Cardiac Arrest and Sudden Cardiac Death in Athletes
Damar Hamlin: Separating what is provable versus speculation based upon clinical medicine, pathophysiology, and published research.
By now most of us are familiar with Damar Hamlin’s cardiac arrest during Monday Night Football’s game January 2, 2023. There is much speculation and emotionally charged discussion on social media.
First and foremost, let’s be respectful of the player’s critical condition (still in ICU) and family’s grief and stress. Prayers and warm wishes for him and his family.
In this discussion it seems many (on all sides of the discussion) are subject to some confirmation bias and some deference to authority (quoting someone they respect but not understanding the pathophysiology themselves). While some aspects of the situation are speculative at best, other aspects can be interpreted with 100% confidence.
It really helps to put aside personal ego and not take any aspects of this discussion personally (and refrain from ad hominem attacks). Much of this can be explained or not explained with provable pathophysiology.
My background:
Interventional Cardiologist having seen MANY ACLS (code blue, cardiac arrest) situations in the hospital and outside the hospital, in the ICU and outside the ICU, in the Cath lab and outside the Cath lab. I also have been evaluating post COVID and post vaccine cardiac complications for past 2–3 years.
1. Cardiac arrest
Eye witnesses at the game confirm he received CPR and AED. Using the AED indicates he had a “shockable rhythm” which would most likely be Ventricular Tachycardia or Ventricular Fibrillation (can also be for atrial fibrillation and SVT but that would not correlate with CPR and subsequent ICU care).
VTach does not necessarily lead to immediate syncope. Stable VTach can quickly degenerate into pulseless VTach or VFib. The fact that he did not immediately have syncope and collapse doesn’t prove or disprove anything.
According to family, patient had a second cardiac arrest at the hospital. We don’t know when this occurred. If this occurred during hypothermia protocol it is not uncommon due to the massive electrolyte shift during cooling and subsequent rewarming. Additionally, during initial intubation short acting sedatives (Versed and Fentanyl) are usually administered. Until continuous infusion (possibly propofol) is started in the ICU, when the short acting sedatives wear off, there is a return of adrenaline and sympathetic drive resulting in recurrent ventricular rrhythmia. I have seen this many times in Cath Lab when the sedation after intubation wears off. This by itself does not portend worse prognosis nor does it add much value to the assessment of potential etiology.
2. Commotio Cordis
We can say with 100% scientific and medical confidence that such a diagnosis was premature and impossible to make the night of the incident (YouTube videos and social media pundits declaring it to be Commotio Cordis within a few hours of the incident). This is not hubris. It’s scientific and medical fact because the diagnosis requires exclusion of cardiac contusion (which could not be done until he reached the hospital and an echocardiogram were performed). The diagnosis also requires exclusion of other structural abnormalities.
Furthermore, Commotio Cordis is due to high impact to the left precordium. It is most often seen in baseball, hockey, and lacrosse due to high speed impact of ball / puck hitting the left precordium. This impact delivers Energy (Joules) to the heart at the wrong time of the cardiac cycle disrupting the electrical conduction system leading to Ventricular tachycardia or fibrillation. A precordial thump (fist to chest) can deliver 30 J of energy.
E= (1/2)mv^2. Thus the velocity of the object is a major factor (more than the mass). A 90 mph baseball will deliver more E than a 100 kg player hitting another player (a 100 kg player is not putting full force of weight onto the other other player unless jumping on his chest). Running into another player at full sprint (? 15 mph max even at full sprint) is not the same as a 90 mph fast ball to an unprotected chest (most of the weight of the running player is transferred to the ground, not the opponent).
[EDIT: the transfer of energy in such collisions is far more complex than my oversimplified explanation. Elastic versus inelastic collisions differ, and there are other factors like rotational energy, center of gravity, rigidity of one or both of the masses involved in the collision, surface area of distribution for area of impact, etc. to assess the amount of E that is actually transmitted at point of impact versus lost /dissipated in other forms.]
