theory one can sum the cost of the two procedures and then derive a ratio of QALY s per dollar spent. Ignoring for the moment the difficulties and ultimately the arbitrary nature  of teasing out cost from charges in the context of what is certainty not a free market unencumbered by price control  but rather one whose costs exist behind a veil of various variable negotiated prices between providers groups and third party payers with an even more opaque series of subsidies and discounts.


When you brush past the bewildering display of statistical artifacts and step to view the overall landscape what you see is another utilitarian procedure. Some new wine is there but the bottles are stamped underneath with the imprint  "utilitarian analysis" A  resurrection of Benthams "greatest good for the greatest number." in the form of a cost benefit analysis done in the tradition of and with the tools of Neo-classical economics.

Has the movement to debase medical ethics become a done deal now

In 2013,  when I posted the essay found below in a slightly revised version found ,there was still considerable resistance to the "New Medical Professionalism" which had been introduced in 2002 by the American College of Physicians and the European Federations of Internal Medicine. and published in the Annals of Internal Medicine in an article entitled  "Medical Professionalism in the New Millennium: A Physician's Charter." Numerous medical blogs protested and there was some public debates.Now I find little comment or concern about what I believe was a effort to destroy traditional medical ethics.

Here is my earlier essay entitled "The Great Linguistic Coup of 21Th Century Medical Ethics"

"George H. Smith in his book "The System of Liberty" in the chapter entitled "Liberalism,Old and New" discusses how the concept of liberalism and its advocates were victims of a linguistic coup in the latter part  of the nineteenth century.

 The classic liberals considered freedom as the absence of coercion.They championed   limited government whose function was to secure the rights of individuals.Enter a group of thinkers who proposed a " new liberalism" , one that would,in their view, correct this inadequate,limited definition of freedom.To the newcomers liberty without equality was freedom in name only  and true freedom involved equal opportunity and power to enjoy one's life. They wanted to replace the idea of "negative freedom" of the classical liberals with what would become  the focus  of  the welfare state.True freedom in their view was more than mere removal of compulsion or coercion.  The new liberals were paternalistic and believed  the state should do much more than secure the people from internal and external predators but rather protect them from the effects of their own uncoerced actions.The classic liberals defended their position in part by asserting that the new liberalism was old wine in new bottles, with the wine being advocacy for a paternalistic government.The new liberals continued to dispense rhetoric that seemingly supported liberty but they had redefined the word liberty.

The new liberals won the day and the old or classic liberals lost much influence  but re-appeared in the 20th century with a new label, libertarian. The new liberals were simply known as liberals and later referred to by some as progressives.

I argue analogously that the traditional ,classical medical ethics and its advocates ( physicians themselves) were victims of a similar linguistic coup. Throughout most of the 20th century and earlier the core of medical ethics was primacy of patient welfare and respect of the autonomy of the patient,the later gradually replacing an older paternalism of medicine.Physicians were considered to have a fiduciary duty to the patient.

At the end of the 20th century and the early years of the 21th century a new medical ethics emerged,one in which -while  its proponents claimed nothing had really changed-there was a radical sea-change in regard to the duties of the physician.This was accomplished by nothing more rhetorically solid based  or intellectually justified  than a simple gratuitous assertion.The notion of social justice was simply declared to be part of medical professionalism and medical ethics.The degree to which this bogus concept has been accepted and endlessly repeated in medical publications is a tragic shame.The victims of this linguistic coup are the physicians themselves but to a greater degree the patients are the real losers as they have lost their advocates at a time when they may need them the most.

Will the quality crusade be the final corruptor of the medical record?

 File this under "The corruption of the medical record".

  The topic today is the " After visit summary"(AVS).

In my case this was a collection of mistakes,misstatements and falsehoods all neatly printed out in a manner that  may facilitate the physician getting credit for various quality measures.  After reading the AVS I asked myself do I really want a serious medical problem that I may develop to be  overseen by someone who signs off on such a pile of crap.

Recently I saw my primary care physician (PCP) for an annual check up.

Several aspects are worth a blog entry. Today it is the "After visit Summary" (AVS) which was available the next day on the practice's web site .Actually it is the hospital web site's patient portal,
This group of internists is "hired" by the hospital under the guise of being a practice group somehow affiliated with the hospital.Remember there previously was something call the Corporate Medicine Doctrine.

My particular  AVS is a sleek , multicolored document replete with little icons by such entries as your weight (icon of a dial),pulse ( icon of a valentine style heart). etc.

