European Heart Journal (2021) 00, 1–4
doi:10.1093/eurheartj/ehab440
Global Spotlights
Screening professional athletes for
cardiovascular diseases at risk of cardiac arrest
1,
Domenico Corrado *, Antonio Pelliccia2, Cristina Basso
Alessandro Zorzi 1
1
Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padova, Via Giustiniani, 2, Padova 35121, Italy; and 2Institute of Sport Medicine and
Science, Largo Piero Gabrielli, 1, Rome 00197, Italy
There was a moment of real panic during the Denmark’s opening Euro
2020 match with Finland, when the professional soccer player
Christian Eriksen suddenly collapsed with the loss of consciousness
due to a cardiac arrest (CA) (Figure 1A). The anxiety for the life of the
athlete lasted a short time because he recovered his cardiovascular
function a few minutes later, thanks to the efficacy of the manoeuvres
of cardiopulmonary resuscitation including the use of the automated
external defibrillator (AED) (Figure 1B). Although the identification of
the cause of the CA is still under clinical investigation, the mechanism
was clearly ‘arrhythmic’ in nature, i.e. an episode of ventricular tachy-
cardia or ventricular fibrillation leading to the sudden interruption of
cardiac pump with the block of circulation and cerebral perfusion. The
miraculous resuscitation with the recovery of cardiac function and
consciousness of the athlete was the result of early defibrillation of the
potentially lethal arrhythmia that was triggered by sports activity and
would have been fatal without the shock therapy delivered by the
AED.
This episode of aborted sudden death (SD) brings back the memory
to the past tragic events of professional soccer players, such as Marc
Vivian Foe, Antonio Puerta, and Pier Mario Morosini who experienced
CA in the pitch, rapidly and inexorably evolving to death because of
unsuccessful treatment. The story of Eriksen is emblematic of the
extraordinary advances in the last years of the management of CA
occurring during sports activity, mostly due to the availability of in-the-
field AED. For this reason, we are really enthusiastic to entitle this
CardioPulse piece ‘Screening professional athletes for cardiovascular
diseases at risk of cardiac arrest’ (rather than sudden death): indeed, the
increasingly consistent evidence that early electric shock is life-saving
makes the use of the terms ‘cardiac arrest’ and ‘sudden death’ in the
athlete fortunately no longer interchangeable, being CA a successfully
treatable event.1
The Eriksen’s case has revived the interest of media and medical
community on the reason why healthy professional athletes can
* Corresponding author. Tel: þ39 0498212458, Fax: þ39 0498212309, Email: domenico.corrado@unipd.it
C The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.
Published on behalf of the European Society of Cardiology. All rights reserved. V
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1
, and
unexpectedly experience CA during sports activity and what preven-
tion strategy might have avoided such a dramatic event. Relevant ques-
tions are: may some causes of CA in top level athletes remain clinically
concealed? and is cardiovascular screening before participation in sports of
limited efficacy for identification of athletes with at-risk cardiovascular
disorders?
‘Competitive athletes’ are individuals who are engaged in exercise
training on a regular basis and participate in official sports competition;
a subgroup is the ‘professional athletes’. Several studies demonstrated
that atherosclerotic coronary artery disease is the most common con-
dition responsible of CA/SD in middle-aged and senior athletes, while
younger (<35 years) competitive athletes have a wide range of cardio-
vascular causes including congenital and inherited disorders.2
The most prevalent causes of CA in young competitive athletes are
genetic heart muscle diseases, such as hypertrophic cardiomyopathy
and arrhythmogenic right ventricular cardiomyopathy, followed by
congenital anomalies of coronary arteries, aortic rupture in Marfan’s
syndrome, myocarditis (either acute myocardial inflammation or post-
inflammatory myocardial scar), and valvular diseases, including aortic
valve stenosis and mitral valve prolapse. A sizeable proportion of ath-
letes experiencing CA/SD has no evidence of structural heart disease
and the cause of their CA is related to primary electrical cardiac condi-
tions, namely inherited cardiac ion-channel defects (channelopathies)
including long QT syndrome, catecholaminergic polymorphic ventricu-
lar tachycardia, and Brugada syndrome.
Preparticipation screening evaluation offers the potential to identify
asymptomatic athletes who have potentially lethal cardiovascular
abnormalities and, then, to protect them from the risk of sport-related
CA/SD.3,4 The target athletic population and the screening protocol
vary among European and extra-European countries. Screening by his-
tory and physical examination only, which is recommended in the
USA, has limited sensitivity to identify athletes at risk because most
individuals with undetected cardiovascular diseases are asymptomatic
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Figure 1 The Denmark player Christian Eriksen collapsed on the pitch because of a cardiac arrest just before half-time in the Euro 2020 match
between Denmark and Finland (A). Although his heart stopped working, thanks to life-saving cardiopulmonary resuscitation including external defib-
rillations he was awake when left the stadium (B). By courtesy of ilgazzettino.it.

and CA/SD most often represent the first clinical manifestation. The
long-running Italian experience showed that adding an ECG definitively
improves the screening sensitivity and substantially reduces the risk of
fatalities among competitive athletes.5,6 The screening protocol of
Italian professional athletes, in addition to history, physical examination,
and basal ECG, includes by law annual maximal exercise testing and
biannual echocardiogram. Additional tests such as Holter monitoring,
cardiac MRI, or coronary CT scan, are requested for selected athletes
who had positive findings at the initial evaluation. Athletes diagnosed
with clinically relevant cardiovascular diseases are managed according
to currently available guidelines. Of note, in Italy, preparticipation
screening is repeated on a regular basis every year in non-professional
athletes and every 6 months in professional athletes.
