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Wednesday, February 22, 2017

Cardiac remodeling -some old and new theory and some data

Following the 1975 echocardiographic study by Morganroth (1) of endurance athletes and resistance exercise athletes and several cross sectional studies that seemed to validate his work the  "Morganroth  Hypothesis" became  the standard exercise physiology party line.

The story goes like this:

Endurance exercise brings about a volume overload or a preload stimulus to the ventricle that lead to eccentric hypertrophy which is an increase in ventricular cavity size and only slight increase in wall thickness. Resistance exercise brings about a pressure overload or an afterload stimulus which leads to concentric hypertrophy in which there is little change in cavity size but thickening of the ventricular wall.,The 2 types can be defined  by the relative wall thickness (RWT) which is 2 x the posterior wall thickness divied by left ventricular diastolic diameter with  a value greater than 0.42 indicating  concentric hypertrophy.

Skeptics have argued that echo studies have inherent  methodological error  ranges too great   to separate groups whose absolute values are not that far apart and MR is a much more precise method and that cross-sectional studies have limited ability  to sort out group difference that  are due to training  from other causes of individual differences. So, what did a longitudinal study with MR imaging show.

A 2011 MRI longitudinal study, Spence et al (2) provided interesting data from which one might conclude that endurance exercise does bring about eccentric hypertrophy but resistance exercise does not increase wall thickness-at least not in the small group of resistance exercisers who worked out three times a week for six months reported in this publication

It is certainly possible that the six months training program in Spence's study was  not enough to bring about concentric hypertrophy. A more recent  meta analysis supplies data and analysis that indicate that there is a typical pattern for endurance exercisers and a pattern for resistance exercise more or less consistent with Morganroth's hypothesis  and a in- between pattern for those who engage in activity in which there is both significant amount of volume and pressure overload such as rowing and cycling.

 Plium et al (3)analyzed echocardiographic data  on 1451 athletes gathered up from some 59 studies.All subjects were  under the age of forty, older athletes excluded so as to not muddy up the data with the effects of aging on heart function and structure.

 Basically the data conformed with Morganroth's hypothesis. Quoting the author's conclusions;

"Divergent cardiac adaptations do occur in the athletes performing dynamic and static sports..However,the classification as an endurance trained heart or a strength-trained heart is not an absolute and dichotomous concept but rather a relative concept."

So a stereotypical runner will have a different  pattern from a wrestler or body builder  but ventricular volume changes and wall thickening occur in both  to varying degrees with the runner tending to a eccentric hypertrophy-remodeling pattern and the wrestler to a concentric pattern while athletes such as cyclists and rowers demonstrate the most marked changes in ventricular volume and wall thickness. 

More surprisingly and maybe more importantly  is the observation that a sedentary life style may evoke a remodeling pattern  characterized  by concentric changes, i.e.  no increase in ventricular volumes and a tendency to develop diastolic dysfunction.

This is what was reported by Brinker et al (4) from Southwestern Medical School in Dallas in their study of  cardiac function and structure in 2900 subjects from the Cooper Center Longitudinal Study.The subjects age ranged from 42 to 67 years of age and all were either self referred or physician referred to the clinic  and had a normal stress test.Based on the exercise levels achieved on the stress test four fitness levels were designated.  They found that the lowest fit subjects ( presumably  those with a sedentary lifestyle) had a higher prevalence of concentric remodeling as well as diastolic dysfunction than the fitter subjects. There was a 40% prevalence of concentric hypertrophy and 9 % prevalence of diastolic dysfunction ( defined as an E/A ratio greater than 1) in the lowest fit group versus less than 20 % concentric change and 2% diastolic dysfunction in the most fit group. So it is not an all on none thing and fitness does not seem to immunize against concentric  hypertrophy and diastolic dysfunction but made both less likely.

 Both resistance and endurance training cause cardiac remodeling but there may also   be a "inactivity remodeling", as might occur in a sedentary lifestyle The ventricles remodel  whether  you exercise or have a sedentary lifestyle and Brinker's group suggest that the inactivity remodeling may be a precursor to diastolic heart failure (aka HFpEF) and further suggest that long term exercise might be preventive.

That is a thesis I would like to believe. I would be more convinced if it were not for the fact that while  66% of the low fit group were hypertensive so were  only 38% of the fittest group were hypertensive. You wonder if that might not play a role in the concentric hypertrophy. I discussed other work by the Dallas group (see here) which,IMO, provides better evidence for the idea that long term aerobic exercise can reduce the risk of diastolic heart failure.

1. Morganroth, J et  al. Comparative left ventricular dimensions in trained athletes.Annl Int Med. 1975,82(4), 521-524

2. Spence,A et al .A prospective randomized longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise J of Physiology 14 nov 2011

3.Pluim,B The Athlete's Heart. A Meta-analysis of cardiac structure and function. Circulation 1999:100: 336

4.Brinker, SK et al. Association of Cardiorespiratory Fitness with Left Ventricular Remodeling and diastolic dysfunction. JACC Heart Failure.Vol 2, no.3, 2014, p238

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


Sherry said...