Under "Today's Visit" we see small head shot photo of the physician and a listing of the addressed issues.This was a collection of mistakes,misstatements and outright falsehoods which are now part of my permanent record.

I was said to have atrial fibrillation. I do not have AF. The diagnosis of AF was erroneously placed on the  chart by the EP clinic but was later ( 8 months) corrected and removed from my problem list. I mentioned to my PCP that do not have AF and that the earlier entry was the results of a error in the EP clinic.This was the second time I explained about the diagnosis of AF to him and his scribe with no effect on my permanent record.

I was also said to have "osteopenia of both hips" .WTF. I have had no imaging of my back or hips at that facility .

I was said to have "hypercalcemia"  and "hypergammaglobulinemia "When  first seen by this PCP one issue was a metabolic profile done by my previous PCP that was stuffed with errors, namely elevated, calcium,elevated K and elevated globulin ( all likely the results of hemolyzed blood sample). These were all repeated and found to be normal but some how the diagnosis of hypercalcemia and elevated globulin level remain.

Nevertheless, on my AVS I was told that those issues were addressed.

What is the AVS all about? it is about "meaningful use".It is one of the eligible professional meaningful use core measures. It all began in 2009 with the HITECH act that was designed to "encourage physicians" to use an EHR.There were monetary carrots and sticks. Neither of which seem to me to be much more than chump change particularly after considering the care and feeding of a EHR .

Kaiser Health News and Fortune Magazine have a detailed article describing what a utter disaster the EHR has become.The title is "Death by A Thousand Clicks".

Recent changes in AHA/ACC atrial fibrillation guidelines

One of my favorite EP cardiologists, Dr. John Mandrola,gives his thoughts regarding the 2019 focused update on  atrial fibrillation (AF)  from the AHA/ACC ,Heart Rhythm Society task force.

Here are some of the highlights and the entire article by Mandrola (full text is available) is recommended.

Aspirin is no longer recommended for low risk AF patients. As Mandrola says , just like that, without much of an explanation .

Both the FDA and CMS have approved percutaneous left atrial appendage closure with the Watchman device  and the panel gives it. a class 11b recommendation. Apparently, the panel did not see fit to comment on the 4% risk of device associated thrombosis reported with Watchman.

DOACs now is  officially preferred over warfarin. Not mentioned by Mandrola is the observation that the fewer strokes with DOACs versus warfarin is driven by the fact there  are fewer hemorrhagic strokes with DOAC while there is little if any difference in the number of ischemic strokes.

The task force stated that female sex alone is no longer considered  a risk factor  for stroke in an AF patient per se.

The guideline writers gave a class 11 b (additional studies are needed-procedure may be considered) recommendation for AF ablation in heart failure.Mandrola believes the data supporting AF ablation in HF patients is sufficient for the panel to have given a higher recommendation quoting the positive results of the CASTLE-AF trial that showed a 12% absolute risk reduction in death and in heart failure admissions in the ablation cohort.


Mandrola shares my views on the CHA2DS2VASc score . It is "simple to use , but at its core distills a decidedly continuous risk for a future event down to an integer." He references D. R. Quinn's 2017 review of 34 studies of AF ( reference can be found in Mandrola's review) that illustrate the large variation in the baseline risk of stroke in untreated AF patients. Quoting Mandrola " Translation: We have no idea of the risk in untreated patients.",and yet every day cardiologists and other docs crank out the CHA2DS2VASC and mater-of-factly tell their patient that they have x% annual risk of stroke and suggest how much that risk will be reduced by oral anticoagulation."


I have written about Quinn's study before and quoting from Quinn's article "' 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."

Left anterior fascicular block-comments on epidemiology and ventricular function

Left anterior fascicular block (LAFB) was previously known as left anterior hemiblock (LAH) .The earlier designation can be attributed to the widely accepted   writings of Maurico Rosenbaum whose work ( 1967) seemed to indicate that in humans the left bundle divided into a left  and   a right branch.

This "trifascicular" concept (right bundle branch and the two branches of the left bundle) was widely accepted and persisted  even though  work in 1972 by Demoulin and Kulbertus  make it clear than there was also frequently a septal branch of the left bundle and more importantly that the anatomy of  left bundle is much more complex that simply consisting of two (or three) branchs, i.e. more of a spiderweb or fan.There is great variation in the interconnections and  in only  few of the 49 careful dissections by Demoulin can a simple pattern of 2  or even 3 fascicles be seen. (the patterns can be seen on page 283 of reference 1, full text is available)

Realizing that all models are wrong but some are useful ( George Box, circa 1978),it may be that the LAFB model has some value.

