Left ventricular remodelling due to pacing


I know there have been some papers that suggest a certain percentage of ventricular pacing can result in ventricular remodelling and that this can increase the risk of heart failure in the long run.

I cannot find the answer to the following two questions though.Has anyone seen any studies or even have their own experiences to answer them?

1) if remodelling occurs is the ultimate indication of this the left ventricle ejection fraction?

2) is there any evidence that regular exercise can counteract the effect of remodelling or even stop it happening? 


Left Ventricular remodelling (enlargement and functional deterioration)

by Gemita - 2020-12-28 07:35:12

John, if I understand the first part of your question correctly, I believe they use left ventricle size as a more accurate marker to determine degree of remodelling rather than relying on EF (ejection fraction), since the latter can be influenced by so many factors.  There are many good meds that claim to inhibit or reverse remodelling (like Beta Blockers or ACE Inhibitors) as well as biventricular pacing.

Physiological causes of remodelling, say from exercise, I believe is reversible, while pathological remodelling, say from scarring caused by disease as in myocardial infarction is probably not.  Based on this assumption, I presume LV remodelling from high percentage RV pacing may well be reversible with say CRT, since this clearly seems to be the case for many?

Regular exercise is healthy for all of us, but depends how vigorous the exercise and on our heart condition.    I believe pushing too hard or the wrong type of exercise for a particular patient could cause problems.  Exercise as part of a healthy lifestyle though could make a real difference and possibly tip the scales in our favour to help overcome many obstacles.  They even wanted to experiment on hubby between stent placement versus meds/lifestyle changes.   But because his blockage was in his LAD artery and he was found to be almost 100% blocked, surgery was the preferred option !!

I don't think LV remodelling that we're concerned about is caused by high percentage Vent-pacing

by crustyg - 2020-12-28 11:37:35

Leaving aside the discussions about the athletic heart (larger, thicker ventricles, lower resting HR), what I believe we're all concerned about is LV-remodelling due to RV-apical pacing that leads to reduced %LVEF.

The problem with RV-apical pacing is that the electrical impulse is supplied at the 'wrong' place, and at the 'wrong' time of the cardiac contraction cycle - by which I mean that the PM has to wait a long time to be sure that a vent activation hasn't occurred naturally before it can safely pace the RV, whereas a normal A=>AV-node=>bundle activation may be activating the top of the ventricles tens of milliseconds earlier than a PM dares to.

Normally, the contraction impulse (from the SA-node) spreads through the RA, reaches the AV-node and then propagates rapidly down the bundle of HIS, activating the papillary muscles (which contract and close the mitral valve) and then spreading quickly to the main ventricular tissues, carried by the Right- and Left-bundles, top-to-bottom.

By contrast, RV-apical pacing delivers the activation impulse to the bottom of the RV muscle, and the activation then spreads (more slowly than it would in the two bundles) across the septal wall to the LV, and causes the LV to contract.  How much the RV-apical lead is paced appears to be a factor, but I don't think anyone currently has certainty about who will get LV-remodelling that results in reduced %LVEF.  It seems to be *much* less common in folk with CCHB - who start with healthy heart muscle - and commoner in those with existing heart muscle problems who are then paced a lot through an RV-apical lead.

I haven't been reading this up, but I understand that the *hope* is that delivering ventricular pacing through the bundle-of-His may prevent this remodelling (as it matches the normal activation pattern).  But it would need a large series of patients and a lot of years follow up to prove this.

The more this anatomically incorrect pacing occurs, the more likely it seems to be that LV-remodelling may occur, but there seem to be other factors as well.

I think that where heart muscle disease (e.g. partially blocked coronary arteries, cardiomyopathies) is not thought to be a factor, that %LVEF *is* considered a valid marker of LV-remodelling and used as an objective assessment of the effectiveness of CRT.  How you measure %LVEF is debatable.  MRI is supposed to be better than echo, but it's a lot more expensive and the actual measurements are probably prone to the same observer errors.

