Dear colleagues Gennadiy and Benito, there is an interesting case and no less mysterious ECG changes. I largely agree with your thoughts and opinions. However, I would very much like to see the ECG in leads I, II, III, avR, avL, avF, since it is very important to us. And it's even better to look at the previous ECG retrospectively (6 -12 months ago ... or before sports).

1) In the present part of ECG is a dominant R wave in right precordial leads (V1- V2, and including fragmented R in V1 lead) with no Q-wave in leads V5-V6. Left medial fascicular block would be postulated, however this pattern may represent a variant of incomplete RBBB. It can also be due to many normal variants, including a variety of LV Purkinje distribution (less Purkinje fibbers in the anteroseptal zone that induces a delay in the activation of this area without pathologic block; this hypothesis of different distribution of Purkinje fibers, has been also used to explain the presence of SI- SII- SIII pattern in healthy people). Taking into account the presence of DG1 myоcardial bridge, and the fact that right bundle and the middle septal fibers receive perfusion from the LAD septal branches, and therefore, the mechanical dynamic obstruction of the DG1 may induce block of either of the structures or both.

2) Attention is drawn to the macroalternation of the T wave in lead V1 (compare the first complex and the second, third and fourth) and QRS alternation (compare the first complex and the third).

3) Biphasic T-wave pattern in V3 - V5 leads (pseudo 2 type LQTs) can be a result of increased transmural dispersion due to greater increase in action potential duration in the M-cells of the myocardium compared to the endocardium or the epicardium.

What do you think about it?

Dear Dr. Benito Jonas Baldauf,

thank you for this interesting clinical case. I think the pesented data deserve an attentive analysis and I'll outspeak that I have yet any conclusive opinion. But I'd like to note as you did - on some interesting findings which would be helpful in future. ECG in rest: in the setting of lower rate of cardiac rhythm and normal duation PR interval (0.156 ms) we can see slight deformity of an initial part of QRS complex (upward, slurred small "r") which resembles Δ-wave of WPW syndrome. We can trace it through almost all pecodial limbs to V6. Probably the presence of the deformity is "responsible" for a slight QRS elongation. It is not such evident, total PR interval is normal but some deformity of the initial part of QRS presents, as I suppose.

Secondly, it is a strange position of ST segment in V3-V6: since S wave we see no isoline itself but upsloping line connecting S end with T peak.

There are questions concerning the exercise test: what load level these changes were detected from? Particularly downsloping ST depression, biphasic T in V1? It would be interesting to assess local wall motion abnormalities during stress-Echo but it's not advise now but rather thoughts aloud. Am I right estimating the tendency of "normalization" of ST depression during the load increasing in V2?

What is more detailed Echo description? Concerning "minimal pouches". Where are they located: within myocardium, subendocardial, involvement of IVS, LV free wall, RV? It would be interesting to see the desciption of all measurements (diameters, IVS and LV thickness, RV).

Dear colleague Gennadiy Taradin,

thank you for your thoughts.

I totally agree with your findings resembling a deltawave. During exercise we did not find any sign of fast antegrade pathway, slurring disappears with heartrate above 110/min...we did not perform cardiac mapping. But we should still consider. For my part, I tend toward ablational therapy in any sportsmen presenting with WPW independent of conduction speed of pathway.

We do see the ascending ST-segment coming from high j-point leading into U-wave quite often in young athletes with history of a couple of years of strenous exercise training. In this athlete though, presenting with fragmentation of QRS and development of ST-depression during exercise it did catch notion and I exspected HCM or even HOCM in the echo...which didnt show.

Very good question and thoughts about wall movement and V1 deterioration:

As matter of fact we can see preterminal T-negativity starting as early as 3 minutes into exercise test with 40 Watts and a heartrate of 80/min!! It then aggravates to descending ST-segment depression leading into a terminal T-negativity as we can see it in the sheet i published here recently, at about 70-100Watts and heartrate of about 110-131/min. A MRI with perfusion will be performed in two weeks. Wall motion and perfusion will be an issue, and I will update for shure.

You are right, ST-depression seems to be inconsistent. This is due to strong artefacts during load in the lead.

The little pouches can be seen in the RV wall apical subendocardial and apical lateral endiastolic in apical 4 chamber view as well as 4 chamber subcostal, IVS and LV are free of pouches in apical 4-chamber, 2- and 3-chamber view, as well as parasternal views or subcostal. TAPSE is well above 20mm, slight reflex in thin modurator.

Measurements:

LV EF 64% endiastolic volume about 90ml/m², endsystolic volume about 30ml/m²

RV EF 50% endiastolic volume about 75ml/m² endsystolic volume about 35ml/m²

myocardial mass abot 170grams

LA 35mm RA 38mm RV 26mm LV47mm IVS 8mm LV lateral wall 12mm

Again thank you for your thoughts.

