Tuesday, May 19, 2015

Can a regular exercise program improve cardiac function in asymptomatic diastolic dysfunction with and without heart failure?

 Well ,at least one recent research paper answered that question in the affirmative.

 Dr. Nole and colleagues  (see below for reference) did a detailed study on the effects of endurance and resistance exercise on a small group of patients, some of who only had diastolic dysfunction (DD) and others who in addition had heart failure (HF) with preserved ejection fraction.

 For purposes of the study normal diastolic function was defined as having: the following echocardiographic findings 1) E/A greater than one,2)E/e prime less than  10 and 3) preserved E/A greater than one during the valsalva maneuver.The E/A ratio is the ratio of early diastolic filling of the ventricle to the late filling (aka atrial kick).The E/e prime ratio is the ratio of velocity of early diastolic filling to the movement of the mitral value annulus as determined by tissue Doppler  and is thought to be a reasonable estimate of the pulmonary capillary pressure.

 See here for the full text article.

Basically the exercise program which was mainly endurance training with some resistance exercise added later in the program lead to improvement in symptoms in those who were symptomatic and in indices of diastolic function as determined by cardiac echos.

Other studies have also demonstrated that exercise training can improve diastolic function.I have commented before about the effects of long time endurance exercise and the possible mitigation of age related diastolic dysfunction.

.WNolte K., Schwarz S., Gelbrich G., Mensching S., Siegmund F., Wachter R., Hasenfuss G., D√ľngen H.-D., Herrmann-Lingen C., Halle M., Pieske B., and Edelmann F. (2014) Effects of long-term endurance and resistance training on diastolic function, exercise capacity, and quality of life in asymptomatic diastolic dysfunction vs. heart failure with preserved ejection fraction, ESC Heart Failure, 1, pages 5974, doi: 10.1002/ehf2.12007

Wednesday, May 13, 2015

Summertime running in the south, quicker glygogen depletion and possible value of ice slurries

You don't have to be an exercise physiologists to know you cannot run as fast or as long in the summer.

One of the reasons that long training runs don't work out as well is the mater of glycogen depletion occurring sooner in hot weather. .This seems to be a fairly well demonstrated physiological fact.See here. Of course volume depletion is a more dominant limiting factor.

 First a brief taste of stylized "glycogenology". The classical 70 kilogram person of physiology textbook lore carries around about 100 grams of glycogen in the liver and about 500 grams in muscles.Liver glycogen can be broken down and released into the blood as glucose while muscle glycogen can only be directly used locally to fuel muscle action,getting ATP to the myosin heads.After a 24 hour fast some 50-60% of liver glycogen is depleted to supply glucose for resting metabolic activities. Indirectly, muscle glycogen can function as a blood sugar source by producing lactate which can be transported to the liver and converted back to glucose (Cori Cycle).Glycogen depletion is a major factor in endurance exercise adventures and this can be mitigated a bit by glycogen loading,ingesting carbohydrates during the event,repleting liver glycogen before the event and by lots of training which hopefully shifts the fuel mix somewhat to fat utilization delaying the time of glycogen depletion.When that occurs you slow down appreciably as muscles fuled mainly by free fatty acids cannot contract as rapidly. 

 So, maybe if you can keep cooler you can delay glycogen depletion.

One thing  you can do to keep cooler seems to be to drink ice slurries.

I quote from an article in the Scandinavian Journal of Medicine and Science in Sports By authors Tan and Lee from the National University of Singapore.See here for abstract.

"The ingestion of ice slurry during exercise is a practical and an effective strategy that greatest the greatest heat sink because of the additional energy required to effect a phase change from solid ice to liquid water.A smaller volume of ice slurrry ( as compared with that of cold drinks is required to achieve similar reductions in body core temperature and improvements in endurance performance."

An earlier paper by J Dugas compared running times in the heat ingesting slurries with cold water and found his subjects could run further before exhaustion with the slurry. See here.

A similar study from Australia   by Siegel and co authors also showed a increase in running duration ( about 20%) in the heat when cold water ingestion was compared with ingestion of ice slurry.See here.

The ice slurry function as a Heat Sink, a concept well known to folks who fiddle around inside computers.The small ice particles have a high surface area to volume ratio which facilitates heat transfer.

If you like snow cones you might give it a try on a hot summer days. I find the  slurries refreshing and fun to eat whether my endurance is enhanced on not. 

