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The Charter ( Medical Professionalism in the New Millennium.A Physician's Charter) did not deal with just the important relationship of ...

Monday, April 09, 2018

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


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

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

The final study cohort included 12043 patients referred for a treadmill exercise test and were followed for a median time of 14 years (9-17).They were classified into four groups based on functional aerobic capacity (FAC) .Each 10% increase in FAC was associated with an decreased risk of incident AF ,stroke and mortality by 7 %.

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

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




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

Thursday, April 05, 2018

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

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

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

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

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

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

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

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




Tuesday, March 20, 2018

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

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

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

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

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

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

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

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

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

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

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


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


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

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

"Humans are pattern-seeking story -telling animals and we are quite adept at telling stories about patterns, whether they exist or not".Michael Shermer.
In 2008, Shermer coined the term "patternicity" -the tendency to find meaningful patterns in meaningless noise. I am not suggesting that the extensive,very carefully done research referenced above is meaningless noise.I just really like the quote but I certainty hope the "Dallas hypothesis" ( my term) proves to be of significant value, having spent a lot of time running a lot over the years.

Sunday, March 18, 2018

Mitochondrial function in octogenarian endurance athletes

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

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

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

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





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

End note 1.Rather than considering estimated 02 max from a table we can see actual measured values done on Ed Whitlock on two occasions. From the excellent blog entitled "Canute's efficient Running Site" we learn that just before his 70th birthday Whitlock's measured V02 max was 52.8 and at age 81 it was measured at a physiology lab at McGill to be 54!. Conventional   wisdom and more than a little data indicate that the 70-80 decade is typically a time period in which there is an accelerated decline in 02 max,perhaps twice that of the 10 % per decade decline than is widely quoted. Whitlock did not get the memo.The VDOTvalues that are referenced on Canute's website and found in detail on Jack Daniel's VDOT Running Calculation web site appear to give more realistic estimates of running times that those that I have been using for comparison with exercise testing comparison that those  found on Noake's table.


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

Tuesday, March 06, 2018

What does reduced ejection fraction in elete athletes mean?

Some NBA  and  professional European cyclists (1) have been shown to have reduced cardiac ejection fractions (EF) and some NFL players(2 )have EFs in the lower range of normal. In regard to the cyclists this observation has , at least in one review, been used to bolster the argument that "too much exercise" is harmful , i.e. support for the  "U-Shaped" curve theory."Too much " exercise certainty can be harmful  (maybe that is what "too much" means) but reduced resting EF in elite . athletes is not proof of that contention.

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



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

Monday, March 05, 2018

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

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

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

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

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

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

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




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

Wednesday, February 21, 2018

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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





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

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


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

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