STEMI Maskers vs. Mimickers: the problem with a wide QRS November 02 2018

The QRS complex reflects ventricular depolarization and by most standards, should be no greater than 0.12 seconds. When the QRS complex is wider than 0.12 seconds the ST segment automatically becomes altered in the opposite direction to the QRS complex.  This normal opposing ST-to-QRS complex phenomenon is known as ST discordance.  There are various reasons why a QRS will widen and when it does, it signifies that the time it takes for ventricular depolarization to occur is taking longer than normal.

A bundle branch block is the most common cause of a wide QRS complex; however, other causes include a pacemaker rhythm, a ventricular rhythm and the use of an accessory pathway such as Wolff Parkinson White.  Hyperkalemia may cause a ventricular rhythm. Whenever a new wide QRS complex is seen we need to be concerned about “WHY”. One of the most common causes of a sudden widened QRS complex, such as a bundle branch block, is an Acute Coronary Syndrome or Coronary Artery Disease.  In our assessments of the causality, we will conduct a cardiac workup consisting of an ECG, Echo, and some form of Stress Test. Depending on these findings, the person may then require diagnostic cardiac catheterization to determine appropriate therapy: medical vs interventional management.

The biggest problem with a wide QRS complex and the ST discordance is that the ECG is often rendered non- diagnostic in determining if an ACS is present. Some call this phenomenon of ST discordance a STEMI Mimicker, meaning the ECG will look as if the patient is having a STEMI when they are not. The concern in a STEMI Mimicker is that the patient will be inappropriately treated as a STEMI which may lead to harm. Others call this phenomenon of ST discordance a STEMI Masker, meaning the patient will not be diagnosed and treated as a STEMI because the ECG was non-diagnostic. Mortality and morbidity are higher if we do not provide reperfusion therapy to a STEMI.

I’m of the camp that feel an ECG with a LBBB should be considered and treated like a STEMI until proven otherwise, especially if the patient is having cardiac symptoms. Err on the side of caution that time is muscle. As a CCU nurse in the pre-fibrinolytic and PCI era, patients who presented with chest pain and a LBBB had very high mortality. Then came the numerous GUSTO and ASSENT studies looking at Streptokinase, t-PA, r-PA, TNK and we were given an amazing drug intervention that could dissolve the clot in a STEMI resulting in reduced mortality.

In those days, the patient who was experiencing classic symptoms of a MI but who also had a LBBB would not be giving fibrinolytic therapy because the risk of harm in getting this drug was thought to be too high given we weren’t 100% sure of a STEMI on the ECG.  As it turned out, research showed that the mortality was greater in not treating these patients and it was discovered, with the advent of cath labs, that these patients who presented with symptoms and a LBBB were often experiencing an occlusion in the proximal left anterior descending artery causing a massive anterior or anterolateral MI.

Given this new data, the guidelines for inclusion of fibrinolytic therapy were then revised so that a patient with symptoms of a STEMI plus a presumed new LBBB could be given fibrinolytic therapy as long as there were no contraindications. The harm in not giving an anterior or anterolateral STEMI intervention is that they will end up with any of the following: severe left ventricular dysfunction (Grade IV LV; a.k.a. HFrLV), left ventricular remodelling leading to a high rate of cardiac arrest, ventricular rupture, NYHA Class III symptoms (inability to do most of their activities of daily living without having symptoms, a.k.a“cardiac cripple”), and high burden of cost on the health care system

Then new research came out indicating that we sent too many patients to the cath lab who were having symptoms plus a LBBB and many of these patients were actually not having a STEMI. The inherent risks of going to the cath lab caused a shift, yet again, in practice guidelines. Instead of erring on the side of caution in treating the symptomatic LBBB like a STEMI until proven otherwise, the shift trended to erring on the side of caution and treating the LBBB as a STEMI mimicker. I predict that research will show this less-aggressive management will result in high mortality... time and research will tell.

For those of you who believe more that a LBBB should be treated like a STEMI Mimicker I would strongly suggest you become very familiar with Dr. Sgarbossa and Dr. Cai’s work on diagnostic criteria of a STEMI on an ECG with a LBBB. There are numerous case studies that have demonstrated the positive predictive value of this assessment tool and I believe strongly that we should all incorporate this tool in assessing the ECG with a LBBB in a patient presenting with symptoms. Also consider the diabetic who is presenting with vague symptoms and a LBBB. If this is a known new LBBB, we need to ask ourselves why they have suddenly developed it.

In my opinion, an ECG with a LBBB should be considered neither sensitive (diagnostic for a MI: masker) nor specific (not diagnostic for a MI: mimicker). The assessment for Sgarbossa criteria needs to be examined further and applied to all ECG with LBBB. However, as Dr. Sgarbossa said herself, the absence of meeting her criteria in a LBBB does not rule out the presence of a MI. Bottom line: the management of a patient with symptoms of a STEMI and a LBBB needs to considered high priority and the age old saying “time is muscle” needs to be kept in the forefront of our approach to treatment.

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Cai, Q., Mehta, N., Sgarbossa, E. 2013. Am Heart J
Sgarbossa E., et al. 1993 N Eng J Med
Smith,S., et al. 2012. Annals of Emerg Medicine