Recognizing Left Bundle Branch Block and When It Matters

Yogesh N. Reddy, MBBS; Siva K. Mulpuru, MD; Suraj Kapa, MD


April 30, 2018

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Yogesh N. Reddy, MBBS: Hi. This is Yogesh Reddy, cardiology fellow at Mayo Clinic. Today we will be discussing the very common clinical scenario of a left bundle branch block (LBBB) on electrocardiogram (ECG). I am joined today by my colleagues, Dr Siva Mulpuru and Dr Suraj Kapa, who are both specialists in this area. Welcome.

Suraj Kapa, MD: Thank you.

What Is LBBB?

Reddy: Dr Kapa, how does a LBBB affect electrical activation and mechanical contraction?

Kapa: A LBBB basically refers to abnormal conduction where ventricular response to an impulse beginning in the atria does not go down the normal highways of the heart. After the atria beats, an electrical signal is sent to the atrioventricular (AV) node. From the AV node, it propagates through the bundle of His and then goes through two major highways, the left and the right bundles.

Image courtesy of Mayo Clinic

In this picture, you can see that the left bundle branch takes that signal and sends it down three further major highways. Typically, those include the left anterior fascicle, the left posterior fascicle and, in many patients, the left upper septal fascicle. Beyond that, those fascicles further go into multiple Purkinje fibers that activate many areas of the left ventricle, almost nearly simultaneously. The reason for these highways and these areas of rapid activation, compared with normal myocardial activation, is to allow for multiple areas of the heart to activate near-simultaneously.

The last area of the heart to activate in the left ventricle is the posterobasal section. Allowing multiple areas of the heart to activate simultaneously results in the potential for greater mechanical force. One way to think of it is the game of tug-of-war: When everybody pulls together, it is much more effective than if individuals pull separately. The effort of those highways in activating multiple areas of myocardium near-simultaneously permits the opportunity for activation and for optimal mechanical contraction.

When we talk about mechanical dyssynchrony resulting from electrical dyssynchrony, it essentially results from the fact that the left bundle branch [is out], so now you have to go down the right bundle branch. After activating the right ventricle, you have to walk over to the left ventricle through slower myocardial activation and then start activating the left ventricle. This means that the right beats somewhat before the left, as opposed to both together. That, in part, contributes to the development of mechanical dyssynchrony and, in many cases, lower ejection fraction and heart failure.


Reddy: Dr Mulpuru, because these are important implications for the diagnosis, how do you recognize a true LBBB on ECG?

Image courtesy of Mayo Clinic

Siva K. Mulpuru, MD: ECG is one of the greatest tools we have today to recognize LBBB. The QRS becomes wider when you have electrical dyssynchrony, and as the left ventricle is posterior in lead V1, you have a negative QRS complex. There are certain criteria used to recognize true electrical LBBB. Let's go over them.

In general, when you have a true LBBB, the septum is activated from right to left. Therefore, you will not see any negative tiny Q waves in lead 1 and aVL. You tend to have discordant T waves. The wider the QRS, the more likely it is a true LBBB, and you also see some signs of fractionated or delayed activation in the lateral precordial leads. The first peak is the activation of the right ventricle, and the second peak is the activation of the left ventricle.

Image courtesy of Mayo Clinic

In summary, a wide QRS (more than 120 ms) which is negative in lead V1, discordant T waves, and fractionation in the lateral precordial leads help you recognize a true LBBB on ECG.

Correcting LBBB

Reddy: We established that LBBB is a bad thing, so how do you correct it?

Kapa: Good question. The effort to correct a LBBB lies in the desire to restore this near-simultaneous activation of left and right ventricle to make them beat together, getting back to that tug-of-war idea. In order to achieve that, we primarily use a special type of pacing device or defibrillator device wherein an extra wire—not just one that goes to the right ventricle, but one that also goes to the left ventricle—is used. Research is ongoing, but we traditionally use a wire that goes to the left ventricle via the coronary sinus vessel.

When you come into the right atrium, most venous blood return from the heart returns into that right atrium via the coronary sinus. That coronary sinus allows access for a wire to be placed that can wrap around the epicardial or outside surface of the heart and extend to the left ventricle.

Image courtesy of Mayo Clinic

As you can see in these anteroposterior and lateral chest x-rays, the lead placement includes a wire that has two coils (those thicker white areas that are extending to the right ventricle) and a separate wire that is more visible in the lateral view that is extending to the more posterior aspect of the heart where the left ventricle lies. This allows the device to have the opportunity to deliver pacing stimuli via both the right ventricular and left ventricular pacing wires simultaneously.

Due to recruitment based on where the left ventricular lead is, you will typically see a very positive deflection in V1 and V2 because, as you pace the left ventricle, you are going to have forces that primarily go out towards V1, V2. And because you are pacing and contributing more from the lateral surface of the heart, similarly, you will see that lead 1 and aVL will be negative because it is going to be going away from the lateral portion of the heart as you see in the ECGs below.

