At follow-up in 2004-2006, 37 had died (most in the older age group) and 11 were lost to follow-up.  Among the 78 remaining ones, 17% had AF and 13% lone AF.  Broken down by age group, the AF prevalence was 18% in group I, 14% in group II and 25% in group III.

Click to enlarge

As expected, the subjects with AF had larger atrial sizes when measured at follow-up.  LV mass was not measured (the less sensitive wall thickness was similar among AF and non-AF subjects).

The baseline data were limited to physical examination, PFT’s, ECG at rest and with exercise, as well as VO2 max measurement.

A slow heart rate and prolonged PQ interval, both indicators of vagal tone, were strong discriminant of the future risk of AF in the younger age group (HR 44 ± 5 for LAF and 53 ± 9 for sinus subjects; PQ 0.17 ± 0.05 for LAF and 0.17 ± 0.02 for sinus subjects).  A similar pattern was found for the overall cohort, although the effect was not as strong.

Intensity and duration of training, height (at follow-up), thyroid tests and HgA1c (at follow-up) were not associated with AF status.

Take-home:  This supports the hypothesis that AF in endurance athletes may be significantly impacted by autonomic tone. A speaker at this year’s ACC meeting emphasized the same point.

I previously reported on the very unusual story that broke out a year ago about the French pharmaceutical regulator being potentially the subject of criminal investigation for allowing the continuing sales of the anorectic drug Mediator despite the publication of data suggesting it could be harmful.

The case is currently on the desk of judges and it appears that ANSM (formerly AFFSAPS) may be facing charges of manslaughter!

I commented that the scientific data with which the agency is getting indicted is incredibly meager, but the criminal aspect of the conduct may not be so much that AFFSAPS allowed a harmful drug to be sold on the market, but that it allowed it on the market longer than the other EC countries.

With bureaucratic principles and legal doctrine becoming more similar among Western nations subjecting themselves to the oversight of supranational organizations, I suspect US trial lawyers will be watching this development with great interest.

Until recently the reason for the delay was obscure, but in the March issue of Cardiology News inside information is provided by cardiologist Sidney Smith.  The UNC professor of medicine, who has made a career out of writing practice guidelines for the American Heart Association, is a senior writer on the JNC-8 panel and this is what he had to say:

The delay has been due in large part to an unprecedented degree of prerelease review by numerous government agencies at a multitude of levels. This extensive and time-consuming advance scrutiny was instituted mainly because many health officials felt blindsided by the publication of the U.S. Preventive Health Services Task Force controversial mammography guidelines, which kicked up a hornet’s nest of criticism in the breast cancer and public health communities. Government officials don’t ever want to be caught by surprise like that again, explained Dr. Smith, professor of medicine at the University of North Carolina, Chapel Hill.

That’s right.  There is nothing more frustrating for a government official than to be caught by surprise by a body of medical experts sifting through scientific data for the benefit of practitioners.  The report must first be approved by the authorities!

We suppose that when the government pays for so much of health care and medical research, it’s only natural it would try to ensure that scientists have the national interest in mind, No?

This paper is yet another report from the Physician’s Health Study, a very large and very old clinical trial/prospective cohort study that followed some 22,000 physicians by questionnaire administered at various time points.  One initial aim of the study was to test any mortality benefit of some primary prevention measures (daily aspirin, beta-carotene), but enough data was collected that numerous other associations (or lack of) have been reported over the years.  This particular report looked at the association between responses to exercise questionnaires administered at the 3-year and 9-year time points in the study, and subsequent development of atrial fibrillation (self-reported).

Again, these data mining efforts are always difficult to interpret.  Quite a bit of effort was put into adjusting for confounders for the development of AF, including alcohol intake, BMI, etc.  Three multi-variable models were tested and the statistical analysis is mind-numbing, as expected.  In addition to controlling for variables, they had to look at answers to risk factors and exercise questionnaires at various time points and adjust the analysis accordingly, since not all who were exercising vigorously at first necessarily kept up the lifestyle later one, etc.

There were enough participants that the level of exercise could be categorized into several buckets.  The referent group were the non-exercisers. Note that they treated frequency of exercise as a continuous variable and assigned the ‘mid-point’ value between the response to the 3-year questionnaire and to the 9-year questionnaire.  Adjustments of that sort are inevitable in these kinds of study, but naturally they impact the realism of the model.