In football, Commotio Cordis is documented with helmet to left chest, not with shoulder pads to chest. Shoulder pads are well designed to absorb the shock of the shoulder’s force onto the opposing player. This is well documented and described.
We don’t have to be equivocal and say it probably wasn’t Commotio Cordis. I can say with 100% scientific and clinical confidence that such a scenario (right shoulder pad hitting left precordium as I saw on multiple replays) is virtually impossible and cannot be deduced conclusively the night of the incident. This has never before occurred in 103 years of NFL.
More on Commotio Cordis.
3. Age of Commotio Cordis
Yes, it usually occurs in those < 20 yo. However, this could simply be because there are FAR more high school and college players than pro players. For example, there are about one million high school football players in the US., 71,000 college football players, and 1,700 NFL players.
The age itself doesn’t prove or disprove Commotio Cordis. Pro sports also have more sophisticated and higher quality protective equipment.
3. Common causes of cardiac arrest and sudden cardiac death in athletes
Yes, it is true that athletes are rigorously screened. Pro athletes are even more thoroughly screened. However, this screening usually entails EKG and perhaps echocardiogram. One of the most common causes of cardiac arrest is HCM (Hypertrophic cardiomyopathy). HCM would have already been identified during screening.
However, screening usually stops there (EKG, echo, maybe treadmill stress test).
Other causes sudden cardiac death in athletes that can be missed during “rigorous” routine screening for athletes:
* Electrical channelopathies (likely requires genetic testing and other testing)
* Anomalous coronary artery (requires cardiac CTA)
* CPVT (difficult to prove in screening, usually diagnosed in retrospect, requires provocative testing). CPVT is catecholinergic polymorphic ventricular tachycardia.
* Aortopathy (would require a CT aortogram, which is not part of routine screening)
* Acquired long QT syndrome (will not always appear on screening EKG, depends upon timing of new QT prolongation and preceding toxic insult)
* Coronary artery dissection from toxic insult, hormones, or vasculitis. Cannot screen for this in advance
* Also, cannot overlook substance abuse
More on sudden death in athletes.
4. Being ventilated after cardiac arrest
After cardiac arrest, it is normal (standard of care) to have the patient ventilated “to protect the airway”. This does not prove patient is “not breathing on his own”. Vigorous CPR can lead to rib fracture and difficulty breathing. Because the patient is “unresponsive” (no purposeful response to stimuli) after cardiac arrest, the patient is intubated and on mechanical ventilation.
According to family, patient was in prone position (due to lung injury) and initial ventilator settings have now decreased from 100% to 50%. There is no such thing has 50% dependence on mechanical ventilation, so this is probably referring to FiO2 (Oxygen requirement) decreasing from 100% to 50%. During CPR, aspiration is possible (regurgitating stomach contents and inhaling them into respiratory tract). Aspiration pneumonitis can cause initial high FiO2 requirements that quickly improves.
Vigorous CPR can also cause rib fracture and pneumothorax. However, this would require chest tube placement and thus far there are zero reports from family indicating chest tubes.
All we know as of today is patient is sedated and on a mechanical ventilator and the ventilator settings are improving.
5. Anoxic brain injury
After cardiac arrest, it is common for there to be cerebral edema and transient neurological deficit (no purposeful neurological response). Therefore, the standard of care is medically induced hypothermia (cooling blankets or cooling catheters to drop the body temperature). Cooling and subsequent rewarming can take 24–48 hours. During this time zero conclusions can be made about anoxic brain injury. Anoxic brain injury would be evaluated >24 hours after rewarming is complete and all sedation is discontinued. If there is no purposeful meaningful response then brain MRI would be performed (possible some other studies) to assess for anoxic brain injury.
At present we cannot conclude anoxic brain injury nor can we conclude favorable recovery. It’s too soon to know with certainty.