Can exercise prevent LV-remodelling due to prolonged/extensive RV-apical pacing?  IMHO, probably not.  You could even argue that it *might*, in theory, hasten the process, but that's a nihilistic approach.  The number of heart beats per day isn't massively different between patients.  Yes, my HR is high when I exercise, and then it sits at 50BPM for hours (about 63% of each 24h period), so overall my heart beats per day isn't that high. Someone with a resting HR of 70BPM who doesn't see the giddy heights of 160BPM probably manages the same number of beats per day.


by AgentX86 - 2020-12-28 13:55:37

Crusty makes good points.  LVEF is the "measure" of cardiomyopathy because it's really what matters and it can be measured.  AIUI, computing LVEF involves a deck of funny cards and tea entrails because of the limitations of echocardiograms.  An MRI can give a much better number because it is a true 3-D image (or model, if you will) of the heart.  Its volume can then be calculated pretty accurately throught the cycle.  The expense of an MRI isn't justified for this, however.  An echo is good enough since an exact number isn't needed (10% is really good enough).

I attach a couple of links

by Gemita - 2020-12-28 14:03:50

John, I attach a couple of links which might be helpful in the assessment of ventricular remodelling.  My EP mentioned that (%EF) is not used in isolation to assess Left Ventricular problems, several other factors need to be taken into account.  The following links hopefully cover this point



I don't wish to start a flame war

by crustyg - 2020-12-28 19:04:22

Hi Gemita: I've had a quick read of Konstam's paper (the first of your two references).  I think we're talking at cross purposes here.  He criticises use of %LVEF as a tool to understand the cardiomyopathies - e.g. HOCM and dilated cardiomyopathy, and, *if* I understand what he's written, then I agree, as he makes the point that %LVEF can be the same either side of the apex of the Starling curve.  But with very different consequences for the patient.

What I wrote above: "I think that where heart muscle disease (e.g. partially blocked coronary arteries, cardiomyopathies) is not thought to be a factor, that %LVEF *is* considered a valid marker of LV-remodelling" was a shorthand way of trying to avoid a discussion of HOCM etc. and focus solely on the LV-remodelling from prolonged RV-apical pacing.  The second paper touches on the same issue (where any given heart is on the Starling curve) and mentions the paradoxical beneficial effect of beta-blockers in heart failure (due to improving the heart's response to previous Ca++ saturation), and then mentions the proven benefits of CRT.

Heart failure is a huge topic (and how that used to drive us mad as medical students, trying to understand how a failing heart could continue to provide an apparently sufficient BP whilst allowing the patient to drown): what I believe we're discussing here is the HF caused by RV-apical pacing.

crustyg and John

by Gemita - 2020-12-28 22:23:16

No flame war intended this end - perish the thought crustyg. 

My understanding of John’s post is that he was asking two very specific questions and nothing more.  He has obviously read all about the risks of prolonged RV pacing and I was attempting to answer the first question in the best way I possibly could. I subsequently posted the links to support my claim that I believed left ventricular size is an important marker too in heart failure, not just EF.  Too much attention seems to be paid to EF and this often fails to see the wider picture and we all know so much can affect EF.

John specifically asked for any studies or any experience any of us had had and asked quite specifically  1) if remodelling occurs, is the ultimate indication of this, the LVEF?  I understood John to mean, is the only indication (evidence) that remodelling has occurred (following a high percentage of RV pacing) likely to be the LVEF?   I was trying to make the point that an enlarging LV was an important indication too.  If I have misunderstood your question (1) John, then I hope you will correct me. 

I sincerely hope the links I posted are of some interest to members suffering from heart failure from whatever cause, including potentially from prolonged RV apical/septal pacing.  I hope members will appreciate that far more than ejection fraction needs to be taken into account when assessing degree of heart failure/LV remodelling.

great discussion thanks

by quikjraw - 2020-12-29 07:28:24

My concern in question 1) was very much the statement mentioned “ LV-remodelling due to RV-apical pacing that leads to reduced %LVEF” but I suppose ultimately my concern is heart failure from RV apical pacing and spotting this early or even preventing due to optimised pacing strategies.

I know during my particular implant they did try to place the second lead somewhere other than the apex but this was discussed very quickly so I do not know where they tried. They tried for probably 45-60 mins achieve it but they could not get the right “signals”. I could hear them trying to get the right resistance and potential difference but to no avail.

I am little confused as to why they would not choose a more accurate method of calculating LVEF such as MRI even if it is more expensive as +/-10% makes it very tricky to understand a trend if that is what is needed to see a precursor to LV-remodelling?

I read through the links too Gemita thank you and it is clear I need to do some deeper reading on this as every time I think understand this I realise that there is even more to learn. I’m a mechanical engineer so this is all alien to me.

There are clearly medical solutions to an already remodelled left ventricle so I expect that will give some comfort to those it may affect. 