Thursday, May 07, 2015

The U.S. medical care boondoggle depends on hookwinking the physicians

The terms hoodwink and boondoggle are so appropriate. My comments here were inspired in large measure by Dr Michel Accad's Jan 2009 insightful  blog entry from which I quote:

'... beyond ignoring the obvious tension between the individual and the group,hoodwinking physicians into practicing "population medicine" is of course the essential  means to confuse practitioners into thoughtlessly carrying out sweeping intervention whose primary benefit is the profit of third parties."

 to this I add and the profit-not necessarily in monetary terms-of the academics whose writings give a scholarly veneer to this monumental hoodwinking enterprise.

See here for Dr. Accad's entire essay,

In this regard several terms and concepts are important:  population medicine, physicians as stewards of finite resources,cost  effectiveness research and  high value care. The key idea is to establish the notion that medical resources is a collectively owned resource and all are entitled to it by virtue of their existence. From this follows that the  utility of the aggregate matters and not that of the individual and that  some one has to manage this collectively owned resource and the elite medical progressives are the self nominated candidates for that job.

The medical  progressive's claim  to being egalitarian advocates of social justice is contradicted by their advocacy for a utilitarian approach to the allocation of these finite resources. Utilitarianism is not a subset of egalitarianism.A leading egalitarian, John Rawls accurately characterizes utilitarianism as being inattentive to the separateness of individuals and treating people merely as means for the achievement of some aggregate or social end. The medical progressives claim to promote social justice in the abstract but operationally sponsor utilitarian calculus in which some individuals may suffer from some alleged statistical benefit to the collective. The progressives play the social justice card frequently in their polemics profiting from this polymorphic notion's lack of generally agreed upon specificity - the term social justice is loose , vague and indeterminate.

The medical progressives causally dismiss the notion of rationing by their unilateral re-definition  which excludes the limiting of "low value" care from their universe  of rationing. Rationing according to this formulation means only limiting high value care and they presume they will be the arbiters of what value is high and what value is low. 

Another linguistic trap is to speak of a given medical expenditure as a "cost to the system" rather than an exchange.  So when someone goes to the ER with chest pain or severe headache that is considered to be a cost to the system or even more ridiculously a drain of resources rather than providing a service for a fee and the transfer of funds as part of various exchanges that are part of the ER medical encounters.

 When someone goes to a car repair shop to replace a radiator or visits a barber for a haircut why do we not speak of draining the car care industry's resources or depleting the finite hair care resources?It is because to a large degree we are paying for the medical care with someone else's money It is the third party payers and their academic facilitators that have accomplished a monumental hoodwinking of the public and most of the medical profession by distorting the language of medical care and shifted the emphasis from a long standing  oath based imperative to care for the patient to one of limiting care the effect of which is to benefit the third party payers

 The language of medicine has been transformed into the language of medical collectivism and the third party payers owe a large debt to the efforts of the collectivists in medical academia and in some of those individuals in influential leadership positions of certain professional medical associations.

In support of the claim that many physicians have been hoodwinked is the amazing amount of support  from professionals medical organizations for the passage of the so-called "doc-fix" or MACRA which mainly replaced one centrally planned system of price controls with another such system , one that placed even more control of medical care in the hands of federal planners and administrators and some "thought leaders" who have arisen from the leadership of various national medical organizations with important input from the lobbyists from the "Bigs" (big pharma,big hospital, big insurance,etc)

In closing I quote Dr. Accad again with this masterful summary:

" But beyond ignoring the obvious tension between the individual and the group, hoodwinking physicians into practicing “population medicine” is of course the essential means to confuse practitioners into thoughtlessly carrying out sweeping interventions whose primary benefit is the profit of third parties.  Only clever sophistry can claim to reconcile the needs of patients with the profit margin of insurance companies, the bottom line of hospital administrators, the end-of-the-month income of practitioners, the annual reports of employers, the promises of legislators, the zeal of government regulators, the self-importance of academics, the confused intentions of voters, and the pocketbooks of taxpayers.  The term “society” simply conceals the myriad of interest groups that partake in the boondoggle we call the health care system."

Monday, May 04, 2015

endurance exercise and the right ventricle-some thoughts

The issue of the effect(s) of endurance exercise on the right ventricle bothers me from time to time and I have blogged about it before.(see here)

A number of studies have shown that endurance exercise marathons,triathlons, etc,  may result in transient changes in right ventricular function  (increased volume , decreased ejection fraction), while such changes in the left ventricle are typically not the case although some transient changes have been documented..But an important question is- do repeated episodes of prolonged exercise lead to some deleterious changes in the right  ventricle  which could include a predisposition to ventricular tachycardia or worse.Is there an exercise induced clinical picture of ARVD in someone who does not have the recognized genetic profile for ARVD?(see below).After thinking about it again and reading more about it,I think maybe but it does not seem to happen very often.

