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 relaxation 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 sentences 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