LAFB is diagnosed on EKG when the frontal plan axis is between minus 30 and minus 90 with QRS duration less than 120 msec and the patient does not have an inferior wall myocardial infarction,LVH  or WPW syndrome.So, typically LAD equals LAFB in the EKG reading context.

Mandyam et al ( 2) from UCSF studied long term outcomes in patients with LAFB who at the beginning  of the data collection did not have evidence of heart disease. Using data from the Cardiovascular Health Study (CHS), they compared 39 subjects with LAFB with 1625 patients without LAFB over a 19 year period.The average age of the control groups with 71.4 and the age of LAFB group was 74.9

They report LAFB was significantly associated with atrial fibrillation (AF) Heart failure(CHF) and death with the following p values-AF .02,CHF .02, and death .001.

This was a small  ( 39  patients),coarse grain study.The authors point out that although CHS tries to exclude preexisting disease on entry to the program hypertension or asymptomatic coronary artery disease may have been missed. The authors referenced no corroborating studies .

This UCSF article received considerable medical press coverage in part as it offered some suggestion that the previously accepted notion that LAFB was a  "benign" finding might not be correct but within a year their findings were seeminly contradicted by research from Copenhagen.

JB Nielsen (4) studied the cardiovascular outcome of 222,227 subjects with a 5.7 year  follow-up period. They did find a statistically significant correction between LAFB and AF, HF and both all cause and cardiovascular mortality. However, after adjusting for age and gender only the all cause risk retains statistical significance.

Quoting the authors: "current EKG definition of LAFB is not always clinically important marker of cardiovascular morbidity and mortality beyond what can be expected by age and sex."

What is the effect of LAFB on left ventricular function?

Leeters and colleagues from The Netherlands studied 28 patients  with RBBB,LAFB and heart failure with 2D speckle tracking regional strain measurements as well as healthy controls and 28 LBBB patients. This is not a study of "lone LAFB" as the patients had RBBB and HF and a number of them had scars detected by CMR. Since the RBBB per se would  not affect Left ventricular activation sequence it is reasonable to assume the delay in activation of the anterior LV is due to the LAFB.The study indicated wall motion abnormalities between the anterior wall and inferior wall of the LV analogous to the classic pattern of septal and lateral LV wall dyssynchrony characteristic of LBBB but apparently less disruptive of cardiac function.


1) Fisher,JH Hemiblocks and the fascicular system:myths and implications. J. Of Interventional cardiac electrophysiology 2018 52: 281-285

2)Mandyam, ML Long-term Outcomes of left anterior fascicular block in the absence of overt cardiovascular disease, JAMA 2014 309 (15)1587

3)Leeters IP, et al Left Ventricular regional contraction abnormalities by echocardiographic speckle tracking in combined right bundle branch block with left anterior fascicular block compared to left bundle branch block.J Electrocardiol 2016 49 (3) 353

4)Nielsen, JB et al Left anterior fascicular block and the risk of cardiovascular outcomes.
JAMA Int Med June 2014, 174(6),1001-1003

More data on lifelong exercisers-this time from Ball State

Scott Trappe and colleagues (1) from Ball State Human Performance lab  studied 7 women and 21 men all in their 70's who were lifelong ( fifty years or more) exercisers and compared them to elderly,apparently healthy sedentary  subjects and to heathy young exercisers (average age 25)

The lifelong exercisers exercised 5 days/week with a weekly hourly total of 7 hours. for the past 52 =/- 1 years.

Maximal oxygen uptake was measured on a maximal cycle test and muscles biopsy done to determine a "muscle aerobic profile" (MAP for short). MAP refers to the degree of capillarization and metabolic enzymes eg. Citrate synthase,B-HAD and glycogen phosphorylase  were determined by muscle biopsy in the lateral thigh.

While the MAP was the same as in the young exercising controls the 02 max  of course was not .The set of long time exercising women was small, but rounding up women who have exercisers for fifty years is no small feat.

Comparing the 02 max in young women,exercisers and elderly control women we find: 44,26 and 18 .

The authors conclude : " the data suggest that skeletal muscle metabolic fitness may be easier to maintain with lifelong aerobic exercise than the more central aspects of the cardiovascular system."

