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Pathophysiology
Contention exists around the exact mechanism for commotio cordis. However, experimental studies have shown that there are several factors involved. First, contact occurs directly over the heart in the anterior chest.[4] The contact occurs during ventricular repolarization, specifically during the upstroke of the T-wave before its peak. If the impact occurs later than this, it is more likely to result in a transient complete heart block, left bundle branch block, or ST-segment elevation.[5] While this period occupies only about 1% of the cardiac cycle, the relative proportion is increased with increasing heart rate, as may occur during exercise.
The impact energy must be sufficient to cause ventricular depolarization, estimated to be about 50 joules. This is easily achieved by a thrown baseball, for example, and the risk for commotio cordis appears to peak around 40 miles per hour. At higher speeds (with more energy), there is more likely to be resultant structural damage to the heart and/or chest wall rather than isolated ventricular fibrillation.[6] Smaller balls also carry a higher risk for commotio cordis, likely due to the impact being concentrated on a smaller surface area.[7]
The mechanical force resulting from the precordial impact causes a stretch in myocardial cell membranes, which likely activates ion channels (mechanical-electrical coupling).[8] If the right number of these channels are in a vulnerable period of repolarization, the result of the depolarization may be ventricular fibrillation.[9]