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Friday, December 04, 2015

Left Bundle Branch Block (LBBB) is not just a EKG finding, it is a really big deal

The EKG pattern of left bundle branch block (LBBB) has been known for decades and that pattern was considered an indication of heart disease. In Dr. George Burch's text book, written over fifty years ago, A Primer of Heart Disease,  I read that LBBB was a pathognomonic sign of heart disease.

However,at the time, It was not known what was the role of LBBB  in altering cardiac function.Did it cause heart disease- this point is debated still. Did patients with heart disease and enlarged hearts develop LBBB or similar EKG patterns as their disease progressed? Some patients have LBBB secondary to coronary artery disease and an infarct involving the interventricular septum,some have heart failure and some  "just" have a LBBB, the so called lone  or isolated LBBB.

 We know the following about the cardiac functional consequences of LBBB in patient with lone LBBB:

1) Abnormal movement of the interventricular septum early in cardiac contraction ( systole) ie in the pre-ejection phase the septum moves to the left.
 (In most cases the septum moves to the left while lateral left ventricular wall relaxes.The septal movement is observed with cardiac echo and termed as "septal beaking")
2) delayed contraction of the left ventricular wall) reduced ejection fraction (EF)
4) Impaired filling of the left ventricle (diastolic dysfunction)
5) More time wasted with the heart valves  closed ( Technically  measured as prolonged IVCT and IVRT) and measured by the MPI or myocardial performance index
6) Mitral regurgitation due to asymmetrical contraction of the papillary muscles
7) increased in left ventricular end-diastolic  pressure
8) Increased pulmonary artery pressure during exercise in some patients with normal resting echo
9) impairment of the normal ventricular twisting motion

Basically the right and left ventricle are designed to contract at the same time. In LBBB they do not- the right contracts milliseconds before the left.So there is inter-ventricular loss of synchrony.

The heart's electrical wiring system is designed so that the impulses that cause muscle contraction spread out more or less simultaneously from the two bundle branches. In LBBB the activation pattern is markedly altered so that the  septum is activated from right to left and  there is delay of  the impulses arriving  at the lateral and posterior left ventricular wall delaying muscle  contraction.

There is also asynchrony within  the left ventricle  apart from that of the septum and lateral wall being out of sync. Various segments of the Left ventricle  also do not contract as an organized system , some segments contracting and relaxing out of tune with others.This is referred to as intra-ventricular  dysynchrony.

Consider what the development of LBBB does to an otherwise healthy heart and consider how that effect would be more manifest clinically in a diseased heart with failure.

Two studies have shown that the ejection fraction decreases about 10-15%. while another reported only 5.8%. The EF does not tell the whole story as there is also impaired filling of the left ventricle.So not only is the stroke volume diminished by a lower EF but impaired filling leads to less blood to eject.Cardiac output falls and is particularly evident during exercise.

Details regarding cardiac function in patients with LBBB and normal coronary arteries ( most were shown not to have coronary artery disease by angiography) were provided by Ozdemir who studied 45 cases of isolated LBBB ranging in age from 48 to 72.(Effect of isolated left bundle branch block on systolic and diastolic function of left ventricle),  see ref 3 below.

Although the ejection fraction was reduced  "only" 5.8% from controls,there were statistically significantly higher values in the LBBB group  for the left ventricular end-systolic diameter,and the isovolumic relaxation  time and the isovolumic counteraction time and importantly the invasively measured ( done at the time of  coronary angiography)left ventricular end- diastolic pressure ( 14+/-3 versus 10 +/-3) with a normal of 3-12.Earlier work had shown that some patients with "Lone" LBBB -those with no coronary artery disease or obvious heart failure- may have normal or nearly normal  echocardiograms ( but typically have evidence of impaired relaxation on Doppler mitral flow studies) and may  have  clinically significant increased pulmonary artery pressure with exercise.

With increases in the IVRT and IVCT there is less time for the ejection time which leads to an elevated or abnormal MPI ( myocardial performance index).The failing heart  both contracts and relaxes more slowly and the MPI has been proposed as a useful prognostic indicator. There is more time spent with the aortic and mitral values in the closed position leaving less time for the basic work of the heart , which is  ejecting blood, to occur.But in lone LBBB it is not the muscle cells defects that are the problem but loss of the normal incredibly well coordinated contraction and relaxation of the ventricles.