The authors mention the fragility index and quote that the value for men is 17.5 ml/kilo/ min and make their educated guess about what it is for women giving 14 ml/kilo/min as the value. I am not sure why women would have a lower number since the index is corrected for weight. Folks fortunate to have values well above those numbers are said to have more physiologic reserve to withstand and survive various homeostasis challenges whose frequency is a function of age.

This index should not be confused with another fragility index which gives an indicator of how robust are the results of a clinical trial.See here for more on that.  (A clinical trial would have an FI of 1 if the hypothetical movement of one patient from the success column to the failure column would make the study no longer statistically significant ( at the p of 0.05 level)

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1) Gries,J et al Cardiovascular and skeletal muscle health with lifelong exercise
JAP 125: 16736 2018 (full text available on line)

In the long run ( or ride) do runners wear out sooner than cyclists?

 Tim Noakes, the MD, PhD exercise physiologist from South Africa has suggested that perhaps many years of running and the gravity assisted  pounding might accelerate the aging process at least as regards muscles and tendons.

If that is the case, might a comparison of the decrement in performance over time between long time runners and long time cyclists be useful  tend to confirm or deny that hypothesis.

Noakes and colleagues made that comparison (see here) and things look better for the cyclists.

We knew all along who would be the collateral damage from the "war" on opioids

This NYT article puts faces on those who bear the collateral damage. No satisfaction from "I told you so" here

Anyone remember "Cure sometimes,treat often,comfort always."

All cases of LBBB do not have the same ventricular contraction pattern or same response to CRT

The block in left bundle branch block (LBBB)-and this can apply to right bundle as well-may not be actually in the left bundle branch, as least as it has been traditionally described.And  the "block" may not mean complete disruption of the electrical cardiac system perhaps just a delay.Further amazingly, at least sometimes,electrical stimulation of the His Bundle can "fix" LBBB obtaining a normal QRS complex.

The traditional text book electrical  anatomical pathway is from sa node to av node to His bundle and then a division into  left and right bundle branches and then to branching purkinje fibers out to the myocardium.

Anatomical work at least as early as 1971 and physiological studies in 1977-1978 demonstrated in both the canine and human heart that the right and left bundles were actually anatomically distinct within the bundle of His.This was described as longitudinal dissociation.

It has been known at least as early as 1978 that stimulation of the his bundle can normalize the ekg pattern of LBBB and RBBB,Presumably-according to the longitudinal dissociation model - in these situations the lesion or block in the bundle  branch was in the His bundle and that stimulation distal to the lesions resulted in a normal ekg.

In other words the left and right bundles are organized longitudinally and separate within the His Bundle.So a lesion in the His bundle could cause LBBB and could be corrected by stimulation distal to the block.

The work done in the 1970s did not really apply to clinical situations  until  cardiac resynchronization (CRT) was proven effective in the treatment of heart failure in the 1990s.  About 30% of patients did not seem to respond to CRT and it was soon realized that the presence of LBBB was a favorable prognostic factor and that , in a sense it was  the impaired electrical conduction system which was the culprit that caused  mechanical dyssynchrony that could markedly impair cardiac function and in some after a variable lag period  lead to disadvantageous cardiac hypertrophy, chamber enlargement and remodeling and heart failure

Further it has been suggested ( Strauss et al ) that the  traditional ekg criteria for LBBB need to be replaced with critieria that make the diagnosis much more specific  and therefore useful in predicting response  from CRT.The QRS duration should be 0.14 seconds for men and 0.13 for women and there should be a double humped QRS either in lead i and AVL or V5 and V6 ( i.e. 2 contiguous leads) .Using the old criteria,according to Strauss, lead to overdiagnosis of true LBBB and included patients who actually had LVH ( left ventricular hypertrophy) and left anterior hemiblock). It was suggested   that patients with "true "LBBB" by EKG are the ones who are likely to benefit from cardiac resynchronization therapy (CRT).

However, results from Denmark and Pittsburgh by Dr. Niels Risum (2) indicated that the sine qua non of "true" LBBB is not necessarily the EKG pattern but rather the mechanical activation pattern ( basically delayed left ventricular activation )which they described in terms of 2D strain echocardiography and that  neither the supposedly specific Strauss criteria nor the traditional criteria   always would  indicate which patients would have that contraction pattern and  would therefore be more likely respond to CRT.See end note # 1for Risum criteria:

Risum and colleagues content that all patients with LBBB diagnosed on EKG do not have delayed left ventricular activation which correspond to their criteria for "classic" LBBB activation pattern.