A relationship between exercise and risk of AF could be found only in the “regular vigorous” group, .e. those who broke a sweat with exercise and exercised 5-7 days a week.  If those were divided according to sporting activity (those who practice more than one activity were excluded), a significant relationship could only be found among the joggers.

For the joggers in the study, the main findings are in the graph below:

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For the group of vigorous exercisers as a whole, a relationship between AF risk and exercise was somewhat stronger if one looked at participants who were younger than 50 at entry.

Take Home:  This study adds a little bit to the evidence linking chronic vigorous exercise to risk of AF.  No new aspects of that relationship are revealed.

The coroner Philip Barlow (not to be confused with Philip Marlowe!)  is decidedly non-committal:

She had taken a supplement containing DMAA, which on a balance of probability, in combination [with] extreme exertion, caused cardiac failure, which resulted in her death.

Apparently, there was no obvious cardiac abnormality at autopsy.  William McKenna, a world authority on hypertrophic cardiomyopathy was also involved in the case and is quoted in The Guardian as saying:

In an apparently fit and healthy young woman who dies suddenly in the last stages of the London marathon, with no abnormalities identified to explain her death, the toxicology identifying an amphetamine-like substance does suggest its contribution to her [cardiac] arrest, particularly after excessive exercise.

The Guardian article also quotes cardiologist Sanjay Sharma, the marathon’s medical director, who suggests that she had massive pulmonary edema.  But the reported  coroner’s findings do not specifically corroborate this.  Significant pulmonary edema or hemorrhage would support a “toxic” effect on the pulmonary capillary bed, as opposed to a “simple” VF arrest.

Another finding of the inquest is the testimony of Squires’ acupuncturist that she had incidentally detected an irregular heart beat a year before.  However, the runner apparently did not seek any formal evaluation for this.

As we have seen before, stimulant use is likely to be very prevalent among competitive athletes.  The potential role of these drugs in the development of cardiac complications associated with high-performance sports should not be overlooked.

For this particular study they looked at outcomes after consecutive cases of atrial flutter ablation performed between 1999 and 2003.  Their EP center happened to routinely administer an exercise questionnaire to all ablation patients as part of another study on cardiac risk factors.  The questionnaire was apparently reasonably detailed.  Here is what they used to define endurance exercise:

Patients performing at least 3 h of sports per week were considered as performing regular sports activity and analysed versus those performing less. Sports activity needed to be intense, defined by competitive participation or aiming for a maximal training effect (semi-competitive).  Endurance sports was defined as semi-competitive participation in cycling, running and/or swimming for
3 h/week.

So clearly, we are not necessary talking about super intense training, but nevertheless, probably more than your casual jogger.  The endurance sports patients were younger than the sedentary group and dominated by males, otherwise baseline characteristics were similar, including LA size.  There was less hypertension in the exercise group:

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By univariate analysis, pre-ablation endurance training was a factor in post ablation afib (post ablation endurance sport was not, but the numbers were small):

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The difference in outcomes between those who were not engaged in endurance sport before ablation and those who were is noted in a Kaplan-Meier curve.

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Take home:

Because the group as defined is heterogeneous (or at least, not well described in terms of exercise intensity and duration), it is hard to know what to make of this.  Notice that afib post flutter ablation is quite common early on, regardless of activity level.  The number of data points followed out to one year is very small (7 athletes) and even smaller beyond that.

Also there was no systematic attempt at following these patients.  The incidence of AF was ascertained by looking at the clinic charts.  It is possible that the patients in the endurance exercise group (who are younger) are more likely to be symptomatic from the AF and therefore more likely to bring it to the attention of the electrophysiologists.

I don’t think this study adds any solid data to our understanding of the relationship of exercise and A-fib.

ROSE:  What took you so long?

SOCRATES:  Sorry, a sporting interest has distracted me…Where were we?

Socrates, sportsman

ROSE:  You were going to give me my report card back.

SOCRATES:  Ah yes!  Well, it’s mixed…

ROSE:  I could sense as much.

SOCRATES:  You see, Geoffrey, I think that you let your political sensitivities get ahead of your science.

ROSE:  What do you mean?

