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Early Repolarization Syndrome

Is anybody here familiar with ERS or been diagnosed with it?  Not the benign ERS, more along the lines of type II.  
7 Responses
Avatar universal
      First of all you are correct to say that there are different types of early repolarization. I have never actually heard them referred to as type I, II, and III, but you are right that the kind of early repolarization that is common in young males and carries a benign prognosis is most often confined to the lateral precordial leads (V5 and V6). I don't know for certain why it most often show up there, but it just does. This time of early repolarization is thought to be due to increased vagal tone which is obviously more pronounced in young fit males, but can sometimes just be so for anyone of any age. It is actually interesting to note that in people with spinal cord injuries or hypothermia patients a similar ST elevation occurs, as both of those situations also result in higher vagal tone. Additionally, black males are more likely to have benign ERS and with it being caused by higher amounts of vagal tone this makes sense, as there have been some links between testosterone levels and vagal tone (correlation or causation we do not know for certain) and black males tend to have, on average, higher testosterone levels than white or Asian or Hispanic males. It is also true that with age testosterone decreases and so does the incidence of benign ERS. Finally, it is obviously more common in males than females, so it would appear that hormonal mediated vagal tone might be the cause of this, along with environmental factors such as acquired levels of fitness.
        Now, it has been shown that having early repolarization (which is really just a reference to J point/ST seg. elevation) in  the inferior or lateral leads may be dangerous. The reason for this is not the actual lead location, but rather that something entirely different is often happening when there is J point elevation in the inferior and lateral leads. The benign sort of early repolarization has J point elevation followed by a rapidly ascending ST segment and a positive T wave. The malignant form has J point elevation with a descending or horizontal ST segment and a negative T wave.
          If that pattern sounds familiar it is because it is the pattern we see in the septal/anterior precordial(also known as the "right precordial leads") in Brugada Syndrome. Brugada syndrome has long been thought to be a purely electrical disease, but recent successful ablation procedures involving the RVOT (right ventricular outflow tract), which have been curative for Brugada Syndrome seem to hold the potential to eventually confirm a previous suspicion that Brugada Syndrome is actually due to a lack of symmetry in the layers of the heart (endocardial, myocardial, and epicardial) over the Rq2t8y2VOT area (which happens to be represented on the EKG by leads V1-V3, where the Brugada sign would show up). It is this lack of symmetry that leads to the J point elevation, which then has a rapidly descending ST segment returning to baseline before going into the negative T wave.
         Whenever we have a situation where the ventricle of the heart is not depolarizing and repolarizing symmetrically we have the potential for arrhythmias. Arrhythmic potential is often assessed by looking at T wave alternas, QRS dispersion (QRSd) and QT dispersion(QTd). Things across the heart should work at roughly the same speed. We don't want one part "getting ahead" or "falling behind." Brugada Syndrome can be caused by many things (the most common of which is a mutation in the SCN5A sodium channel gene), but the end result seems to be the same. But who is to say that this same pattern, or a very similar pattern could not occur, for various reasons, in other parts of the heart (and thus other EKG leads), and carry the same potentially disasterous risks? In essence, it may very well be that "malignant ERS" is just Brugada Syndrome in the inferior and/or lateral leads, while Brugada is that same pattern in the right precordial leads. Obviously, the more areas of the heart that have a problem like this the worse off one is (hence why it is worse to have it in both the inferior and lateral leads vs just one, and even worse to have it globally). Furthermore, the higher the J point elevation, the more asymmetry there is between the layers of the heart in that spot, so the worse off your arrhythmic potential is. The lateral precordial leads are not immune either. Just because they most often carry the vagal tone mediated benign early repolarization (which has nothing to do with what we call malignant early repolarization) does not mean it cannot show the malignant ERS sign. Really any lead could show thinks sign (J point elevation with a descending ST segment and inverted T wave) and the degree to which it is present (amplitude of the J point elevation) and how widespread it is (how many leads it shows up in) is key. Obviously, there could be a sort of genetic link to this problem, just as there is a genetic link to Brugada Syndrome. That's all I can really share on this topic. Hope some of this helps.
1124887 tn?1313754891
I'm not "diagnosed" with early repolarization, it's not a diagnosis and my cardiologist doesn't care about it. But as you can see from my EKG attached to my profile, I have a slightly slurred S wave in the inferior leads (II, III, F) and slight ST elevation in the ateroseptal leads.