Risum's work offers an explanation for  at least some of the widely quoted 30% CRT poor response rate .Interestingly, as early as 1979 several different patterns of septal movement were described on echocardiogram in LBBB.( Fujii et al )

Their data demonstrated that during a 4 year follow-up 40% of patients without the classic pattern had an adverse event (combined end point of death,need for LVAD,or heart transplant) versus 14 % in the group with the classic pattern.So since it is not 100% versus 0 % the presence or absence of Risum's classic pattern does not explain all cases of CRT failure.



 It would not be expected, on mechanistic grounds, for Bi-Ventricular pacing to improve cardiac output in patients with right bundle branch block since in RBBB the electrical activation and the contraction pattern of the left ventricle would not be abnormal.There is considerable clinical data that CRT results in RBBB are definitely worse than in LBBB; However, there may be an exception.

Rosenbaum described an RBBB pattern in which there is left axis deviation and broad slurred r waves in I and Avl which was termed LBBB masquerading as RBBB in which an argument has been made that Bi-V pacing might be on benefit.(1)


1)Auriccho, A Does Cardiac Resynchronization therapy have a role in patients with right bundle branch block.irc. Arrhymia Electrophysiol 2014 pg 532

2)Risum,N et al, Identification of typical left bundle branch block contraction by strain echocardiography is additive to electrocardiography in prediction of long term outcomes after cardiac resynchronization therapy. Journal American College of Cardioogy  2015 vol 66 no 6 pg 632

3)Fujii, J K, et al  mode and cross sectional echocardiographic study of left ventricular wall motions in complete left bundle branch block. Brit Heart Journal 1979 42 (3) 255

end note 1
Risum 2d strain echo criteria:
1)early shortening of at least one segment of the septal wall atnd early stretching of at least one segment of the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure

Lone Left bundle branch block and increased afterload -bad combination

I have commented before on functional impairment associated with LBBB. See here.

J Aalen and colleagues  (1) see here demonstrated that  cardiac output in asymptomatic patients with isolated LBBB is very sensitive to afterload as  in elevated arterial pressure as would also occur with strenuous exercise.  (Full text is available on line,)

Dr Aalan studied the effect of increasing afterload on left ventricular ejection fraction (LVEF) in 11 asymptomatic patients with isolated ( or lone) LBBB. Afterload was increased not by exercise by increasing blood pressure (increase of 38 +/-12 mm Hg) by pneumatic extremity constrictors and handgrip exercise .

The controls subjects decreased their LVEF from 60 to 54 while the LBBB patients decreased their LVEF from 56 to 42. The increased heart rate and after load accentuated the effect of the left ventricular dyssynchronous contraction which consists of early septal contraction with bulging of the lateral left ventricular wall and delayed lateral wall contraction and bulging of the septum. In LBBB both the IVCT and the IVRT are increased, i.e slowed contraction and prolonged relaxation.

The severity of cardiac functional impairment is not reflected by the resting LVEF. Most studies have indicated at most a mild decrease. On a personal note, when I developed a LBBB my decrease in running speed was by about 20% -close to the 25% decrease in LVEF note in Aalan's paper. (decrease from a fairly comfortable 12 minute mile run  to a difficult 15 minute mile with unusual calf discomfort)

I received 2 comments on the blog post mentioned in the first paragraph from readers indicating their exercise history after LBBB onset was similar to mine.

Lone LBBB is often considered asymptomatic and  often is at rest.  A person not doing strenuous exercise would likely not notice any problem and probably for that reason many texts describe LBBB as asymptomatic. For example, Mayo Clinic Patient website -" in most people BBB does not cause symptoms " and Up to Date "LBBB can also be seen in  asymptomatic patients with structurally normal hearts."(Both accessed on 2/6/19) The key here is "with structurally normal hearts". Patients with already reduced EFs may experience significant worsening of exercise ability with onset of LBBB.

1) Aalen J  et al Afterload hypersensitivity in patients with left bundle branch block . Jan, 2018 JACC Cardiovas imaging.

Is the link between atrial fibrillation and obesity epicardial fat?

The epicardial fat pad image on chest x-rays was long regarded as nothing more than a barely  interesting incidental finding of no clinical importance. That no longer appears to be the case.

