Damar Hamlin & Commotio Cordis

It is important in medicine to maintain a differential diagnosis and not to “diagnostically anchor” to one diagnosis. There are several possible causes of Damar Hamlin’s cardiac arrest. Commotio cordis is the leading candidate but cardiac contusion, and even direct injury to the left anterior descending coronary artery are possible. I favor commotio cordis as the explanation, although the reported second arrest in the hospital does make a contusion or LAD injury possible. Here are some notes from our textbook on Sports Cardiology on commotio

Kumar, Mandleywala, & Link. Chapter 7: Commotio Cordis: Pathophysiology, Prevention, and Treatment. From Sports Cardiology. Thompson, PD & Fernandez, AB editors. Volume 3, p.121–133. World Scentific Publishing. 2018.

· Impact to the heart by a small hard object during the last 30 or so msec before the peak of the T wave can cause VFib

· Variables include: it appears more frequent in males (greater than sports participation alone, so may have hormonal component like LQTS), pliability of chest wall (because it has to increase LV pressure in pig model to cause the event), possibly genetics, location, hardness of object velocity, and shape of object (a flat disk, the size of a baseball won’t do it).

· Sudden increase in LV pressure increases dispersion of repolarization to trigger both PVC and a wave of depolarization — both appear necessary.

· It is one of the most common causes of SCD in young athletes.

· A 1900–1910 report from baseball (ie, first part of the 20th century) found 19 cases due to baseball strikes to the heart.

· Apparent commotio cordis was previously reported in workplace accidents (and I think from horse hoof strikes).

· There is a National Registry started in 1996, and up to 2018 there were about 220 cases reported.

· Usually occurs from impact of a small dense object, baseball, hockey puck, lacrosse ball directly over the ventricle.

· Can also result from sharp fist blow to the chest, even from child discipline.

· Age is usually 11 to 19, median about 14, probably because you need a flexible chest wall.

· Victims are overwhelming male — may be due to differences in ion channels with sex.

· Resuscitation is successful in only about 60%.

· Mark Link when he was at Tufts developed a swine model. They shoot an arrow at an anesthesied pig’s chest with a special compound bow (of bow/arrow fame). This demonstrated that both Vfib and complete heart block (CHB) can be produced by chest hit.

· CHB was not related to time of the cardiac cycle and was always transient.

· VF in swine model only occurred if strike was 10–30 msec prior to T wave peak.

· Higher impact speeds more frequently produced VF, but if speeds were too high there was also cardiac contusion.

· Impacts over the center of the heart were most productive of VF.

· The impact has to increase LV pressure and in the pig required a pressure >250 mmHg.

· There is variability among animals suggesting a genetic susceptibility.

· Animals with longer QTs were more vulnerable.

· It is Thought that both increased electrical dispersion and a PVC are required to cause VF.

· This may be an example of “mechanic-electrical’ coupling, where mechanical stretch (from increased LV pressure) produces electrical changes.

· This mechanic-electrical coupling has been attributed to stretch sensitive ion channels in the myocardial cells — possibly a K+ channel, since K channel blockade reduces VF.

· Chest protectors have not been universally shown to be preventive in the Link swine model, but are now required in some lacrosse leagues for goalies and in some baseball leagues for catchers. Soft baseballs do reduce VF.

· Early recognition and early defib are keys to survival.