There is a lot of debate regarding the significance of this. From one article I've read, the risk is slightly higher but still extremely low (if I remember correctly, the risk of cardiac arrest is 1:20.000 instead of 1:33.000 without early repolarization or so). I guess if I should be afraid of that, I would have to be afraid of almost everything in this world.

Early repolarization (which is a fairly stupid expression, by the way, as it has nothing to do with early repolarization or repolarization at all) can in some cases be "late depolarization", which if I understand it correctly can in some cases trigger arrhythmias. If you are worried you can consider asking your cardiologist for a signal averaged EKG, which may reveal late depolarization potentials. The problem with this test is, however, that even if it's positive (which it is in approx 10% of us), the risk is still extremely low and you risk ending up worryed about something completely benign (which you probably already do ;)

Avatar universal
I have never heard of Early Repolarization Syndrome type II. ERS apparently is often seen as a common and benign  ECG abnormality  in young adults  and often associated with athletes. There have  been  some recent  studies refuting ERS is always benign.  
I have 3 sons 15 20 and 22 . All have ERS   mainly in the inferior leads + bradycardia.   My 20yr old is athletic,  the other 2 not at all.. No abnormality seen in there ECG 's except for ERS and bradycardia.
Only my  youngest son is symptomatic, he has recently had 2 blackouts  is very easily tired his pulse is around 50 normal, he has episodes when it is around 40  that is when he feels  dizzy and  might blackout.
Drugs challenge ruled out brugada syndrome, he has since been implanted with a permanant  cardiac monitor. It will be 'read' in November.
There has been 4 family members on my side with sudden death between the age of 36 and 57.
My older sons are scheduled to have a drugs challenge, and we have been tested genetically.
So, is it just a coincidence  they all have ERS??   is it really benign??  is it heredity??  Research is ongoing for us. There is so  very little information  regarding  this  ' ERS 'terminolgy.   I'm interested to hear about others with similar symptoms.  Regards.
Avatar universal
Actually it is a diagnosis and it isn't always benign.  There is actually a genetic link to it as well, which happens to be something worth looking into with my family.  The type of ERS that I'm referring to isn't even the type you are referring to.  Type II and III aren't common and aren't in 10% of the population.  Those types are not considered benign and can cause problems whether it's just syncope, palpitations, or at the worse cardiac arrest.  The fact that I came on here and asked if anybody here is familiar with it doesn't mean that I am "worryed" about something completely benign or that I sit around and worry about benign issues.  It would be me trying to find somebody who is actually familiar with it (which apparently isn't you) so that I can ask them some questions.  I would be careful about making assumptions.
Avatar universal
I cant answer your question but if you contact the SADS foundation, they should be able to help by providing you with information on the condition, support groups, and doctors with expertise in this area.
1124887 tn?1313754891
First, I didn't say that 10% of us have ERS, but up to 10% of us can have a positive signal averaged EKG.

It's not a "type II and type III" early repolarization syndrome, Brugada syndrome on the other hand, can manifest as type 1, 2 and 3, depending on the EKG changes. The possibly dangerous early repolarization you refer to, is concerning the EKG changes in the leads II and III (also known as the inferior leads). It's not uncommon.

I'm very familiar with this, as I obviously have this myself. And, I've asked my cardiologist about it and he is not concerned at all. Early repolarization is common in young people. May I ask, are you diagnosed with early repolarization?

I'm sorry if my previous answer somehow offended you.
Avatar universal
Actually there are 3 types of ERS

"Type 1: ERS observed predominantly in the lateral
precordial leads, prevalent among healthy male athletes
and rarely seen in IVF survivors; Type 2: ERS
predominantly in the inferior or inferolateral leads
and associated with a higher level of risk; Type 3:
ERS globally in the inferior, lateral, and right precordial
leads and associated with the highest level
of risk for development of malignant arrhythmias.
Type 3 is often associated with IVF storms."

"J-point elevation in inferior leads
– >0.1mV (5.8%)RR cardiac death: 1.30 (CI:1.05 –
1.61, p=0.02)
– >0.2 mV (0,33%)RR cardiac death: 3.03 (CI 1.88-
4.90, p=0.001)
RR arrhythmic death: 2.99 (CI 1.49-6.03, p=0.005

Stronger predictors than QT interval and LVH"

I think what offended me the most about your post was
" you risk ending up worryed about something completely benign (which you probably already do ;) "  You assumed this from the fact that I simply asked if anybody was familiar with this syndrome.
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