J. Ector and co workers studied right ventricular  (RV) function  in a group of  22 endurance athletes who had experienced episodes  of ventricular arrhythmias and concluded "Endurance athletes with arrhythmias have a high prevalence of right ventricular structural and/or arrhythmic involvement." ,the implication being the repeated endurance events predisposed to the rhythm problems (Eur Heart J. 2007, Feb 28 (3),345-53)

LaGerche studied 39 endurance athletes, see here, immediately after an endurance event,and one week later with echocardiography and Magnetic resonance Imaging. with gadolinium. Transient RV function changes noted immediately after  the event resolved by one week but 5/39 demonstrated  late deposition of gadolinium (delayed gadolenium enhancement or DGE) in the interventricular septum.The authors seemed to assume that the MR findings were fibrotic lesions and were causally related  to multiple bouts of endurance exercise but the actual cause of the late deposition of gadolinium has not been determined but it is true that  in some contexts ( maybe most) the histologic basis of the delayed gadolenium uptake does  represent fibrosis.

Arrhymogenic right ventricular dysplasia (ARVD)-also called Arrhymogenic right ventricular cardiomyopathy) is an inherited condition primarily involving the right ventricle with replacement of cardiac muscle with fibrous tissue and fat, leading to decreased  right ventricular function and predisposition to arrhythmias including ventricular tachycardia and ventricular fibrillation.. Typically it is inherited as an autosomal dominant and involves several mutations in the genes that code for the desomsomal adhesive proteins which function to help bind muscle cells together.

ARVC is much more common in Italy and naturally there is more awareness in Italy and more more published research. The most common cause of sudden cardiac  death in the young in Italy is ARVC accounting for 22% of deaths versus 7 % from hypertrophic cardiomyopathy (HCM) in contrast to  HCM being the most common congenital problem found in sudden deaths in young athletes..See here for details of the long standing cardiac screening program in Italy.

While it seem reasonable to conjecture that a person with one of the ARVD gene patterns might hasten the clinical manifestations of ARVD by endurance exercise , is it possible/likely that a person could bring about an  ARVD-like clinical picture by repeated endurance training and endurance events in the absence of the Italian or other recognized  genetic patterns ?

Earlier work in 2009  by Breuckmann et al ( see here ) also demonstrated some marathoners with delayed gadolenium enhancement (DGE) but in a different distribution that seen in LaGerche's subjects. Of 102 marathon runners age 50-72 who had run at least five marathons in the preceding 3 years,12 showed a DGE .Of those, 5 had a "coronary artery disease" pattern along the distribution of the left anterior descending coronary artery while 7 showed a "predominantly midmyocardial patchy pattern".Could these midmyocardial patches of presumed fibrosis be the earliest lesions of a endurance athlete's cardiomyopathy, which to my knowledge, except for arguably ARVC , has not been reported. Have autopsies been done on Tarahumara runners?

Monday, April 27, 2015

Standard maximal heart rate prediction formula may result in an underestimate

For stress tests purposes ( regular treadmill and nuclear exercise imaging) physicians  typically use the formula : Maximal heart rate =220-age.

Another formula is the Tanaka formula; Maximal heart rate =209-.7

More recently based on a Norwegian study by Nes  and co workers the following formula is suggested :

Maximal heart rate= 211-.64 with an error term of +/- 10.8. See here for reference.

For the three formulas applied to a 75 year old we get maximal heart rate predictions of
145,156 and 163 . (Standard,Tanaka,Nes)

Frequently stress tests are terminated at when the patient reaches 85% of the predicted max heart rate.
For the three formula we get :


The validity of a stress tests depends in part on having the patient exercise to a high enough level to induce some degree of stress into the stress tests and use of 220-age formula would seem to make  false negative tests more likely.This is not breaking news, Tanaka said as much in his 2001 article in the American College of Cardiology Journalo  but still some  stress test facilities still use the 220 formula . See here.

Thursday, April 23, 2015

Do we neeed to worry about the right ventricle in endurance exercise?

Is the right ventricle the Achilles heel of endurance exercise? I wrote briefly about this subject in 2007 .