Regards

Dear colleagues Gennadiy and Benito, there is an interesting case and no less mysterious ECG changes. I largely agree with your thoughts and opinions. However, I would very much like to see the ECG in leads I, II, III, avR, avL, avF, since it is very important to us. And it's even better to look at the previous ECG retrospectively (6 -12 months ago ... or before sports).

1) In the present part of ECG is a dominant R wave in right precordial leads (V1- V2, and including fragmented R in V1 lead) with no Q-wave in leads V5-V6. Left medial fascicular block would be postulated, however this pattern may represent a variant of incomplete RBBB. It can also be due to many normal variants, including a variety of LV Purkinje distribution (less Purkinje fibbers in the anteroseptal zone that induces a delay in the activation of this area without pathologic block; this hypothesis of different distribution of Purkinje fibers, has been also used to explain the presence of SI- SII- SIII pattern in healthy people). Taking into account the presence of DG1 myоcardial bridge, and the fact that right bundle and the middle septal fibers receive perfusion from the LAD septal branches, and therefore, the mechanical dynamic obstruction of the DG1 may induce block of either of the structures or both.

2) Attention is drawn to the macroalternation of the T wave in lead V1 (compare the first complex and the second, third and fourth) and QRS alternation (compare the first complex and the third).

3) Biphasic T-wave pattern in V3 - V5 leads (pseudo 2 type LQTs) can be a result of increased transmural dispersion due to greater increase in action potential duration in the M-cells of the myocardium compared to the endocardium or the epicardium.

What do you think about it?

Dear colleague Vaikhanskaya,

thank you for your thoughts. Very distinguished and in detail...

I added the missing leads. See below.

I agree on to your point of view it might be the ecg normovariant of a healthy individual with incomplete RBBB in the present ECG, stress testing did reveal significant development of ST-depression, which in this case lead to further testing. We did perform all of these tests to narrow down differential diagnosises (HCM, HOCM, ARVD, channelopathies, myocardial infarction, myocarditis, sarcoidosis) since we need to attest fitness for FIFA licensing (professional soccer player). Cardiac MRI adenosine stress test will be performed to show significance of stenosis due to myocardial bridge-ing. Computed FFR in this case also due to radiation reduction protocol was not performed. Again myocardial brigde-ing is very superficial (see coronary CT reconstruction), changes in V2 start very very early (warm-up)... I will keep you updated.

...and you are totally right with your referring to induction of bundle blocks by obstruction of the DG...

The T-wave alternation does meet the eye, as does the fragmentation of QRS in the third QRS komplex in difference to all the others....might be due to projection and breathing (very lean patient, small chest, 120% vital capacity in bodyplethysmography)...but I am not shure.

As for your explanation for biphasic patterns of the T-wave...yes!

Thank you again for your thoughts

Regards

Dear Dr. Benito Jonas Baldauf,

Thank you for your comprehensive answer and ECG. I completely agree with your diagnostic research. The diagnostic algorithm is an excelent. I hope that the young athlete will show good result of cardiac MRI adenosine stress test and and will be certified for FIFA licensing. I hope to hear updated results further.

Best

Thank you Benito, Gennadiy and Tatiyana for the nice discussion. ECG shows QRS of 100 msec with some fragmentation especially towards the latter part. The myocardial bridge seems to be an incidental finding and the ST T changes in the exercise testing do not appear significant. My only concern is the possibility of ARVD, before it becomes full blown satisfying the criteria for a definitive diagnosis. Before labelling as a "benign rbbb variant" it will be desirable to do a detailed echo and a targeted MRI to look for early evidence of ARVD. Follow up imaging is certainly desirable. I only hope that it is only a " normal variant".

Dear colleagues, i hope so too. You can image the state this young soccer player is in right now...

I will keep you updated

Thank you for your participation in the matter, the great discussion and sharing excellent views.

Regards

I find it very interesting, as are all discussions. In my opinion of an old cardiologist, it seems that at the end of all examinations the definitive diagnosis will be: benign incomplete RBBB in an otherwise normal heart.

Dear Benito,

Peace and blessings.

Very interesting scenario.

Beside the aspects already well commented by the colleges I wish to share some thoughts based on data made available, if I may. My comments are merely academic.

This seems one of those cases with undetermined QRS electrical axis, with thickened S waves, indicating a right bundle branch conduction disturbance. Slight QT lengthening is not uncommon in this case.

He is very tall for the age, and lean. Does he have any thoracic abnormality like pectus excavatum or carinatum?