In terms of exercise I take your point about the exercise Crustyg assuming that every beat is a paced beat but it could be a different story if intrinsic beats occur during exercise? These may have a more positive effect than intrinsic beats at rest? I am somewhat making this up as I type so I appreciate it could all be very far from correct.

Try not to focus on it too much

by crustyg - 2020-12-29 12:18:13

Hi John: I agree, if some of your vent-activations are intrinsic from your AV-node then that shouldn't promote the LV-remodelling problem.  Which not everyone gets: it's still a minority of RV-paced folk who get into this problem.  As to treatments, I don't know that there's any evidence of medical treatment fixing the potential problem of LV-remodelling due to RV-apical pacing.  In any case, it makes more sense to address the root cause of any problem.  HF is a huge topic, with many different causes.  Ischaemic heart disease is still by far the commonest, but we're not talking about that here.  Stephen Westaby relates a fascinating case which illustrates the enormous potential for recovery if suitable stem-cells are still available and functional, and which he says is now his main research aim - instead of flogging old, damaged cells, try to grow new healthy ones.

Early detection: good luck with that.  I doubt that anyone is going to organise an annual echo 'just in case', and for the sort of reduced %LVEF due to prolonged RV-apical pacing an echo is quite good enough.  I don't know if you've yet had to run the gauntlet of an MRI as a PM patient, but it's tedious.  They *really* don't want to do them if they can avoid it.

From what you say it sounds as though your EP team tried mightily to achieve His-bundle pacing.  It's not easy and not possible for everyone.

So it would have been His Bundle pacing

by quikjraw - 2020-12-29 13:24:35

Yes Crusty I had an MRI with contrast medium during my stay in hospital.

The stem cell research looks very interesting but I guess some way off until human trials have been conducted.


How you are feeling is what matters most

by Gemita - 2020-12-29 13:24:55

John yes, I believe a slightly better position for lead tip placement now is the RV septal area (this is what I have), although obviously not thought to be as good as HIS bundle pacing which should more closely match what nature intended.  However HIS bundle pacing would need long studies to confirm that it really is the best option and as crustyg says, years of trials with sufficient number of patients to give an accurate picture of the pros and cons.  

In the meantime John, the best indicator to assess how well your heart is working is often to go by “how you feel”.  Feeling well, being well, being able to carry out your normal daily activities, without chest pain, breathlessness, fatigue, these are the important indicators that your heart is coping well.

I would be less inclined to spend your time worrying about something that may never happen, since it clearly doesn’t happen to everyone with prolonged RV pacing and spending time worrying about what might happen is clearly unhelpful.  Many are paced for years in the RV - even from an early age - without any adverse effects.  

My EP mentioned that if at some stage in the future I developed heart failure symptoms from RV pacing, then a pacemaker upgrade to a CRT would be considered.  He also advised that CRT was not routinely prescribed under the NHS as a “preventative” measure since he felt there was absolutely no benefit in using CRT until it was really needed. He further said that if heart failure was going to happen from RV pacing it would happen quickly for many patients - as quickly as in the first few months to 1 year.  If it didn’t happen within say 4 years, in his long experience it probably never would.  I believe another contributor has also posted a similar dialogue with her EP.

I hope you are feeling better John and getting some decent sleep, that is what matters most now.  Thank you for all your searching questions

You are right!

by quikjraw - 2020-12-29 13:38:48

Yes Gemita I know you are right that I should not be worrying about things that might never happen but it's still proving a little difficult for me to settle into this new stage of my life.

My sleep is still not good to be honest but last night was a lot better. If my watch is to be be believed my heart rate is never going below 55 so I probably didn't need the settings dropping to 40bpm so not sure why they went so low.

From The Pacemaker Patient Advocacy Group

by Terry - 2020-12-29 15:50:52

We have a sample of 167 scientific papers related to remodeling and correction offered by His bundle pacing at <http://www.his-pacing.org/the-list-his-bundle-pacing-papers/>. The papers are organized by topic, for elample "If I have heart failure subsequent to conventional pacing, can my heart heal itself if I convert to His bundle pacing?"