In 2019: I had a 50+ yo patient with late presenting (>12 hours) anterior STEMI (heart attack involving 100% block of LAD which is the “widow maker”). Patient had VTach in the field and then again on the Cath table. In total, we performed CPR for 53 minutes and patient received 33 shocks during my LAD PCI (opening the artery and placing a stent). Patient received hypothermia protocol after the LAD PCI was complete. Patient walked out of the hospital one week later with zero neurological deficit. The key to survival without neurological deficit is immediate high quality CPR (survival without neurological deficit decreases by 10% each minute that CPR is delayed).
6. Subclinical myocarditis
I have searched extensively on this topic for 2 years (for my vaccine associated myocarditis articles on Medium). There are zero published data to prove subclinical myocarditis increases the risk of future cardiac arrest and sudden cardiac death.
Previously, the gold standard for myocarditis was biopsy. With the advent of cardiac MRI and improved diagnostic protocols as well as screening MRI for surveillance in research trials, Cardiac MRI became the de facto gold standard for diagnosing myocarditis. Subclinical myocarditis is a phenomenon diagnosed on Cardiac MRI during routine surveillance in the absence of symptoms. However, I have not found any research that correlates subclinical myocarditis and future risk of cardiac arrest.
Elevated troponin alone does not equate to a diagnosis of myocarditis. Recently there are several post vaccine studies that identified elevated high sensitivity troponin (but below the diagnostic threshold for myocarditis) without corroborating cardiac MRI. Many have concluded this is “proof” of vaccine associated myocarditis. Troponin elevation (especially high sensitivity troponin) in the absence of cardiac MRI does not prove subclinical or clinical myocarditis.
Troponin does indicate myocardial injury. True. However, injury is not the same as inflammation. Other cause of mild elevated high sensitivity troponin in an asymptomatic patient during screening / surveillance in a research trial:
A. False positive (subsequent regular troponin is normal even though high sensitivity troponin is elevated)
I see this monthly. Outside hospital uses HS-trop which is mildly elevated and transferred to us for further cardiac evaluation. Our lab troponin (not high sensitivity) is completely normal (as is EKG, echo, and nuclear stress test).
There are more false positives for HS-troponin thad traditional troponin.
Other causes of elevated HS troponin:
* Microvascular disease
This could be from atherosclerosis, hypertension, autoimmune disease, vasculitis, or idiopathic.
* Demand ischemia (tachycardia or stress)
* Rigorous athletic training (marathon, excessive endurance sports)
* Chest wall trauma (motor vehicle accident)
* Rhabdomyolysis
More detailed discussion and references on my previous analysis of subclinical myocarditis here.
This does not mean I am clinically and morally dismissive of elevated troponin after vaccination. It may in fact be of grave and significant long term concern. I’m simply stating that we do not yet have any proof of clinical prognostic interpretation of subclinical myocarditis.
If you find any published scientific paper that proves otherwise (that subclinical myocarditis is linked to future risk of cardiac arrest), please share it and I happy to be corrected.
7. LGE on CMR
Late Gadolinium Enhancement (LGE) on cardiac MRI (CMR) does not prove “scar”. LGE can occur from edema, inflammation, or scar / fibrosis. LGE in the acute phase of myocarditis does NOT prove scar later. If follow-up CMR is normal, one cannot assert scar. Scar is of clinical significance because myocardial scar has been proven to be associated with subsequent increased risk of fatal ventricular arrhythmias.
LGE can be false positive (depending upon location) in adaptive athletic conditioning (athlete’s heart) whereby there are areas of hypertrophy from high intensity athletic training. This was well documented in the COVID myocarditis MRI studies that were conducted in college athletes (to distinguish from true COVID myocarditis).
LGE without symptoms (subclinical myocarditis) has indeterminate clinical significance. We truly do not have any data to assess the long term clinical implications.
More on LGE on CMR here.
8. Myocarditis prognosis
Most of the studies we have on this are pre-COVID (in the context of traditional viral myocarditis or autoimmune myocarditis). We can only extrapolate that to vaccine asociated myocarditis.
