Week 13

Death by Sports
Sudden death in athletes has been a  tragic occurrence in the field of sports medicine,
cardiology, primary care , and pediatrics. By far, the most common cause of unexpected death
for a younger athlete on the competitive  field is cardiac illness, usually that of congenital
etiology. However the use of anabolic steroids, peptide hormones, and stimulants has led to the
emergence of acquired  heart disease in younger and middle -aged athletes. In contrast,
sudden death in an older athlete is typically due to atherosclerotic coronary artery disease.
Sudden cardiac death (SCD) is a sudden unexpected and rapid natural death due to cardiac
disease, occurring within 1h from the onset of symptoms such as chest pain, in individuals
without any prior condition that appears fatal (Yeda Wu, et.al.,The forensic pathological analysis
of sport-related sudden cardiac death in Southern China;Forensic Science Research,2020).
There are so many triggers, which can cause SCD, such as physical activity, mental stimulation,
over eating, etc. As for physical activity, it is well accepted that regular physical activities play a
positive role in health, especially the cardiovascular system. On the contrary, physical
exertion,including intensive exercise and heavy physical activity, is associated with cardiac
fatigue and increases the risk of SCD (Leischik R. Spelsberg, et al. Exercise Induced arterial
hypertension,2014)
There are a variety of congenital heart illnesses that occur in the general population. Most of
them are categorized into structural and non-structural varieties. Congenital structural heart
disease will generally affect blood flow within the heart and flow from the heart. Examples
include hypertrophic obstructive cardiomyopathy (HOCM), arrhythmogenic right ventricular
dysplasia (ARVD)  and coronary artery anomalies. Non structural  heart disease involves
defects in the electrical system of the heart, which may induce unstable and dangerous
arrhythmias (e.g., long QT syndrome, Brugada Syndrome, Wolf-Parkinson-White Syndrome,
and catecholaminergic polymorphic ventricular tachycardia). Anabolic steroids  and peptide
hormones induce structural changes in the heart. Stimulants can cause dangerous arrhythmias.
These conditions can clinically manifest as syncope/presyncope, and in some instances, can
present as sudden unexpected death. The associated morta existing lity underscores  the
importance of early screening and identification of heart disease in athletes. Many athletes with
pre existing heart disease are often asymptomatic, with a cardiac arrest being the first
manifestation of underlying pathology. The challenging aspect of identifying affected athletes is
adequately screening the general population without excessive  and unnecessary invasive
testing. A thorough physical examination, including assessment of personal history, physical
exam and an electrocardiogram, can be useful screening tool in asymptomatic and low-risk
athletes. Higher-risk athletes, such as those who have abnormal findings or have symptoms,
may require more extensive testing.
Etiology
Cardiac etiologies
Structural Abnormalities:
a. Hypertrophic Obstructive Cardiomyopathy (HOCM)
b. Dilated cardiomyopathy
c. Coronary artery anomaly
 d. Left ventricular  hypertrophy
e. Atherosclerotic coronary artery disease
f. Left ventricular noncompaction
g. Arrhythmogenic right ventricular dysplasia
h. Aortopathy
i. Congenital aortic stenosis
j. Mitral valve prolapse  
Structurally Normal Heart:
a. Wolf-Parkinson-White syndrome
b. Congenital long QTsyndrome
c. Acquired long QT syndrome
d. Brugada syndrome
e. Atrioventricular blocks
f. Catecholaminergic polymorphic ventricular tachycardia
g. Short QT syndrome

Other:
a. Stimulant use
b. Anabolic steroid use
c. Commotio cordis
d. Aortic rupture
e. Myocarditis
Differential Diagnosis
The evaluation of sudden death in athletes must include non cardiac etiologies. 
a. Blunt trauma
b. Drowning (sports dependent)
c. Heatstroke
d. Dehydration
Given that syncope in athletes is a key alarming symptom, other probable etiologies should be
considered in evaluating  syncope.
a. Vasovagal events will be common cause of syncope in both the general population and
athletes
b. Heatstroke
c. Dehydration
d. Anorexia in female athletes and associated electrolyte abnormalities
e. Anemia
f. Seizures
g. Hyponatremia
Pathophysiology
The function of the heart is to effectively pump blood throughout the body, hence disturbing the
blood flow and/or the  rhythm of the heartbeats negatively impacts the heart’s functional goals.
Structural defects prevent the heart from effectively pumping blood, especially during times of
increased demand. Ion channel defects disturb the regularity  of necessary electrolytes, which
maintain the heart’s rate and rhythm. Consequently, untreated, structural defects can result in
arrhythmia, while persistent arrhythmia may lead to structural heart changes. An example is
dilated cardiomyopathy which can develop due to an excessive premature ventricular
contraction (PVC) burden.
Normal Physiologic Findings on ECGs
Athletes may have findings on their ECG that would otherwise be considered abnormal in the
general population. Sinus bradycardia (under 60 beats per minute) is among the common
benign abnormal ECG findings, but very low heart rates should not be ignored. Infrequent PVCs
and premature atrial contractions (PACs) are also considered normal among physically active
people. However, specific findings on ECGs considered normal among athletes but abnormal in
the general populations include:
a. Left ventricular hypertrophy (QRS voltage criteria)
b. Right ventricular hypertrophy (QRS voltage criteria)
c. Sinus arrhythmia
d. Early repolarization
e. First-degree atrioventricular block
Physiologic versus Pathologic Left Ventricular Hypertrophy
Left ventricular hypertrophy is a common occurrence among athletes. A mild to moderate
degree of hypertrophy occurs as a natural response to exercise, particularly endurance-based
and isometric exercise. Large level of hypertrophy are generally noted to be pathological and
are known to be induced either genetically and/or as a result of anabolic steroid or peptide
hormone use. One differentiating factor between physiological and pathological left ventricular
hypertrophy is the wall thickness itself. On an echocardiogram, a normal ventricle will be 6 mm
to 11 mm. Under  13 mm is generally not considered to be hypertrophic from a clinical
perspective, although 11 mm to 13 mm is borderline thickened. Over 16 to 18 mm is considered
significantly enlarged and crosses over into the territory of hypertrophic obstructive
cardiomyopathy.
The grey area of  13 mm to 16 mm requires clinical evaluation to differentiate between
physiological adaptations to exercise and cardiomyopathy.