A time-trend analysis of the incidence of SD in young competitive ath-
letes in the Veneto region of Italy over 26 years (1979–2004) showed
a decline of mortality by 90% after the introduction of the nationwide
screening program.7 Most importantly, the study demonstrated that
the mortality reduction was a reflection of a lower incidence of SD
from ECG detectable cardiomyopathies and channelopathies. Up to
two-third of at-risk cardiovascular diseases are diagnosed by virtue of
serial (annual) screening that intercepts genetic cardiomyopathies with
a late-onset phenotypic expression or newly acquired heart muscle
disease.8
It is noteworthy, however, that no screening strategy is able to
identify all athletes at the risk of CA/SD (Figure 2). Acute myocardi-
tis may occur unpredictably and some cardiac conditions such as
atherosclerotic coronary artery disease and congenital anomalies of
coronary arteries usually are asymptomatic and non-associated with
abnormalities on basal 12-lead ECG.3–4 According to the ESC
guidelines, asymptomatic middle-age/senior athletes, in whom the
most common cause of SD is coronary artery disease, before
engaging in a vigorous physical activity should be evaluated using
the ESC risk score systems and then by exercise testing and/or
coronary CT, which are reserved to those with a high or very high
estimated cardiovascular risk.9
Recent clinical and pathological studies have demonstrated that a
non-ischaemic left ventricular myocardial scar may be a not so uncom-
mon and clinically concealed substrate of life-threatening arrhythmias
in the athlete.10 This myocardial lesion may be caused by a variety of
myocardial diseases, including myocarditis, sarcoidosis, and genetic car-
diomyopathies. Although non-ischaemic left ventricular scar is a poten-
tial source of effort-induced ventricular arrhythmias detectable by
exercise testing and/or Holter monitoring, the diagnostic power of
standard ECG is limited because suspicious abnormalities such as low
QRS voltages in limb leads and T-wave inversion in lateral leads are
found in a minority of affected patients. Moreover, the segmental
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Figure 2 Efficacy of preparticipation screening, diagnostic tests, and prevalence of cardiovascular diseases at risk of cardiac arrest/sudden death in
professional athletes. The dotted red arrow denotes the decreasing efficacy of preparticipation screening of professional athletes in relation to the
increasing complexity of diagnostic tests required for identification of at-risk diseases. The routine screening protocol (medical history, physical
examination, basal electrocardiogram, echocardiogram, and exercise testing) provides a good sensitivity for the identification of most prevalent con-
ditions associated with the risk of cardiac arrest/sudden death in young professional athletes, such as cardiomyopathies, channelopathies, Wolff–
Parkinson–White syndrome and mitral valve prolapse. The screening shows a lower diagnostic yield for less prevalent causes of cardiac arrest/sudden
death, i.e. non-ischemic left ventricular scar, coronary artery disease, congenital coronary anomalies, acute myocarditis, and idiopathic ventricular
fibrillation, whose detection needs advanced imaging examinations (cardiac magnetic resonance and coronary computed tomography angiography)
or invasive tests (endomyocardial biopsy and electrophysiologic study). The importance of in-the-field automated external defibrillator increases for
treating unexpected arrhythmic cardiac arrest due to cardiac diseases more difficult to identify by preparticipation screening. Generally, genetic char-
acterization by molecular testing is indicated in the presence of a disease overt phenotype. AED, automated external defibrillator; Brugada, Brugada
syndrome; CA, cardiac arrest; CAD, coronary artery disease; CCA, congenital coronary anomaly; CMR, cardiac magnetic resonance; CCTA, coro-
nary computed tomography angiography; CPVT, catecholaminergic polymorphic ventricular tachycardia; ECG, electrocardiogram; ECHO, echocar-
diography; EMB, endomyocardial biopsy; EPS, electrophysiologic study; ET, exercise testing; HCM, hypertrophic cardiomyopathy; Hx&PE, medical
history and physical examination; LQTS, long QT syndrome; MVP, mitral valve prolapse; NILVS, non-ischemic left ventricular scar; SD, sudden death;
VF, ventricular fibrillation; WPW, Wolff–Parkinson–White syndrome.

nature of the left ventricular myocardial scar involving the epicardial-
midmyocardial wall layers, but sparing the subendocardium which
most contributes to myocardial thickening, explains why it is usually
missed by echocardiography and only evidenced as late gadolinium
enhancement on cardiac magnetic resonance.10 The difficulty to iden-
tify affected athletes by routine preparticipation ECG screening makes
this condition one of most challenging and unpredictable causes of
CA/SD during sports, as shown by the fatal event of the Italian profes-
sional soccer player Pier Mario Morosini in 2012.
To conclude, the best strategy to fight SD during sports is to synerg-
istically combine primary prevention by preparticipation identification of
athletes with at-risk cardiovascular diseases and secondary prevention by
the availability of on-site AED which provides life-saving early defibrilla-
tion in case of unpredictable arrhythmic CA, like that experienced by
Christian Eriksen.
Conflict of interest: none declared.
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