SOCRATES:  Let’s reflect on the tension between individual freedom and social constraints, a topic which you naturally discuss.  You would agree that people have diverse viewpoints about what is an appropriate constraint on individual freedom and what is not, wouldn’t you?

ROSE: Naturally.

SOCRATES:  People can disagree both on the kinds of constraints that are appropriate, as well as the degree to which a given constraint should be allowed.  For example, some people may be very comfortable with military conscription when the nation is facing a certain level of perceived threat, yet readily object to mandatory vaccination even if the nation were to face a serious health threat.

ROSE:  I grant you that, although this particular position seems quite irrational to me.

SOCRATES:  I’m not saying that it is rational or not, I’m only pointing out that people do hold different opinions on the subject, and those opinions cannot be placed on a simple scale.  Other people may favor both military conscription and mandatory vaccination.  For the most part, most will be able to articulate some reasoning behind their position.  One can disagree with a given position, but you cannot outright accuse people of being irrational for holding a certain position.  One’s choices in that regard are complex and governed by a number of factors.

ROSE: Including social conditioning!

SOCRATES:  Yes, but you yourself admit that social reality is not strictly determinant of individual behavior (1).  In that, you seem to have some reservation about Emile Durkheim‘s theory, although some scholar’s have highlighted some commonality between your perpective and his.  A bit further in your book, you jab at Margaret Thatcher and her view that “society does not exist, there are only individuals and families.(2)”

E. Durkheim, sociologist

M. Thatcher, ferrum domina

ROSE:  That’s a most appalling moral viewpoint and I still can’t get over that we allow ourselves to elect governments with such disregard for the effects of social conditions on people’s behavior and chances in life!  But where are you going with this?

SOCRATES:  Would you agree that your political views gravitate toward the cluster of opinions that might be called progressivism?  In general, that worldview calls for social reforms, support for welfare programs, particularly in health care, and dislike of militarism.

A little Rose book of preventive medicine

ROSE:  Socrates, if your point is that my political views have shaped my preventive strategy, I think you really missed my point.

SOCRATES:  It is, and I don’t think I have.  But let me ask you point blank:  you don’t think your research shaped your political philosophy, do you?  Nowhere in your book, which is quite personal, do you mention any sort of “conversion” in your worldview as a result of your work as an epidemiologist.

ROSE:  I think that’s correct.  My views, like those of most people, were formed by the time I was a young adult.  But I tell you this, Socrates, nothing in my work has challenged my political convictions.  If anything, my research has affirmed them.

SOCRATES:  That’s pretty much where I was going, Geoff.  Let me take you back to the first chapter of your book, which we have not really covered and where you lay out the foundation arguments for your interest in prevention.

ROSE:  I didn’t think there would be anything controversial there!

SOCRATES:  That may be precisely why the chapter is worth examining.  You start the very first paragraph of your book with a simple observation, if I may quote:

Few diseases are the inescapable lot of humanity, for a problem that is common in one place will usually prove to be rare somewhere else.  Cervical cancer is twenty times commoner in Colombia than in Israel, 10 per cent of Indian children die before their first birthday whereas in Western countries 99 per cent of babes survive, and according to UK census figures 3.1 per cent of adults in Wales report that they are permanently sick, compared with only 1.2 per cent of residents in southeast England.  There is no known biological reason why every population should not be as healthy as the best.(3)

And you end the chapter with a pithy remark which you call “The Humanitarian Argument:”

It is better to be healthy than ill or dead.  That is the beginning and the end of the only real argument for preventive medicine.  It is sufficient.(4)

Dr. Rose, humanitarian

ROSE:  What’s wrong with that and why are you smirking?

SOCRATES:  It’s because it seems you are taking issue with the one thing I’m most famous for!

ROSE: Come again?

SOCRATES:  Come on, Geoffrey!  You took elementary logic, didn’t you?  How do students learn the basic form of a syllogism?

ROSE:  All men are mortal, Socrates was a man, blah, blah, blah.  I get it… but again, what’s your point?

Socrates, mortal (man)

SOCRATES:  You claim that “few diseases are the inescapable lot of humanity” and you contrast being healthy with being ill or dead.  But while no single disease is the inescapable lot of mankind, some disease surely is, don’t you agree?  Sometimes, being dead is the healthiest thing that can happen.

