This is the second UG Guest Blog from Dr. Jon Lucas, MD.
Preventing Combat Sport Deaths
The tragic death of a fighter is always accompanied by questions of “what could have been done to prevent this.” There has been a lot of discussion recently in the mixed martial arts community about the best way to protect fighters from brain injury and reduce the risk of death from brain trauma during a fight. However, head trauma is not the only risk that athletes face during competition, as sudden deaths also occur in non-combat sports such as basketball and marathon running. The death of an amateur fighter in an unregulated event in Michigan in April of 2013 ruled to be secondary to a cardiac arrhythmic disorder illustrates the risk of non-head trauma related death. This article will discuss some of the cardiac causes of sudden death in athletes and strategies for preventing these tragedies.
Cardiac abnormalities that predispose to sudden death during exertion can be thought of in three broad categories:
•Structural abnormalities; and,
First we will briefly discuss some examples of these cardiac abnormalities, and then discuss prevention strategies.
The conduction system within the heart carries the electrical impulse to the heart muscle cells and causes them to contract, creating the heartbeat. Electrical abnormalities are differences in this conduction system. Examples of electrical abnormalities include arrhythmias and abnormalities of conduction. Ventricular tachycardia and ventricular fibrillation are two arrhythmic causes of cardiac death. Conduction abnormalities include Wolff-Parkinson-White, long QT syndrome, and Brugada syndrome.
Ventricular tachycardia occurs when the bottom chambers of the heart (ventricles) begin beating on their own without the usual control from the normal conduction system. Ventricular fibrillation is when the muscle cells in the ventricles contract erratically without the heart squeezing effectively. Wolff-Parkinson-White syndrome is a second, abnormal electrical connection between the top and bottom chambers of the heart that can allow a “short circuit” causing the heart to race (supraventricular tachycardia), or allow the ventricles to race in response to an atrial (top chambers of the heart) arrhythmia. Long QT and Brugada syndromes are abnormalities of the ion channels within the cardiac muscle cells, leading to an increased risk of dangerous arrhythmias.
Structural abnormalities that increase the risk for sudden cardiac death include coronary artery abnormalities, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, obstructive lesions, coronary artery disease, and aortic arch abnormalities. The coronary arteries are small blood vessels that supply the heart muscle. Changes in these arteries from prior insults such as Kawasaki disease, narrowing from cholesterol related coronary artery disease, or abnormal courses of the arteries into the heart muscle can all lead to a sudden death during exertion secondary to insufficient blood supply to the cardiac muscle. Hypertrophic cardiomyopathy is an abnormality of the heart muscle that leads to significant thickening of the cardiac muscle and predisposes to restriction of the amount of blood the heart can pump during exercise. Arrhythmogenic right ventricular cardiomyopathy causes changes in the heart muscle on the right side of the heart, and increases the likelihood of dangerous arrhythmias. Obstructive lesions include any conditions that restrict the pumping of blood from the heart. A typical example is aortic valve stenosis. Aortic arch abnormalities predispose to sudden death by allowing enlargement of the vessel which leads to an increased risk for rupture during exertion. This can occur secondary to an abnormality of the wall of the vessel, as occurs in Marfan syndrome, or as the result of abnormal forces on the aortic walls from a valve abnormality or high blood pressure.
Situational occurrences include myocarditis, and commotio cordis. Myocarditis is an inflammation of the heart muscle that can occur after certain viral illnesses, which increases the likelihood of a dangerous arrhythmia occurring. Commotio cordis occurs when a sharp blow to the chest causes a ventricular arrhythmia. Commotio cordis is more frequently associated with getting hit by hard objects such as baseballs, lacrosse balls or hockey pucks (as happened to Chris Pronger for the Saint Louis Blues during the 1998 playoffs), but there have been examples in combat sports such as this case at a karate tournament:
What Can Be Done?
There is not currently a wide consensus amongst experts as to how best screen athletes for these conditions prior to participation in sports. Some of the conditions create findings likely to be detected by screening physical examinations, such as murmurs from obstructive lesions or physical features of Marfan syndrome, but the majority of the conditions would not be evident on a physical examination and would require further studies to be detected. A ECG would likely be abnormal in patients with hypertrophic cardiomyopathy, long QT syndrome and Brugada syndrome; but there is a significant false positive rate (ECG is abnormal when patient does not have the condition) when trying to detect myocardial hypertrophy by ECG in athletes, and patients with long QT syndrome and Brugada syndrome can have normal resting ECGs at times. Patients with episodes of ventricular arrhythmias are likely to have a normal resting ECG unless they happen to have an episode of arrhythmia at the time the study is performed. An echocardiogram (ultrasound of the heart) would detect hypertrophic cardiomyopathy, congenital heart disease, obstructive lesions, aortic arch abnormalities, and in expert hands can often detect abnormalities in coronary artery origins.
Unfortunately, even with a normal physical examination, ECG and echocardiogram, there is still a risk for sudden cardiac death due to situational occurrences, abnormalities that could progress after their screening such as hypertrophic cardiomyopathy, and abnormalities that are difficult to detect on screenings such as arrhythymogenic right ventricular cardiomyopathy and coronary artery abnormalities. Many of these cardiac abnormalities are genetic, so there may be warning signs in the fighters family history.
Currently, the most commonly employed screening process is a tiered approach:
•A family history should be obtained that asks about any sudden cardiac deaths, in particular in patients who were less than 50 years of age. In addition, a relative with congenital deafness, seizure disorder, or an unexplained single car accident or drowning should be noted.
•The fighter should be asked if they have ever passed out, had bouts of unexplained dizziness, palpitations, shortness of breath, exercise intolerance or chest pain.
•A thorough cardiac examination should be performed, including blood pressure measurement, palpation of pulses in arms and legs, and cardiac auscultation. If there are any concerning findings on family history, physical examination or the fighters history, then further evaluation of those findings should be performed before the fighter is cleared to compete.
•Some commissions require fighters to have an ECG performed prior to obtaining a license. While I believe that this is a reasonable requirement, there is not currently widespread agreement amongst experts that an ECG should be part of pre-participation physical examinations.
As mentioned above, despite even the most thorough screening evaluations, there remains a risk for sudden cardiac death during a fight. Therefore, it is vital that a medical team including a physician and paramedic trained in ACLS are present during all mixed martial arts events. Since arrhythmia is the final common pathway for the majority of the causes of sudden cardiac death, there should also be a defibrillator or AED available at cageside, as required by most athletic commissions. With proper precautions, the risk of sudden cardiac death can be lowered, but at this time it cannot be completely eliminated.
If you are interested in more details about sudden cardiac death and pre-participation screening, I recommend reading the following articles:
Recommendations of the 36th Bethesda Conference: (J Am Coll Cardiol, 2005; 45:1322-1326)
“Sudden Death in Young Competitive Athletes. Clinical demographic, and pathological profiles” Maron, BJ et al, JAMA, Vol. 276, No. 3, July 17, 1996 (Abstract available through link, full content requires purchase.
I will also be happy to discuss this issue further in the Underground Forum.