I am so happy to find your blog post!!! I'm looking for direction from a failing group of cardiologists.

I'm a young 57 y.o. female with LBBB & a current EF of 40-45% (decrease from 65%). I am currently symptomatic (SOB/DOE, decreased exercise endurance and occasional chest discomfort aka "soreness"). Currently on Toprol XL 50mg for rate control (HR 120-130 when vertical, 60 when horizontal). I've had a complete cardiac workup to include catherization (normal) which prompted referral to Endocrinology to r/o pheo d/t to elevated catecholamines (urine/blood). Repeat labs were WNL. All thyroid were negative. Now I'm back to cardio (new guy) and hoping for some help!

I have intuitively felt I needed more intervention given my age and otherwise excellent health. I recognize you cannot provide counsel regarding my personal care, what are you thoughts on resychronization at my age? I've read it leads to early heart failure...but isn't that where I'm headed anyway?

And for grins & giggles...the cause of my LBBB....elavil! Was taking 25mg q HS for sleep x 16 years....


Sherry Terry

james gaulte said...


Of course I cannot provide specific patient advice on the internet but I will offer some observations that may be of interest to you as you discuss the situation with your cardiologist.Let me say I am not a cardiologist and certainly not an EP cardiologist but my personal health issues gave me mega incentives to learn as much as I could about LBBB and pacemakers,
CRT ( cardiac resynchronization) actually is a treatment for heart failure it does not cause heart failure.What might be confusing there is that in some pacemaker patients the typical means of stimulating the right ventricle ( an electrode in the apex of the right ventricle) may lead to heart failure.It does so by basically causing the same electric and mechanical activation pattern of the heart as does LBBB).

CRT is currently recommend for patients with low ejection fractions ( usually less than 35%) who have heart failure and in whom the basic pharmacologic treatments do not seem adequate).The figure usually quoted is that crt is not successful in about 1/3 of cases and there is controversy as to how to predict who will benefit but I believe there is general agreement that success is much more likely in someone whose ekg does show the typical LBBB pattern.

I said that CRT is a treatment for HF but more accurately, as a cardiologist on the Medtronic web site put it CRT is treatment for LBBB as it to varying degrees corrects the electric and the associated mechanical dyssynnergy that LBBB brings with it.

Another pacing approach is Bundle of HIs pacing which in some cases is able to stimulate the conduction system of the heart past the point at which a bundle branch block is present and with BoH pacing in some cases the LBBB is "fixed".You still have the block but the pacing electrode accesses the conducting system at a point past that block

My EP cardiologist did place an lead in or near my Bundle of His and I am paced that way and now my exercise tolerance is about what it was before I developed the LBBB ( I also had an intermittent exercise induced AV block which was the primary indication for the pacemaker.Since I also had a LBBB so he decided that I needed more than the usual right apical pacing . He also put in the usual three leads necessary for standard bi ventricular pacing as a back up in case the BoH pacing failed. (The three leads are right atrium, right ventricle, and the left ventricle via a wire threaded into a vein on the surface of the left ventricle though a venous channel that empties into the LA (the coronary sinus))

PM implantation is a bit of a big deal with various risk of complications two of which I had.CRT and to some degree BoH pacing require more voltage so a battery change will be more frequent than in someone who had a PM as a backup for AV heart block. (the term battery replacement is misleading as they have to replace the entire PM unit)They tell me my unit will needed to be replaced in about five years after the first implantation)

some EP docs have argued that CRT should be considered earlier than is currently done particularly in patient with LBBB who have good heart muscle otherwise ( that is have not had heart attacks etc)but how often that really happens and how insurance handles that I do not know.)

I believe more EP folks are considering BoH pacing but my sense of it is that they are still in the minority.

I hope you can find a cardiologist who can discuss the situation with more hands on knowledge and experience that I have and give you some useful and practical advice


Sherry said...


Thank you so much for your thorough response. It has provided me with great insight and options/questions for my appt on 3/22. There is an EP in the group with access to a Heart Hosp & UVA if needed. As previously indicated, this came out of the blue (found during lead placement for a colonoscopy!). My exercise tolerance is non-existent, I'm having unpleasant sign effects from the Toprol and my rate issue 130-140's) is still unresolved. I perceive my rate issue is r/t poor LV filling. However, I did have about a 5% improvement in my EF after being on Toprol x 30 days. I'm anxious to have a repeat echo & evaluation.I'm ready to be free of RX, have a PM & get on with my life. (who has time for this?)

My father has a PM for sick sinus syndrome (in his 90's) so have been through the quarterly interrogations as well as a "battery change" with him. My mother had RBBB, so wiring seems to be an issue in our family.

I cannot thank you enough for your response & support. Will continue to keep you posted as well as read the noted research articles.

Thank you again!
Sherry Terry RN