Image courtesy of Mayo Clinic

During right ventricular pacing, because you are often pacing more from the septal portion of the heart, leads 1 and aVL will often be positive, with net forces going towards them and away from aVR, and leads V1 and V2 will also often be more negative because they are looking at the heart from a more anterior view. Whereas during left ventricular pacing, leads 1 and aVL will often be negative because you have forces primarily going away from the lateral surface of the heart.

As you see here, aVR becomes more positive because the forces are flowing towards aVR, and V1 and V2 are more positive because you have these forces coming from the more posteriorly located left ventricle, extending out towards the more anteriorly oriented V1 and V2 leads. We are looking for an appropriately biventricularly paced ECG being negative in lead 1 and aVL and positive in V1 and V2. We are looking for a situation where the net vector is allowing for more left ventricular contribution. You want the primary contribution as you initiate conduction to be left ventricular in order to allow for optimal resynchronization.

Many studies[1,2] have been done in order to look at whether there are specific leads that are optimal or better for resynchronization, such as multipolar leads. Studies have also looked at where in the coronary sinus a lead should be optimally placed. We will not go into those in detail, but suffice it to say, these resynchronization efforts have allowed physicians to permit better activation and more physiologic activation of the heart.[3] While it is not truly physiologic activation, as you would normally see from an intact His-Purkinje system, it does allow, in many cases, for improvement in the myopathy that results from abnormal conduction.

The Future of Cardiac Resynchronization Therapy

Reddy: Where do you feel the field is progressing? What is the future of cardiac resynchronization therapy (CRT)?

Mulpuru: That is a great question. Several advances have been made in the past few years.

As Suraj explained, CRT does not really correct the conduction system abnormality, and we are basically working at the myocardial level. Some investigators thought, "What if we pace the conduction system and restore the normal activation of the heart? Will that correct the electrical abnormality?" That is a very important advance in our thinking and our understanding of resynchronization in the past few years.

Image courtesy of Mayo Clinic

In this [image], you can see the AV node, which then continues as the bundle of His, traversing through the membranous septum, which then continues as a right bundle on the right side and a left bundle on the other side. Some investigators looked into pacing the bundle of His, the conduction system itself, to overcome the LBBB.

Image courtesy of Mayo Clinic

How does that work? Just like we do in our electrophysiology studies, we have specially designed mapping catheters we can use to map areas of His bundle-like signals, Purkinje-like signals.

In this ECG, you can see a high-frequency signal before the complex that lines up with the QRS. When you screw in the pacing lead in this area, that essentially results in a QRS that resembles a normal conducted beat.

Image courtesy of Mayo Clinic

In this tracing, you can see that when you're pacing a high output, the QRS is narrow; and as the output is decreased, the QRS widens, showing that we lose capture of the conduction system at low output.

Image courtesy of Mayo Clinic

A chest x-ray can be a little confusing when you see these patients with His bundle pacing. It almost looks like two atrial leads in two big "Js." But do not be confused: This second lead is placed in the region of the His bundle and causes a conducted beat that results in a QRS, resembling a sinus beat.

Image courtesy of Mayo Clinic

In this tracing, the first two beats on the QRS are very wide and it is a true LBBB. In this patient, we placed a lead in the region of the His bundle and the QRS completely normalized. We narrowed down the QRS to 93 ms. This is a new advance and potentially avoids that lead placement in the coronary sinus.

However, it is not without risk because you can injure the conduction system. In this patient, you see development of complete heart block once you screw in this pacing lead, and we see that in about 10%-20% of the patients.

Kapa: In addition to His bundle pacing, other studies are being done, both clinically and in animal models, in order to understand whether we can achieve resynchronization through other means. People are looking at placing pacing wires on the endocardial surface of the left ventricle.[4] A fear for this is the potential for clot or thrombus formation on these leads, which could cause a stroke if it came off. However, some people believe that this procedure might be safe in the modern era, and clinical research studies are being done. In addition, there are initial clinical feasibility studies using a unique form of leadless pacing. It essentially involves sending pellets into the left ventricle that can be activated via ultrasound, resulting in activation of the left ventricle somewhat through a minimally invasive mechanism without the traditional wires that traverse the entire endovascular system.[5] People are also looking at the use of epicardial wires that can be delivered percutaneously either through a direct epicardial or "outside the heart" approach, through a sub-xiphoid puncture or other mechanisms.[6] In the next 10 -20 years or more, people are thinking about biologic pacemakers where we can transfect viral vectors and recreate an AV node. People have demonstrated this in animal models.[7] People are also trying to change the very nature of cells so that they respond to light stimuli, a term we call "optogenetic stimulation," that might allow for different methods of causing resynchronization without the use of any hardware.[8]

Reddy: Fascinating. Thanks again, Dr Mulpuru and Dr Kapa, for these very important insights. And thank you, the audience, for joining us on the | Medscape Cardiology.


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