ROSE:  I see your point, perhaps I was over-emphatic on this.  But what does that change?

SOCRATES:  You approach things with the enthusiasm of a positivist.

ROSE:  That’s absurd!  Positivism was discredited as a general theory and I do not hold that everything can be reduced to quantifiable phenomena.

SOCRATES:  Did I touch a nerve?  I don’t want to apply a label to you, Geoff.  I didn’t accuse you of being a positivist but only of having the enthusiasm of one.  And that’s a natural and sometimes laudable inclination, provided it is kept in its proper boundaries.

Look who you quote in the second paragraph of your book:

Epidemics appear, and often disappear without traces, when a new culture period has started; thus with leprosy, and the English sweat.  The history of epidemics is therefore the history of disturbances of human culture. (R. Virchow, quoted from Ackerknecht, EH. Therapeutics from the primitives to the 20th century) (5)

My point is this:   Like Virchow, you start off your inquiry with a view that disease (and perhaps much of evil) is the result of faulty social structures. Consequently, the solution lies in improving the social structures.  For Virchow, most disease was infectious or nutritional, and he could directly relate epidemics to social problems of hygiene, war, poverty.

ROSE: Not a bad insight, if you ask me.

SOCRATES:  Yes, but with the improvement in hygiene and water sanitation and the development of vaccines and antibiotic treatment, infectious epidemics vanished but, low and behold, other diseases began to surface: hypertension, coronary disease, diabetes.  What’s worse, those newcomers affected the rich!  One couldn’t easily invoke “disturbances of human culture” here.  It was back to the wrath of God!…Until, of course, the risk factor concept was introduced.

ROSE:  So far, so good, Socrates, no objection to what you are saying.

SOCRATES:  Except that the risk factor is a puny substitute for the germ theory of disease.  Here we have Koch’s postulates, there we have the p value.  Here we have a single etiologic agent, there we have “multifactorial” muck.

ROSE:  Well, that’s reality.  What do you want us to do?  Sit around until we find the cause of heart disease?

SOCRATES:  I understand that you’re limited with what you have to work with, on the one hand.  On the other hand, easy adoption of the risk factor concept opens many doors!  And for you, that was your opportunity to connect social determinants with health and make achievable what Virchow dreamed to see established:  that “Medicine is a social science, and politics is nothing else but medicine on a large scale. (7)”

R. Virchow, politician on a small (cellular?) scale

In other words, you found in the risk factor a scientific justification for your political inclinations.

To summarize your theory:  Disease occurs at the tail end of a continuous risk factor curve —> Entire risk factor curves can be seen to “shift” when social conditions vary, accounting for the changing prevalence of disease —> Social conditions themselves can be viewed as continuous risk factors curves and ultimately account for the majority of diseases —> In order to prevent disease in a meaningful way, we must tackle social “inequities.”

ROSE:  Not a bad formulation. I like it.

SOCRATES:  Perhaps you were conditioned to liking it by your pre-existing political convictions.  Pasteur may have said that “chance favours only the prepared mind,”  but a mind that is too prepared to anticipate certain patterns can be fooled by its observations.  It seems that you were so keen on demonstrating the nefarious effects of social problems that you quickly latched on to your idea of shifting distribution curves, but overlooked many holes in your theory.

ROSE:  And what holes are we talking about?

SOCRATES:  I already highlighted the problems with your view that every disease follows a continuum, as well as the problem of not always knowing what shape the distribution curve follows (which you concede).  There is also the problem that epidemiology cannot usually establish causation—and you concede this point as well.

There is the problem of adequately defining what the “population approach” is and distinguishing it from the “high-risk” approach.  One can define abnormal cut-off values for a risk factor such that its prevalence will be greatly increased and the distinction between the two approaches will be blurred.

In terms of trade-offs between implementing what is good “for the population” and the cost that must be borne by individuals for the benefits of the collectivity, although you acknowledge early on the “prevention paradox (8),” you do not deeply consider its moral implications.  You only emphasize the potential benefits to individuals that the population approach can bring.  And for all your claim that ‘personal freedom is paramount (9),’ you minimize the paternalism of your strategy.