I can add a personal story. When I  recently developed a LBBB my "comfortable "( age appropriate and consistent with what one might expect in an aging runner)  jogging times increased from about 12: 45 minutes per mile to 14 +  minutes per  miles. which represents a 12% decrease. in running speed. Similar stories can be found on the web describing what LBBB does to a person's exercise capacity. It should be noted that all patients with lone LBBB do not have the same cardiac functional impairment nor the same rate of progression of impairment.

But there is more to the functional consequences of LBBB. Some patients  ( many, most ?) with LBBB develop heart failure. Some of the evidence for this occurrence comes from the clinical experience of patients with heart block who have had pacemakers with the traditional right apical pacing electrode, which in effect is an iatrogenic  LBBB.It is thought that the abnormal contraction patterns due to LBBB may lead to a deleterious cardiac remodeling and ultimate heart failure.  

The introduction and advances in cardiac echocardiography made it possible to gain important insights into what are  the functional consequences of LBBB  and ultimately provided a new treatment for heart failure.

Dr.  IG McDonald in 1973 demonstrated by echocardiography that the interventricular septum moved abnormally. The septal problems were defined more clearly by Curtis in 1983 who showed that various abnormal movements of the septum were associated  with lower cardiac ejection fraction.,some patterns being more detrimental than others. Curtis mentioned that cardiac pacing might mitigate the LBBB induced abnormal ventricular contraction pattern.

 "The early studies described how the abnormal and/or delayed left ventricular activation wave front could lead to a reduction in left ventricular efficiency and performance that is largely independent of myocyte contractile function" Ref 1 see below.

 But it was not until 1994 that his theorizing was proven true when two clinical  studies demonstrated that pacing targeted to the site of the most delayed left ventricular contraction could improve overall cardiac function. The dyssynchrony could be "fixed" by resynchronization  ( or at least could  provide an effective work around) which became known as CRT or cardiac re-synchronization therapy.( also known as Bi-ventricular pacing, or Bi-V as most CRT is accomplished with Bi-V although more recently there is increasing use of His Bundle Pacing in re-synchronization therapy) .About 1/3 of HF patients treated with CRT do not show improvement, the 2/3 who do are those with  LBBB because in them the dyssynchrony is a major factor in the cardiac impairment and is often improved with Bi-V.

Cardiac pacemakers are nothing new-the first totally implementable pacemaker (PM) was introduced in 1958 and for decades were used to treat patients with heart block .Now a new use for pacing has improved the outlook for many patients with heart failure. It turns out that that the ones benefited are those with LBBB- so would not patients with lone LBBB also benefit from CRT? Is it necessary for a patient with LBBB to develop overt heart failure before pacing is considered or could/should the patient with NYHA class 1 be offered the implant?What about the patients with normal cardiac echo studies and shortness of breath on exercise? On further thought if a patient with LBBB has shortness of breath I would not expect the echo to be perfectly normal.The EF might not be less than the lower limits of normal but there would at least be delayed relaxation evident on echo . If PM implantation were a completely benign procedure the answer would be easy.


1)Breihardt,G,and Breithhardt ,O "Left Bundle  Branch Block-an Old-New Entity". J of Cardiovasc Trans. Res. 2012 5: 107-116

2)Grines,CL et al, Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony.  Circulation 1989. 79:845-853

3)Ozdenir,V Effect of the isolated left bundle branch block on systolic and diastolic functions of left ventricle. J Am Soc Echocardiog, 2001 Nov 14, 11 , 1075-9

4) Vaillant, C Resolution of Left Bundle Branch Block-induced cardiomyopathy by cardiac
 resynchornization therapy. J. of Amer College of Cardiology.2013, 61, 1089-1095

5)Yu,cm et al Biventricular pacing in patients with bradycardia and normal ejection fraction. NEJM 2009,363

addendum 12/28/15. Minor editing and addition of a 9th abnormality in LBBB,.
addendum 1/17/16 minor editing.5/22/16 Several spelling errors corrected.
addendum 3/19/17 Three sentence were added to the last paragraph.
addendum 10/12/17 more superfluous fiddling with the wording in several places
Addendum 12/3/17 Mention of His Bundle Pacing added


Anonymous said...