The epidemiologic data having   established a  sound correlation between obesity and risk of atrial fibrillation , the electrophysiologic (EP) cardiologists  began to speculate on possible mechanistic explanations. These so far have included activation of pro-fibrotic pathways,atrial fibrosis, abnormal connexin, ( gap junction proteins necessary for heart cell action potential propagation) diastolic dysfunction , paracrine effect due to proximity of epicardial fat to myocytes,  and more recently  detailed scrutiny of  the role or roles  of epicardial fat to which has been assigned the ironic designation, of  EAT (epicardial adipose tissue) in deleterious remodeling of the left atrium.

At least as early as 2003 cardiac fat  acting like an endocrine organ was identified as a source of inflammatory cytokines ( Il-6,TNF-alpha, etc) that could  possibly promote coronary artery disease. Mazurek et al (2) found higher levels of inflammatory cytokines in patients with significant CAD.

Now EAT is accused of playing a role in the genesis of AF.

Dr, Mahajan and co-workers from Australia  studied 27 obese patients and 27 non obese patients who underwent AF ablation for AF. The obese groups demonstrated evidence of electroanatomical remodeling (global reduction in conduction velocity and increased electrogram fractionation) .The obese group had increased EAT and low atrial voltage in the posterior aspect of the left  atrium adjacent to EAT.

Author quotes:

" obesity related conduction abnormalities were most prominent in the posterior left atrium which was in close contact with the epicardial fat. "

"Obesity results in expansion of EAT and marked electroanatomical remodeling of the left atrium,creating a substrate for AF"



1)Mahajan, R etl al Electroanatomical Remodeling of the atria in Obesity. Impact of adjacent epicardial Fat.JACC, clinical electrophysiology vol 4, no 12, 2018 ,p 1531.

2)Mazurk, T et al Human Epicardial adipose tissue is a source of inflammatory mediators.
Circulation 2003, 108 r122-128

Did a third randomized trial for PSA screening reconcile the conflict betwen the first two?

Did the third RCT settle the issue of the efficacy of PSA screening for prostate disease?  The short answer is no - that settling purportedly was   achieved by another statistical analysis. ( see reference # 2 for that) at least for a while .

There are now three large RCTs (1) that have addressed the subject.

1) the PLCO
2) The ERSPC
3) the Cluster Randomized Trial of PSA testing for Prostate Cancer.

Only the ERSPC demonstrated reduction in cancer in an "invitation to screening"  with PSA setting.

So did the two out three being negative settle the issue? Not even close.

In 2012, faced with two conflicting RCTs the USPSTF decided to recommend against screening with PSA.Then a third RCT was completed showing no difference in mortality in the PSA screened group.

So if the score was 2 to 1 showing no benefit for PSA screening why did the USPSTF recant and return to their recommendation of "shared decision making" in 2018?

 The answer seems to be that Tsodikov from the University of Michigan ( and 21 other authors from various institutions)   did some adroit statistical footwork (2) in an effort to reconcile the disparate findings. Their work appears successful with the conclusion
being that when the proper type analysis is done (taking into account mean lead time) both the PLCO and the ERSPC both demonstrated approximately the same decrease in mortality with PSA screening.
Note the original analysis did not show a benefit to screening .

So now the score is two RCTs in favor of screening with one against and the current USPSTF recommendation is for shared decision making.


1)A blueprint for cancer screening and early detection :Advanced screening's contribution to cancer control. Wender RC et al . Ca,A Cancer Journal for Clinicians, Vol 49, no 1 Jan/Feb 2019 ( This is an excellent review of screening for cancer detection in average risk, asymptomatic adults including breast,cervix,colorectal,endometrial,lung and prostate.}


2)Tsodikov, A Reconciling the effects of screening on prostate cancer mortrality in the ERSPC and PLCO trials, An Intern Med. 2018, 168 608


"Life is short,art long,opportunity fleeting, experience treacherous,judgment difficult."Hippocrates.

Left bundle branch block -a really big deal part 2

Left bundle branch block (LBBB) is associated with a contraction pattern(s), that are dyssynchronous in regard to the pattern of left venricular (LV) relaxation and contraction.

The first "big deal " I commented on was the observation that the ventricular dyssynchrony associated with LBBB per se can lead to heart failure. See here.

The next big deal is that the pattern of ventricular dyssynchrony typical of "true" LBBB is determinative of a favorable clinical response to CRT and the presence of a LBBB EKG pattern does not necessary indicate a underlying LBBB dyssynchronous pattern.