Most importantly there is the problem of unintended consequences of population-based interventions: a minuscule error in judgment will have massive consequences.  You did not live to see the rise in obesity in Western countries, which some researchers attribute to misguided dietary public health policies.  You also missed the embarrassment felt by the medical community in finding out that the estrogen replacement therapy which you advocated to reduce osteoporosis and which others promoted to reduce cardiovascular disease led to countless increases in thrombosis, stroke and cancer cases.  There are many such cases where expert opinion is convinced that the proposed intervention carries little risk and can reap great benefits, only to find itself dumbfounded by reality.

In terms of social and political changes, no one will dispute that poverty is the mother of all risk factors.  But the remedy lies in understanding correctly what constitutes prosperity.  The experiment to abolish inequalities has been carried out several times in recent history.  The effects on health have been rather disastrous…

A little red book of preventive medicine

Finally, as much as you side-step the issue, the population-based changes which you advocate can only be implemented under the strong arm of government.  I find your treatment of the role of government to be rather confused.  The State cannot at once “protect the individual’s freedom” and carry out population-wide changes.  Public health services have historically always emanated from the military.  I’m afraid your attempts to shift curves are tantamount to a form of civil war.

ROSE:  A civil war!  That’s the last thing I intended!  I even said that war is the largest threat to public health (6)!

SOCRATES:  Then declare peace on risk factors and let doctors deal with them at the local level.

ROSE: What level would that be?

SOCRATES:  The level of the examination table, of course.

ROSE: Is that all you have to say?

SOCRATES:  I told you my report card was mixed, therefore there must be some good in all of this.  I must tell you that your observation that blood pressure curves can “shift” is most provocative in light of the Platt vs. Pickering debate.

Contrary to what you, think, that debate was never really settled.  The fundamental question about the ‘nature of hypertension’ remains essentially unanswered to this day.  The dispute fizzled in the early 70′s primarily because of therapeutics.  Once the blood pressure could be lowered safely, no one cared any more if hypertension was a distinct disease or the tail end of a spectrum of normality.

For the most part, doctors continue to behave as if Platt was right.  Public health advocates view high blood pressure the way Pickering did.  There is a modus vivendi between the two position that masks a true underlying contradiction.  Platt and Pickering cannot both be right!  Perhaps that’s why the hypertension community seemed to now be tied into a knot and why the Americans have been unable to produce new hypertension guidelines in almost 10 years.

At any rate, if your observation that blood pressure distribution curves shift is correct, it raises questions of major proportion.  For this insight, the medical community owes you a tip of the hat.

ROSE:  Thank you Socrates, but where do we go from here?

SOCRATES:  I’ll leave it at that, Geoffrey.  I’m only wise enough to ask the questions.  If you want to pursue this more, I suggest consulting the student of a student of mine.  He would appreciate the opportunity to be once again solicited in mainstream academic circles.

A former Akademia student

____________________________________________________________

Bold references:

1. Rose ‘s Strategy, 2nd ed.  p. 95-96
2. Ibid p. 129
3. ibid p. 35
4. ibid p. 38
5. Ibid p. 35
6. Ibid p. 157
7. R. Virchow, 1848 Die Medizinische Reform, 2. Quoted in Henry Ernest Sigerist, Medicine and Human Welfare, (1941) 93.
8. Ibid p. 47
9. Ibid p. 148

____________________________________________________________

UPDATE:  This series is now complete and consists of a total of 9 posts.  Beginning with Post #3 I am aided in this exploration by a legendary cross-examiner who interviews Geoffrey Rose’s directly and in depth in an informal Q&A format.  Quick links to the part are here: 1, 2, 3, 4, 5, 6, 7, 8, 9

Subjects in both groups (n=107 in each) were asked to respond to an activity questionnaire and were subjected to a physical and echocardiographic examination.  The questionnaire was fairly detailed and tried to capture years of activity as well as intensity, both in terms of occupational and sports activity.  As we know, such methods do have important limitations.

Here are the main findings:

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Activity level was much higher among the LAF group then among controls.  Note that the data is expressed as median (25th-75th quartiles) which makes the difference between the groups look really striking, when in fact there is overlap for each measure (for example, there are sedentary people in the LAF group and pretty active people in the control group).  Nevertheless, the difference is not trivial.