All the best,



by quikjraw - 2020-12-29 17:31:35

That is a very comprehensive set of papers. I shall bookmark it thank you Terry 


by PacedNRunning - 2020-12-30 05:01:34

I was right where you were when I First got my PM.  I wanted to minimize pacing.  I had intermittent heart block 2:1 with exercise only. I was running one day and felt a run of what I thought was palpitations. The fix, PM. I was very concerned with pacing induced CM or PICM.  My doctor was all for minimizing pacing. The key is to minimize unnecessary pacing.  It was difficult to program my PM just for exercise so in order to give me what I needed with exercise, I needed to pace some unnecessarily. Not too happy but it was what needed to be done.  I paced about 37-50% of the time,  Probably needed about 10%.  Because of this I did a lot of research and reading about PICM.  What I found was most people do not suffer this consequence from chronic RV pacing.  The studies I read (DAVID) made me believe it was a high chance of happening when in fact the actual percentage is quite small.  The issue with the DAVID trial was that most of those patients were older and already had some sort of decreased heart function.  Almost all them were paced unnecessarily.  Unnecessarily is the KEY! If you have heart block it is harder to minimize pacing. It just depends on what type of heart block you have and if it's persistent or intermittent.  Intermittent is easier to minimize. This is why pacemakers have the RV pacing minimizing algorithms now. Anyone with sinus node dysfunction should have this feature on because they should not be pacing in the RV much if at all.  I have read any unnecessary pacing greater than 40% puts you at high risk.  I have seen many people paced for 12-15+ Years 100% and do just fine without affecting their EF.  The one takeaway I had with all this was there is an easy fix.  Place a cRT. Upgrade to a CRT. As Gemita said above certain heart remolding is not reversible but I do believe this one is. I've seen great results for those that needed to upgrade to a CRT due to chronic RV pacing.  

The HIS bundle is the optimal place to help greatly reduce PICM but it hasn't been out long enough to say it's superior to RV septal or RV outflow track pacing site.  I have an RV septal lead and pace 100% now, I'm no longer in intermittent block. Unfortunately my block progressed. I'm glad i did a lot of reading and researching about this prior to all this and feel that since this is something that happens but in such small percent, I'm not going to focus on it anymore. I know it's there and I know it's a possibility but there is a fix! CRT.  The other thing that is an indication is your QRS duration. Based on your RV lead site, your QRS can wide or narrow. Narrow show that the activation between the right and left ventricle are better timed than a longer QRS duration. typically greater than 130ms is a long duration.  So ask what your QRS duration is on your next 12 lead ekg.  I will be finding this out at my next appt.  I'm also going to second what Gemita said above about if it hasn't shown up in the first 4 years of pacing, it most likely won't.  Do you pace a lot?  I'm a runner also. I know a guy whose 36 with a PM, 100% paced 6 years no issues. :). Hang in there! I know it can be stressful knowing the side effects of having a PM but keep in mind it's such a small risk and if your heart otherwise is structurally fine, you should be in the majority.  Hope my 2 cents helped some.  

they certainly do help

by quikjraw - 2020-12-30 10:59:53

Yes that is a good summary of the risks I think PacedNRunning and I should now just concentrate on getting back to my life before and ensuring minimal pacing. I seem to remember the EP who fitted my pacemaker suggesting I had a narrow QRS at that time so now I know that this is a good thing I will ask this on my follow ups.

I was venticular pacing at 46% and then at my first follow up I believe the technicians removed or extended the PR interval on the AAI-DDD mode.  I also have a very long PR interval (I think they said 400ms). Though I have heard that longer PR intervals might be better managed but I need to read more upon that. I think on balance living with a longer PR interval is better than giving a high percentage pacing but I would need to understand the numbers before I could state that was true. I have potentially lived with a long PR interval for many years and it has caused me zero problems to my heart or to my running performance.

It will be interesting to see what that percentage moves to on my next appointment.

John - message from PacedNRunning

by Gemita - 2020-12-31 03:23:28

John I found this message in general comments, so am posting again since it has not made it onto this page for some reason.  Update John this message actually refers to your previous post which PacedNRunning is responding to but I am still leaving copy here to make sure that you will see.