What draw my attention, at first, was the remarkable high frequency notching, in V1 and V2, starting approximately 76 ms from the begging of the QRS complex.

In peripheral leads, those notches were evident, timings were identical, but they changes in amplitude in subsequent beats.

Also, time of QRS onset to notch remained constant in consecutive complexes, and also during exercise testing with increasing heart rate, pointing to fixed conduction abnormalities.

To rule out scars, although you stated 'no major ARVD criterion', was there any spotty late gadolinium enhancement on the apex or the LV free wall? Could you manage to rule out noncompactation?

Finally, pouches in RV reminds me double chambered RV, and could also explain QRS fragmentation, RBB conduction disturbance as well as beat by beat variation in notches amplitude.

Any update on MRI with perfusion?

Best regards,

Dear colleague Paulo,

very distinguished and good thoughts on the case, very good examination of the ECGs conducted.

I am conducting a study of ECG and echo findings in patients born with thoracic deformations. I do see similar ECG changes in some of them with severe types of excavatum. This young soccer player though has no deformation at all.

We did perform three MRI. Hardware is Siemens, software is Circle CVI. Both excellent in performance. We could not detect any subepicardial fibrosis, no endemic showings for CMP nor HCM, no lack of perfusion.

We do see cases in which ECG changes show way earlier than changes in MRI.

Exercise MRI will be conducted next week.

Planning to do an ajmalin as well, maybe. What do you think?

Sehr Geehrter Benito,

Danke für Ihren Kommentar.

Ich bin nicht sicher dass Ajmalin kann etwas zu helfen in diese Scenario.

Auch, wurden Ajmalin benutzen nur wenn Sie Cannelopathie oder frühe Repolarisationen haben bewerten. Keinen klinische Synkope Vergangenheit oder bemerkenswert EKG Signal, Ich denke dass Ajmalin testen ist nicht Klinisch relevant jetzt. In Ihrem Ermessen.

Frieden und Segen.

Geehrter Kollege Paulo,

der Kurvenverlauf ist nicht unbedingt Brugadatypisch, auch ist die Familienanamnese unauffällig, daher habe ich die Frage einmal in die Diskussion geworfen. Nicht zuletzt um die Ausführungen der geschätzten Kollegenschaft dazu zu hören.

Vielen Dank

Beste Gruesse

BB

Dear colleague Paulo

the ECG is not typical for any kind of channelopathy like Brugada, nor is family history arising suspicion. For there is great expertise in the field here, I did throw in the question, to get some thoughts on the matter.

Thank you

Regards

Dear Dr. Benito,

After reviewing the ECG tracings, I have to agree the biphasic T waves in V3 and V4, and the terminal peaked T waves in II, III, aVF, V5 and V6, first highlighted by Dr. Tatyiana (@Tatiyana Vaikhanskaya) above, have drawn my attention.

I agree a challenge with Ajmalin may be useful to rule out some repolarization disorders.

Let us know.

Thank you for your comments.

Sincerely,

Peace and blessings.

Dear colleagues,

MRI with Adenosin has been conducted to rule out lack of Perfusion during exercise due to myocardial bridge-ing of the large DG1. There is no lack of Perfusion. I do have to state the MRI was conducted pro bono for FIFA licensing.

A great discussion has come up wether to conduct Ajmalin or not...for now it hs been postponed and the Soccer was licensed....

I thank you for your Input to this case.

I will shortly be uploading another, wery difficil case...

Regards

During my internal medicine training, when I had to deal with the ECG, I learned to pay attention to clear changes in cardiac disease, i.e. 1) changes in normal sinus rhythm, 2) changes in the excitation process and excitation regression, and 2) significant ST-seg-ment changes >1 mvol as evi-dence of ischemia. Later on, I also commu-nicated this to the students in the practical year, and I am well received. I was even able to convey that to my son when he was six, who later became a bank clerk and forgot everything again. There are numerous nonspecific ECG changes in adolescents and athletes, which, however interesting, neither directly prove heart disease nor rule it out with normal ECG with certainty.

Of course, signs of left hypertrophy, right heart strain, pericarditis, disturbances of elec-trolytes, such as hyperkalemia, regular or irregular pacemaker function, can be detec-ted in the ECG. And there are many other nonspecific ECG changes in adolescents and athletes, which, however interesting, neither directly prove heart disease nor rule it out with normal ECG with certainty.

Addinng something to the many answers, I would suggest to also consider an external coronary compression- This might be the case considering the yound age of the patient. This rare pathology it is mostly seen in young women and is more frequent in the right coronary artery. The external compression may be missed if is fluctuating and one is not specifically searching for this rare condition.