I wish they had provided us scatter plots or histograms instead of summary measures, but the next table tries to give some texture to the findings by listing the number of subject in each activity category for each group:

Notwithstanding the imprecision with which effort intensity was graded (in term of heavy or moderate), there is clearly a skew in terms of moderate and heavier activity among those with lone AF compared to controls.  This goes for occupational as well as for athletic activity.

The statistical tests also pointed to an effect of height as well as of BSA (but not BMI).

As expected, LA size was also greater among patients, but so was LV size and mass.  Mass was greater by a significant margin (187 vs. 158 g and 105 vs. 90 g/m2 for mass index).

In the multivariate analysis, moderate and heavy physical activity, height, and LA anteroposterior diameter were independently associated with LAF.

LV mass was not independently associated with LAF , so mass was presumably related to physical activity.  Notably, measures of LV diastolic function were not associated with LAF.

Looking at tertiles of cumulated moderate and heavy physical activity, there was a graded increase in the odds ratio of AF.

Notes:  This is a better case control study than the previous one by the same group.  The number of subjects is greater and this study shows a more compelling association between AF and total lifetime physical activity than the previous one did.  It seems that assessment of physical activity was more carefully done here.

The authors concede that the selection of controls may have skewed that population toward a more sedentary group, thus possibly enhancing the difference in activity with the patients.

Take home messages:

• The association between physical activity and lone AF in a general population setting found in this study supports the notion that it is also physical activity which is responsible for the higher incidence of AF among top endurance athletes (as opposed to, say, performance-enhancing drugs, unusual diets, or whatever else could distinguish endurance athletes).

• This study adds to the evidence that for AF at least, there is a cumulative dose effect as far as physical activity is concerned.  The fact that occupational activity was included may point to an effect of isometric, as opposed to endurance, effort.  However, much of the “heavy” activity was accounted for by sports (Table 2).

• The abnormalities in LA size and LV mass suggest that lone AF is not so lone after all (this is supported by other studies).

• The finding that height may be associated with lone AF risk is not specific to humans.  Large animals, such as equines, seem to be frequently afflicted by AF.  (Makes one wonder what the prevalence of AF is among professional jockeys…)

Here’s the play-by-play:

O’Keefe starts with Thomas Bassler’s 1977 proposal that “marathon running confers immunity against heart attacks” and counters that claim with an anecdote about a long-standing marathon runner whom he found to have a high coronary calcium score at age 68.  He then states that the patient had no risk factors (adding under his breath “…to speak of….” ).

What is that supposed to indicate?  That marathon running does not make us “immune to heart disease” is certainly not news to anyone.  Unfortunately this anecdote sets the tone for the rest of the monologue.

O’Keefe goes on to quote this Lancet study of 400,000 Taiwainese residents who were asked to complete self-administered activity questionnaires and were followed for 10 years or so.  Here is the graph shown during the talk:

O’Keefe stresses the point that the mortality benefit for those in the “vigorous activity” group levels off with increasing volume of daily activity, while for the moderate exerciser, it continues to increase.  That may well be true, but bizarrely he barely ackowledges the fact that the mortality reduction is far greater for the vigorous exercisers at any volume of activity!

Incidentally, he also makes the comment that he and his colleagues “published an editorial along with this.”   Well, the alleged editorial was actually a letter to the editor in which O’Keefe et al. asked the study authors if any adverse effects of vigorous exercise were seen at all.  Here is the response from the authors:

James O’Keefe and colleagues raise an interesting question as to whether excessive strenuous exercise can become deleterious. We showed graphically that the benefits of mortality reduction peaked at 50 min with a hazard ratio of 0·60, without showing that it continues beyond 70 min. By 120 min, the hazard ratio for all-cause mortality was around 0·55, with even better hazard ratios for cardiovascular diseases (although less than 0·3% did daily vigorous exercise at this level). The adverse effects of strenuous exercise for incremental efforts for more than an hour a day did not seem to outweigh the benefits. We were not able to identify an upper limit of physical activity, either moderate or vigorous, above which more harm than good will occur in terms of longterm life expectancy benefits—an observation similarly made by the 2008 Physical Activity Guidelines for Americans. (emphasis mine)

O’Keefe then switches gear to tell us of his love for “evolutionary medicine,” where supposedly “looking at nature and our deep past we can find the template for ideal health.”   What he means by that is not entirely clear but his bibliography on PUBMED seems to indicate some attraction to the “hunter-gatherer” lifestyle.