In that regard there is more data now about which to fret.  A 2011 article by researchers in Australia and Belgium  gives reason to believe that endurance exercise affects the left and right ventricles differently and possibly  not in a good way .Could endurance exercise induce chronic changes in the structure of the right ventricle such that it is vulnerable to ventricular arrhythmias, similar to those related to an inherited cardiomyopathy (arrhythmogenic right ventricular cardiomyopathy).  See here. ARVC is very uncommon in the US but more commonly seen in Europe particularly in Italy where it is said to be the most common cause of sudden cardiac death in young athletes.

 The authors studied 40 well trained endurance athletes before an event , immediately afterwards and 6-11 days later.Echocardiograms were done at all three times and cardiac MRs were done at baseline. 

 Immediately post race, right ventricular ejection fraction was reduced  and RV volume was increased while comparable   changes were not present in the left ventricle. RV function did recover by one week except for an echo derived index  called "global strain".(In echo lingo strain means deformation which can be determined by tissue Doppler techniques)

Five of the 39 athletes demonstrated delayed gadolinium enhancement (DGE) in the ventricular septum. These changes believed to represent fibrosis were more common in the athletes who had  been competitive endurance athletes longer  and the authors suggested that the areas of  fibrosis noted on the gadolinium scan were in the area of the septum which bulges into the left ventricle as a result of the tissue deformation noted  in the right ventricle.

As the authors stated, the long-term clinical significance warrants further study.Will there be re-modelling of the RV in such a way as to predispose to ventricular arrhythmias?

Another publication by some of the same authors  had previously examined the prevalence of gene mutations in athletes with complex ventricular arrhythmias. Specifically they looked for desmosomal gene mutations of the type typical of ARVC ( Arrhythmogenic  Right Ventricular Cardiomyopathy). Desmosomes are complexes of protein that function to facilitate cell to cell adhesion. In 20 of the 47 cases no desmosome gene mutations was identified.A suggestion was made that prolonged endurance exercise could bring about remodeling of the right ventricle which would predispose to ventricular arrhythmias  even in some athletes who do not have the recognized desmosomal gene mutation..I wrote in more detail about this study here.

The right ventricular issue may well be worth worrying a bit about but the small but consistently  increased incidence of atrial fibrillation in long term exercisers has a more robust data base in its support

Wednesday, April 22, 2015

Is the doc-fix bill worse than SGR?

Here is what Dr. Scott Gottlieb has to say in his Forbes column on 3/19/15:

"The current Medicare reforms being put before Congress ( he was writing before the bill was passed) are better than the existing scheme, the so-called sustainable growth rate or SGR. But the new measures sill envisions Medicare actuaries and  at the center of a price setting process. Now they will also have the authority to mandate clinical practice standards. That this woeful development stands as an improvement to the status quo is a measure of how much our current approach has corroded so many aspects of medical care."

That is I believe the worse and most important part of MACRA. The folks at Medicare will mandate clinical practice standards that it turn will drive physicians compensation.Some well intentioned physicians working within various medical societies sincerely believe they can inject rationality into those yet to be written standards.Those well intentioned few are up against the lobbying powers of the various crony capitalists,the bureaucratic inertia of the administrative state, and the bully pulpit power of a subset of the leadership of professional organizations who either sincerely or cynically advocate for the purportedly calculable  good of the collective over the individual patient.

Yes, of course it is good that physicians no longer have the threat of a 21% immediate reduction in fees and to receive a slight increase (less than the rate of inflation) but after you look past that the slight and temporary  gains made now will seem like a Pyrrhic victory and I believe that Dr. Gottlieb may have been overly optimistic in his comments.

One of the reasons allegedly for the widespread support of MACRA was  that the impending 21% cut would force many physicians to opt out of Medicare. I submit that once the Merit Based Incentive Payment System (MIPS) is implemented and understood by practicing physicians it will be likely that even more physicians will leave Medicare.

Will well meaning  physicians somehow find the time,money and energy to fix the heretofore inadequate or harmful quality measures replacing them with better ones?  Will the CMS quality "metrics" some how escape  the inescapable  reach of Goodhart's law?  A measure of something looses its value as a measure when it become a target. With quality measures as will be defined by CMS and resource utilization embedded into MICRA  more and more medical decisions will be made in Washington and physicians will be less and less able to act as the fiduciary agents of their patients with trust in physicians and reliance on evidence based medicine fading away.

For a detailed and frightening analysis of what MACRA contains please read this commentary by Dr. Arvind Cavale. See here.

There is so much to fret about that is explained by Dr. Cavale  not the least of which is the move to have your physician share the insurance risk with the insurance company. Have a nice day.