BHRS Editorial – The painful LBBB

Parag Gajendragadkar – ST7 Cardiology, Papworth Hospital

A middle aged lady presents to A&E complaining of typical cardiac chest pain. She has no cardiovascular risk factors and during an episode of chest pain has LBBB documented on her ECG.

The new onset of Left Bundle Branch Block (LBBB) with chest pain is suggested in ESC (although not American) guidelines to merit consideration of emergency reperfusion therapy [1,2]. It is certainly well known amongst interventional cardiologists and confirmed from registry data however that isolated LBBB activations for primary PCI uncommonly have blocked arteries needing acute reperfusion [3,4].

The ‘Sgarbossa criteria’ for diagnosing an acute STEMI in the context of LBBB derived from a NEJM paper by Elena Sgarbossa (and others) based on the GUSTO-1 thrombolysis study [5]. ECGs of patients who had an acute STEMI with LBBB and confirmed by cardiac enzyme rise were compared with controls who had chronic LBBB and stable coronary disease. This yielded the ‘Sgarbossa criteria’ outlined graphically in Figure 1. Anecdotally, whilst seemingly well used amongst paramedic crews, clinicians take a more global clinical approach to the patient presenting with LBBB and chest pain when deciding on emergency PCI – ‘true’ LBBB due to a coronary occlusion is associated with a large area of infarction which is usually clinically apparent.

Figure 1: Sgarbossa’s Criteria. 1. ST segment elevation >1mm concordant with QRS complex. 2. ST segment depression >1mm in lead V1, V2, V3. 3. ST segment elevation >5mm and discordant with QRS. (Adapted from


Quite often however the history and clinical scenario is not clear and adjudicating between ‘presumed new’ vs. ‘old’ LBBB is the decision that clinicians have to make. Mark Josephson’s group published data from a large ECG database where serial ECGs where available [6]. LBBB development was studied showing that a ‘new’ LBBB had a large T-wave compared to the depth of the S-wave in the chest leads and that this T-wave amplitude decreased over time [6]. They suggested an S/T ratio of <2.5 had excellent sensitivity (100%) and specificity (89%) for separating LBBB less than 24hrs old from that present for greater than 24hrs – see Figure 2.


Figure 2: Example of change in LBBB over time. Development of LBBB over time. QRS/T ratios listed showing S/T ratio <2.5 predicted ‘new’ LBBB. (From Shvilkin et al. 2010 [6])


The original patient described at the beginning of the article had negative serial troponins measurements and had normal coronaries on an angiogram performed the next day. A subsequent MRI scan also didn’t yield any abnormalities.

Mark Josephson’s group recently published a case series describing a group of patients who developed typical cardiac chest pain with the onset of LBBB which resolved with offset; importantly in the absence of functional ischaemia [7]. This has been termed ‘painful LBBB syndrome’ [7]. The phenomenon has been detected in a variety of ways – from Holter monitoring to treadmill testing. An extensive literature search described within the same paper found 50 individual cases described over the years from the first case report in 1946. There was an even male to female split and the common feature was the simultaneous appearance of chest pain and LBBB during an exercise test. Identical pain was inducible with LBBB at similar heart rates due to atrial pacing, IV isoprenaline and dobutamine. In most of the published cases, pain resolved with resolution of the LBBB. Interestingly, the heart rate at which LBBB and pain disappeared was invariably lower than the rate of onset. The long-term prognosis seems to be good with all patients having normal LV systolic function at rest. With the reduction of the use of exercise testing and with no evidence of functional ischaemia, it is likely that this condition is somewhat underdiagnosed.

The mechanism behind such a syndrome is unclear. The previous prevailing view was that this was in some way linked to myocardial ischaemia. However, nuclear imaging has always been negative for ischaemia in the limited case reports and vasospasm has been ruled out during ergotamine infusion at the time of coronary angiography (although modern practice casts doubt on this as a provocation test). Josephson’s group’s view is that dys-synchronous ventricular contraction may be the primary cause of the chest pain during LBBB as has been postulated previously [8]. Anecdotally, most people can think of a few patients who have had pain during ventricular pacing and it is assumed this is fed back to the central nervous system by local mechanoreceptors. Previous studies investigating patients with normal coronary arteries and chest pain have suggested that in these patients there is some sort of abnormal cardiac sensitivity, judged as a sensation of pain due to internal cardiac pacing or RV catheter manipulation [9]. Interestingly, certain areas of the brain (the insula) show electrical waves contingent on the heartbeat [10]. The amplitude of these evoked potentials appears to correlate with an increased perception of the heart-beat [10], something that may contribute to the perception of the dys-synchrony.

The intermittent LBBB pattern is similar to ‘new’ LBBB with a S/T ratio of <2.5. Interestingly, the ECG in ‘painful LBBB’ tends to have an inferior QRS axis as opposed to normal/leftward axis in the overall LBBB population. Josephson’s group postulate this to indicate a specific ventricular activation and contraction pattern – i.e. not all LBBBs are created equal. Different myocardial contraction patterns have certainly been described in the setting of LBBB using cine MRI (which then can predict response to CRT, which makes sense intuitively at least) [11].

One of the cases described by Josephson’s group is particularly interesting [7]. After exercise induced chest pain and intermittent LBBB, one of their patients underwent coronary angiography. The patient had moderate coronary lesions which were not thought to be significant. The pain persisted however and eventually PCI to these lesions was undertaken, unfortunately with no resolution of symptoms. A Holter monitor was also done and showed evidence of intermittent high-grade AV block so a dual chamber pacemaker was implanted. Initially, there was a resolution of symptoms with RV apical pacing. At the first pacing check when algorithms to reduce RV pacing were instituted, the patient developed typical pain soon afterwards. With resumption of obligate RV pacing, the symptoms disappeared. Josephson’s group go on to make the point that an EP study in such patients may be useful to pinpoint locations for pacing and assess whether some sort of cardiac sensitivity syndrome existed.

In summary, painful LBBB syndrome is an unusual syndrome to consider in patients with exercise induced chest pain in the absence of functional ischaemia. Exercise testing can still be a useful diagnostic tool.



1              Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC), Steg PG, James SK, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2012;33:2569–619. doi:10.1093/eurheartj/ehs215

2              Members* WC, O’Gara PT, Kushner FG, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. Circulation 2013;127:e362–425. doi:10.1161/CIR.0b013e3182742cf6

3              Brown AJ, Hoole SP, McCormick LM, et al. Left bundle branch block with acute thrombotic occlusion is associated with increased myocardial jeopardy score and poor clinical outcomes in primary percutaneous coronary intervention activations. Heart Br Card Soc 2013;99:774–8. doi:10.1136/heartjnl-2012-303194

4              Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J 2010;160:995–1003, 1003.e1–8. doi:10.1016/j.ahj.2010.08.011