There is an increased risk of sudden cardiac death with aerobic activity (competitive sports) for 6 months after myocarditis (hence the activity restriction). This is why current professional society guidelines recommend restriction from competitive sports for 6 months after myocarditis diagnosis.
However, the risk of death and need for transplant can persist for 12 years.
If myocarditis degenerates into dilated cardiomyopathy, the prognosis is poor (27% 5-year mortality). If heart function is normal (no abnormalities on echocardiogram) and LGE on CMR is fully resolved, then the prognosis can be favorable, but we truly don’t know (especially with repeated boosters). I have several patients with cardiomyopathy after vaccine associated myocarditis with heart function not improving on echocardiogram despite maximally tolerated optimum medical management for many months. Long term prognosis is guarded.
I’ve covered much of that previously (myocarditis after COVID vaccination and potential prognosis).
9. Undiagnosed myocarditis
Rather than subclinical myocarditis, the greater concern is undiagnosed clinical myocarditis. Many people (especially children and young adults) have vague atypical symptoms without classic chest pain. Simone Scott (college student) died from complications of myocarditis soon after her COVID vaccination: her diagnosis was missed for a few weeks because campus health physicians dismissed her ‘flu-like’ symptoms and did not initially suspect myocarditis.
I see many patients 4–8 weeks after their initial symptoms which may have been post vaccine myocarditis. The PCP and / or ER physician all missed the possibility of myocarditis. Delayed or missed diagnosis of myocarditis is very very common and of grave concern.
10. Definitive diagnosis of Vaccine Associated Myocarditis
Unfortunately, the definitive diagnosis is only made with biopsy on autopsy (for spike protein). As we know, this is rarely done and few labs / pathologists in then country are performing the appropriate tests. Most families and coroners and physicians (who sign death certificate) are not requesting / demanding this. We know that spike protein is directly toxic to endothelium and myocardium. Spike protein also can cause autoimmune disease also leading to endothelium dysfunction and myocardial damage.
Temporal association of clinical myocarditis (diagnosed on cardiac MRI in a person with symptoms of myocarditis) after vaccination is strongly suggestive if other causes have been ruled out. However, we don’t know what timeframe to use to establish an association. Most current studies use 21 or 28 days as cutoff. However, spike protein persists for at least 4 months on some studies, so there is no scientific reason to believe that 21 or 28 days is an appropriate cutoff for temporal association. I have many young and middle aged patients with unexpected cardiac complications whose only risk factor is being fully vaccinated (>6 months ago). I have no way to prove this yet but I suspect even 6–18 months may be reasonable temporal association for post vaccine complications (and proven with later research).
Vaccine associated myocarditis occurs with far greater incidence than CDC estimates (3–4x more than CDC estimates) as demonstrated on repeated international studies. Prognosis is also far worse than CDC estimates (many are lost to follow-up, many still have activity restrictions and have not returned to normal 3–6 months later). Those who are lost to follow-up (>40%) may have died and CDC is not releasing autopsy reports nor explaining how someone can be “lost to follow-up” in a situation where VASERS report requires CDC to follow-up on outcomes. Vaccine associated myocarditis studies by definition exclude those who may have “suddenly died” and not reached the hospital. A recent autopsy study from Germany indicates 4 of 25 (16%) of those who “died suddenly” within 20 days of recent vaccination had myocarditis from the vaccination (with other causes of death ruled out).
For now, we cannot say with certainty whether Damar Hamlin suffered from post vaccine myocarditis leading to his cardiac arrest. However, the complete media silence (as well as many social media physician ‘experts) on this possibility is deeply disturbing. The rush to summarily explain this tragic incident with Commotio Cordis is scientifically unfounded. All possibilities must be thoroughly and objectively evaluated.
More on myocarditis after COVID vaccination and CDC’s poor follow-up data.
The situation is still rapidly evolving. It’s best to not jump to definitive conclusions. More to come.