Risum et al (1) list 3 criteria for the typical contraction pattern of a "true"LBBB
(these apply to description of a longitudinal stain curve in a 4 chamber 2-D strain echocardiogram)

1)early shortening of one or more segment in the ventricular septal wall and early stretching in one or more segments in the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure

The early shortening of the septum is recognizable on standard echocardiography and referred to as "septal flash". "Apical rocking" is another echo finding in which there is a rocking motion  of the LV apical  myocardium perpendicular to the long axis. These two findings seem to be the findings on routine echo exams that correspond at least to some degree  (possibly large degree) to the Risum's criteria from strain echocardiography and  perhaps share to some degree the predictive power as regards outcomes of cardiac resynchronization therapy (CRT).

Those patients with a ekg pattern of LBBB and these findings on strain echo are much more likely to have a favorable clinical response to CRT.

Not all patients with a typical LBBB EkG pattern have what Risum refers to as the typical LBBB contraction pattern which is predictive of likelihood of favorable response. to CRT.This seems to hold true in regard to both the standard criteria for LBBB and the newer Strauss criteria .


Quoting Risum : "It seems reasonable to believe that the main mechanism underlying the differential effect from CRT according to QRS morphology is whether a significant activation delay is present in the LV". ( my underlining)

Question: Does the presence of septal flash and apical rocking predict likelihood of success with CRT as good or better than Risum's criteria? Have the two set of criteria been directly compared? While I could find no direct comparison ,Stankovic et al (2) published data that indicated apical rock and septal flash could predict reverse remodeling with a sensitivity of 84 % and 79% and the absence of both was associated with unfavorable long term survival.

Bottom line from Risum's work is that a patient may have EKG criteria for LBBB  (either the standard criteria or the new criteria proposed by Strauss) and not have the mechanical dyssynchrony pattern described by Risum  and not respond well to RCT.

So is the evidence strong enough to recommend pre-implantation 2d strain echo and not proceed with Bi-V pacing if the Risum criteria are not met? Is the absence of apical rock and septal flash reason to not proceed with Bi-v (or His Bundle) implantation?



1) Risum , N Identification of typical left bundle branch block contraction by strain echocardiography is additive electrocariography in prediction of long-term outcome after cardiac resynchronization
J Amer Coll of cardiology, 2015, vol 66, no. 631-641

2)Stankovic, I Relationship of visually assessed apical rocking and septal flah and long term survival following cardiac resynchronization therapy (PREDICT-CRT) Eur Heart J Cardiovasc Imaging. 2016,Mar 17 (3)262-9

addendum 1/30/19 reference to the Stankovic paper added

Once I thought I knew how to advise people how to eat to reduce heart disease risk , Now....

Read this recent brief overview of diet and fats and carbs and and cholesterol levels  and heart disease risk and see if you would presume to advise patients on how to eat. I am glad that I am out of that business.

I have written several times on medical hubris . In light of what we think we "know" now and what I advised ten years ago,I think "who is without sin....." I believed I had the answer while having answers was little more than parroting the recommendations of boards and organizations.

You have to remember the lawyer's classic query "Doctor, where you wrong then or are you wrong now/"

Neither the pre-operative beta blocker debacle nor the post menopausal use of estrogen and progesterone missteps seem to be a teaching moment for the population medicine devotees. The pop med folks , as explicated here would presume to take funds away from the treatment of some to fund preventive program to others which would "after a few generations" bring about a utilitarian gain by some metric even as some might suffer now.

At the time of this writing serious doubt has been cast on the previously widely disseminated advice about how to eat to avoid heart disease and who should take aspirin for primary prevention of coronary artery disease and who , if anyone, shovel be screened to detect low vitamin D levels, just to name a few of the ever changing array of medical recommendation to prevent disease and death. 

The internist who once upon a time was thought to be the physician trained to diagnose and treat complex complicated medical conditions has to extent  that she is now a ambulist ( at least those who are not now hospitalists) sends her time in part giving advice about how to prevent disease. How to eat,how often to get a cervical cancer screening test or a colonoscopy , who should take statins of aspirin or vitamins  and how much to exercise. For this you did not need to study four years in medical school and then three of more years of internal medicine training.You just need to subscribe to a service ( an app on your IPAD) to keep you up to date on the latest, and every changing, recommendation of various panels.