Thank you, this was very informative. I am one of the patients you describe. Now 62, was diagnosed with LBBB in my 40s

james gaulte said...

Thanks for your comment.Have you experienced any loss of exercise capacity resulting from the LBBB?

Anonymous said...

James -I'd be interested to hear your opinion on endurance exercise after being diagnosed with LBBB.

I was never an elite athlete, but a good age-grouper, always near or on the age-group podium (running) with a 5km time around 17min through my 20's. I kept very active through my 30's, although slowing down as I put on a little weight and career took over. I was 41 in 2011 when I had severe back to back flu infections (really quite sick for about 2 months). When I recovered, I found that during high efforts runs, I'd intermittently be getting short of breath, the start of which which was always accompanied by a sharp jab in the chest.
Long story short, I was diagnosed with intermittent LBBB which eventually became permanent, probable cause being myocarditis (MRI shows the mild non-ischemic scar). MY EF has fallen from 65% when I developed the LBBB to around 54-55% currently, almost 8 years later. Echo and MRI definitely show the typical pattern of abnormal movement, but no other issues.
I kept active since, but never racing nor training hard. Time with family and career didn't leave me with much time except for a couple runs a week.

That said, I did exercise capacity testing 6 months ago, and even while untrained I still had good VO2 max for my age of 48 (~40ml/kgmin) despite them stopping the test well short of my max heart rate (168 vs max of 183). At that point I decided to improve my diet, quit all alcohol and caffeine and start training to see what I could achieve within the limitations of my LBBB.

Instead of running, I've been riding daily, building up my endurance and power (with a good chunk of time in the middle lost to recovery from 1st rib resection for vascular TOS). I've been progressing well, and have an FTP of ~3.3 watts/kg which I think I can definitely raise with time, hard intervals, etc. That's not bad already for a normal person my age, especially one without a long cycling history., nor LBBB.

My question is what you think about daily higher effort endurance exercise for those with LBBB. Will it put additional stress on the heart, or help it? I'm not talking about crazy high hours of high intensity training - more like 7-10 hours a week with heart rates in the region of 150+ maybe half that time.

james gaulte said...

anonymous 2
. Of course, I cannot give individual medical advise over the web but I can comment about what little I know regarding the topic.

I am aware of no data that might be informative regarding safety or efficacy of high effort endurance exercise in LBBB.Safety concerns would include both possible deterioration of heart function and possible increased risk of inducing an arrhythmia such as atrial fibrillation or ventricular tachycardia or fibrillation or a heart block.

Making an answer even harder to come by is the fact that LBBB is very heterogenous regarding effect of heart function and risk of development of a cardiomyopathy caused by the dyssynchrony. Two patients with the same EKG may have different patterns of abnormal septal wall motion and functional impairment.For example LBBB caused by fibrosis and calcification of the conduction system associated with aging (LEV's disease) may differ in several ways from a LBBB thought to be due to a myocarditis.

Have you discussed the value or risk of a high exercise program with your cardiologist? He may be the best source of estimation of your particular risk. I wish I could be of some help.

Paul Sanders said...

I'm a 75yo man who was Dx LBBB about 4 yrs ago. Although past symptoms indicate the condition probably existed as long as 15 yrs. After having shortness of breath last summer a complete work up was ordered that indicated no CAD. I'M a competitive tennis player who has qualified for Nats in June. My question concerns the amount of time it requires to get my heart rate up so I can compete efficiently. I work out 2/3 wk. Non smoker/drinker. 5-11 162lbs.

Anonymous said...