From PacedNRunning "So to your answer your question to me. Am I back to prePM running pace. No. 😂. Sorry. But the key is I can still run and do all the things I did before. Since I paced 100% in my V lead with exercise that took some time to get use to and tweak. It basically started pacing me 100% when my HR reached 100bpm up to my max of 185bpm. So in the beginning it kicked in too slow and the first 2 mins of exercise I felt awful. Hard to breath etc. just like normal running except a little more exaggerated. You know when you run or exert yourself the first few mins are hard and then things plateau and you feel fine. Well like that except moderately harder. Once my pacemaker paced faster and more physiological for exercise I felt much better. So I would push through each run until I hit my plateau. Being paced wirh exercise in that bottom ventricle at high rates extended periods made me tired. It's way better now but the first year it made me tired. So I would cut back the amount of time I ran to 30 mins and then built up from there. So just listen to your body. Scale back some if you have too and then increase back to where you want after you give your body/heart time to adjust. Now that I'm pacing 100% my settings are as short as they can be, I feel like a normal person exercising. So it's a give and take. I would totally take back intermittent pacing over 100% pacing. But it's what my heart needs so I have no choice. You may have to do a treadmill programming session with your team to get to dialed in good. 

to explain the algorithms to minimize pacing. You typically have to miss 2 beats out of 10 for it to start pacing you. So basically 2 dropped beats. I will say for me. That algorithm did not work for exercise because every time it checked I was in block and it felt like someone punched me in my stomach twice every 2 minutes! Not ideal. After a while that catches up to you hemodynamically. 

as far as your minimum setting. I was at 45 at implant. the following morning my doctor saw I paced all night at 45, so he lowered it to 40. Well my heart didn't like 40, I went into junctional rhythm. So we put it to 60bpm. 60 bpm was too much for me since my PM is not for bradycardia. So it's been at 45 for quite sometime. I will say we did have to bump me to 50bpm bc it made the settings work better. Not sure why but overall 50bpm feels better. 

the reason you pace under 60 is because the bottom lead will pace at any heart rate. It's not looking for HR but block or slow PR interval. So the top lead will pace if you drop below 40 but the bottom lead will pace 40- up to your max rate. Hope that makes sense. 

I hope answered or clarified some information"

His Bundle pacing

by Terry - 2020-12-31 16:57:59

As you probably saw, reports on clinical permanent His bundle pacing have been in publication for twenty years. Similar to DAVID and MOST (on pacing for sick sinus syndrome). Both RCTs in support of physiplogical ventricular activation and minimizing V-pace, without cardiac conduction system ventricular activation that is. That is why His pacing has grown exponentially recently.

Wow lots of information in this post, just wanted to share my personal experiences:

by asully - 2021-01-03 15:18:56

My ultimate conclusion is that it is often a chicken or egg question.

I have left ventricular remodeling (followed by right).  The electrophysiologists will tell you it's from right ventricle pacing (I am 100 percent pacer dependent) and that you may be able to trigger reverse remodeling by switching to a crt device.  They ultimately use your QRS duration to determine if CRT may benefit you.  My QRS duration was super long so they upgraded me.  The surgeons will tell you the remodeling is from your "valve disease, CAD, or cardiomyopathy", basically whatever underlying heart condition you have and will say if you fix that problem (like a bad mitral valve in my case) that there is a "chance" you can have reverse remodeling.  The heart failure docs (the pill guys) will tell you that there are promising studies showing that many heart failure meds can help with reverse remodeling.  

So based on what type of specialist you talk too you may get different answers.  I dealt with it by telling them to be aggressive and do it all, lmao.  I figure there is no harm in using all three approaches, and if they all have a chance of helping then do them.  I am quite pushy however when it comes to my care, I favor an aggressive approach.

Also to answer the question on remodeling measurements, it is not just LVEF.  They use everything from x-ray, CT, cardiac MRI, and echocardiograms to detect remodeling.  You can maintain a preserved ejection fraction while the remodeling progresses, in fact that's how the remodeling occurs by changing the shape and size of your heart to make up for output problems, which in turn causes more output problems and leads to more remodeling.  This loop can continue for a while before you ejection fraction drops.  That is the difference between heart failure with preserved ejection fraction and heart failure with reduced ejection fraction.  Out of all the paper I read I did learn that there is a sort of point of no return, essentially in order to have a chance at remodeling you need to catch it before it hits the advanced stages.  More and more studies show that early intervention gives the heart the best chance to reverse remodel.


by asully - 2021-01-03 15:22:13

My atria enlarged before my ventricle.  So you really have to watch the whole dang thing, and most importantly compare it to past imaging and tests, your looking for changes in your personal physiology so going of "normal ranges" may not always be accurate.

The latest on....

by Terry - 2021-01-03 19:41:45

Reverse remodeling. Scroll down to "If I have heart failure subsequent to conventional pacing, can my heart heal itself if I convert to His bundle pacing?" on the Papers page: http://www.his-pacing.org/the-list-his-bundle-pacing-papers/

All the best in the New Year

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