The differential diagnosis of ST-segment elevation is wide and diverse, and includes the following : myocardial ischemia or infarction, Prinzmetal angina pattern, Takotsubo cardiomyopathy, ventricular aneurysm, pericarditis, normal variant ("early repolarization"), left ventricular hypertrophy, left bundle branch block, other causes of myocardial injury, such as myocarditis, trauma or tumor invading the left ventricle, hypothermia, after DC cardioversion, hyperkalemia, hypercalcemia, type 1C antiarrhythmic drugs, intracranial hemorrhage and the Brugada pattern.
Three aspects are important in the discussion of this case:
Firstly, Loukas et al  divided false tendons into five categories, according to the site of implantation. Ker  described a sixth type of false tendon where the specific location is between the subaortic portion of the interventricular septum and the left ventricular free wall. Six cases were described and in all of them a striking, localized ventricular, hypertrophic response was present at the site of subaortic implantation. This condition was named "false tendon-induced subaortic hypertrophy" and it was proposed as a new variant of hypertrophic cardiomyopathy . This case clearly belong to this sixth group of false tendons with a clear subaortic implantation location.
Secondly, repolarization changes in leads V1–V3 can be associated with Brugada syndrome. This case does not fulfill the criteria for Brugada syndrome : Three ECG patterns for Brugada syndrome have been identified but only a "coved" or type I ECG segment elevation is presently considered diagnostic for the disease . The other crucial aspect in the diagnosis of Brugada syndrome is the criterion for structurally normal hearts . This case clearly does not demonstrate a structurally normal heart, as it demonstrates the false tendon-induced subaortic hypertrophy variant of hypertrophic cardiomyopathy. In order to accept a type II ECG ("saddle-back" elevation) as Brugada syndrome one needs genetic confirmation with a structurally normal heart .
Thirdly, hypertrophy is a mechanism (or response) of the heart to reduce stress on the ventricular wall . It has been shown that mechanical stress on the ventricular wall can elicit a wide variety of auto-and paracrine responses, leading to the local secretion of a wide variety of growth factors, such as endothelin 1, angiotensin II and insulin like growth factor . Therefore, scientifically it is clearly conceivable that a false tendon inserting itself in a subaortic location, will cause a localized stretch response at the implantation site and leading in some instances to a localized, hypertrophic response, as shown before . It is therefore quite plausible that the localized, septal hypertrophic response is the reason for the observed repolarization changes.
In conclusion, a case report is presented of a young, healthy man with a "saddle back" ST-elevation of the precordial leads. The cause for this phenomenon is the sixth type of false tendon, the subaortic false tendon  leading to a localized hypertrophic response. It is proposed that this is a totally benign phenomenon and that care should be taken in the young, healthy patient not to confuse this entity with serious disorders, like the Brugada syndrome.