I know this is an old thread but figured I'd comment since it is relevant to me now. I am a 45 y/o male. I was diagnosed with LBBB after exercised induced shortness of breath and palpatations which was affecting my lifestyle. I was always an athlete in highschool and college with no issues until my 30s. I started having severe arythmias and after many trips to the hospital, some by abulance thinking I was having a heart attack, I was finally able to catch an issue with a holter. I was diagnosed with SVT and my heart rate got to 200 before the monitor shut off. I received an abliation and was cured of the issue. When I was 43 I started having symptoms again of the severe palpataions and shortness of breath with exercise. I had a stress test that was stopped when it showed signs of LBBB at about 150bpm. It would resove itself with lowered heart rate but persisted enough to be a real issue doing any activity like yard work and golf. I had a cath to find out I had no blockages and no other issues seen which would casue this. So I basicially am in the 1% or so that have normal heart but have this issue. I wonder if the abliation somehow casued this with scar tissue over the years. Is there any data for patients who have had an abliation in the past turning into something like this? I did research and found that a calcium channel blocker can help so I requested this from my cardioologist. I started 30mg of cardizem 3 times daily but eventually went to a CD dose at 120 which seemed to help keep my baseline heart rate a bit lower during exercise. After abot six months it didn't work as well so I asked to raise it to 180. Now it has been a year and I'm 45 but having more symptoms. I only exercise mildly with walking and have been having it hit me at about 120-125 now. My Polar heart monitor stops reading and says 0 as soon as I feel the palpations starting. It has casued be to fear exercising hard and is causing me anxiety about living what would be a normal life with kids. I don't want to be playing basketball and drop dead from an anythmia. I know this may be extreme but as soon as it happens I start feeling light-headed and have pretty significant shortness of breath. The other day I moved an appliance to the garage with a neighbor and could barely talk after until my heart slowed down to get into a normal rythym. I am considering either asking to increase the Cardizem 180 to the next level but my nightime sleeping rate gets as low as 42 which is also a scary thought if it goes lower. My other choice is to try to push for a pacemaker. I just want to know if a pacemaker would even help with this condition? My doctor never seemed concerend at all and just said there should be no issues with LBBB. It is easy for someone who hasn't experienced the feeling to say that on paper it should be fine, until the one day I push myself, it isn't. I'm not even sure what type of pacemaker would work (if at all). My mother is in her 70s and was also diagnosed with LBBB so I wonder if this is genetic. In the last fee months she passed out a few times resulting in some seriious injuries but fortunately wasn't driving. The medics said her heart rate was in the 30s last time she passed out. So I'm not sure what to do but I don't want to live my life in fear to exercise. Sorry this is so long but I feel neglected from my cardiologist and would love to seek other opinions or hear if ther are similar experieces. Thank you.

james gaulte said...

Of course I cannot give medical advice over the internet and again someone should not rely on the web for actionable health advice.

I can make some general comments that may be of interest.

The most common cause of SVT is AVNRT which is said by EP cardiologists to be relatively easily fixed by ablation.A heart block (not a LBBB) is a fairly rare complication.I am aware of no reports of LBBB following ablation for AVNRT.

LBBB can cause significant decrease in left ventricular function. This is most apparent on exercise and the resting echo may not reflect the degree to which exercise ability is decreased.Since often the patient is asymptomatic at rest and the echo does not show a major decrease in EF,some cardiologists may well recommend a watch and wait approach.

Over a variable period of time some patients with LBBB develop heart failure(HF) due to deleterious remodeling of the heart secondary to the dyssynchronous contraction pattern of LBBB.

A recent report indicates that patients with HF secondary to LBBB seem to respond much less well to the usual HF medication though some do respond, about 25% according to one recent article quoted below)

I understand that the current recommendation regarding HF and the use of pacemakers to do CRT (cardiac resynchronization therapy ) is that CRT is indicated if the patient has HF not responding to the usual medications and the patient has a EF of less than 35%.I understand that insurance companies may be hesitant (or worse) to pay for PM implantations not being according to generally accepted criteria for indications)and cardiologists may not want to practice outside the guidelines.

For patients with HF secondary to LBBB CRT often is of great value . Also His Bundle Pacing is being used by some EP docs and may be at least as good or better than standard CRT (with Bi-venricular pacing-one lead in the RV apex and one lead stimulating the LV)

Because of the less than optimal response of many LBBB patients with HF to the usual HF medications some EP cardiologists are talking about earlier use of CRT . Dr JP Daubert Chief of EP at Duke has expressed those views recently ( E Sza and JP Daubert " Left bundle branch block-induced left ventricular remodeling and its potential for reverse remodeling" J of interv electrophysiology 2018, august, 52 (3) p 343-352

Among cardiologists the EP docs, ideally one who has adopted His Bundle pacing, are the best equipped to give advice to some one with LBBB

LBBB should not cause a very slow heart rate. If someone develops a Hr in the 30 range they would be advised to see a cardiologist. They may need a event monitor as they may have disease of the sinus node (sick sinus syndrome or a block of the impulse at the AV node ,either of which may require a pacemaker