Next, he advances the point that exercise, like any other pharmaceutical, has a therapeutic window of some sort:  below a certain “dose” it is ineffective;  above another level it is toxic.  O’Keefe then makes claims that sustained high cardiac output can cause “stretching” and “burning” of the heart, pointing to the serum troponin elevations seen after marathon running and illustrated, for example, in this paper and in the graph below:

Click to enlarge

O’Keefe goes on to describe in dramatic terms these troponin elevations and studies showing increases in myocardial fibrosis, coronary calcium, atrial fibrillation, and ventricular tachycardia in veteran athletes, as if cardiac failure was an inevitable outcome of sustained high-endurance training.

Next, we again get an anecdote, this time the story of Micah True, whose autopsy report officially described a dilated cardiomyopathy.  O’Keefe will have us believe that from his reading of the autopsy report, Micah True had “what we might expect to see in some extreme endurance athletes,” as if the putative athletic heart cardiomyopathy bears a recognizable pathognomonic signature.  According to O’Keefe, caballo blanco had a classic case of “Phidippides Cardiomyopathy,” a term coined by Dr. Peter McCullough who seems equally enthusiastic about postulating the existence of an athletic heart disease.*

O’Keefe ends the talk by plugging his 2 yet to be published studies which will “revolutionize” how we think about exercise.  For this we’ll have to wait and see until the details are available for review.

Parting thoughts:

The detrimental effects of long-term endurance training are potentially very serious.  Who’s at risk, what the risk really is, and what should individuals do regarding their level of activity, however, is far from settled.

Is there a thoughtful to approach this problem?  I certainly hope one will emerge.  But at this point in time, athletes young and old deserve dispassionate appraisal of the available data, not hyperbole about “arteries becoming harder than bones,” premature pronouncements on hypothetical pathophysiological mechanisms, or romantic notions that health can be found in the Cro-Magnon way of living.

O’Keefe tells us: “as a cardiologist, I’m in the business of finding the ideal diet and lifestyle.”  I’m afraid that if he has his way, we will be served another platter of a one-size-fits-all recommendation.

For the last 40 years enlightened cardiologists have been telling us the wrong thing on what we should eat.  Does a handful of provocative studies give them now the necessary wisdom to tell us how we should run?

____________

(*)  In my opinion, Phidippides’ sudden death is much more plausibly the result of Octopus pot disease than of any putative fibrosis induced by chronic endurance training.

____________

UPDATE:  As always, Lawrence Creswell does an excellent job of putting things in perspective.  He shares his thoughts on the 2 studies that O’Keefe is alluding to.  He also points to other blog entries, notably one by Alex Hutchinson, the edits “sweat science” at Runner’s World.

Participants in the 1990 Barcelona marathons were invited to participate in a health survey (unrelated to the topic of atrial fibrillation).  A total of 252 runners agreed.  Age range at entry was 20-60.  Of these, 183 agreed to participate in a follow-up examination in 2002-03, on average 11 years after the initial marathon.

The controls were selected from a near contemporaneous, unrelated study of 802 subjects (age range 25-74) performed in the Barcelona region.  All subjects who were sedentary (< 305 kcal/day of leisure activity) were selected.  That made up a group of 305 subjects.  Of these, 290 agreed to respond at the 2003-03 follow-up.  The study design is below:

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Despite being younger and leaner than the control group, the group of marathoners had a higher rate of atrial fibrillation (prevalence ~ 5% among marathon runners).  Note: consumption of alcohol was greater among marathon runners…

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The authors then compared the marathon runners with AF compared to those without AF.  There was no identifiable clinical or echocardiographic difference at the baseline visit.  At the follow-up visit, LA dimension was greater in the fibbers (chicken or egg?).

The data tables are below.

Main take-home lesson: the study solidifies the increased risk of AF in athletes.  Still no distinguishing predictive baseline characteristics and no real handle on whether any monitoring can identify athletes on the verge of developing significant AF (the paper by Furlanello et al. suggested AF could be reversed if caught early and activity level is decreased)

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