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Myocarditis is an important cause of arrhythmias and sudden cardiac death (SCD) in both physically active individuals and athletes. Elite athletes seem to have an increased risk for viral infection and subsequent myocarditis due to increased exposure to pathogens (worldwide traveling/international competition) or impaired immune system (continuing training during infections/resuming training early thereafter, strenuous exercise training or competition, and exercising in extreme weather conditions). Initial clinical presentation is variable, but athletes characteristically express non-specific symptoms of fatigue, muscle soreness, increased heart rate at rest, as well as during exercise and reduced overall exercise capacity. Beyond resting electrocardiogram (ECG), cardiac biomarkers, echocardiography, and 24-hour Holter ECG, diagnostic work-up should include cardiac magnetic resonance imaging (CMR) assessing inflammation, oedema, and fibrosis by late gadolinium enhancement (LGE), respectively, as these measures are crucial for prognosis and sports eligibility. For patients with insufficient cardiac recovery, endomyocardial biopsy is recommended to clarify differential diagnoses and initiate specific treatment options. In uncomplicated cases with normal left ventricular function during acute phase and absent LGE, eligibility for sports can be attested to three months after clinical recovery. In those with persistent pathological findings, even after six months, the risk for SCD remains increased and resuming exercise beyond recreational activities can only be recommended individually based on course of disease, left ventricular function, arrhythmias, pattern of LGE in CMR, as well as intensity and volume of exercise performed during training and competition. For all athletes, follow-up examination should be performed yearly.
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Myocarditis in athletes: A clinical
Martin Halle
, Leonhard Binzenho
, Heiko Mahrholdt
Michael Johannes Schindler
, Katrin Esefeld
Carsten Tscho
Myocarditis is an important cause of arrhythmias and sudden cardiac death (SCD) in both physically active individuals and
athletes. Elite athletes seem to have an increased risk for viral infection and subsequent myocarditis due to increased
exposure to pathogens (worldwide traveling/international competition) or impaired immune system (continuing training
during infections/resuming training early thereafter, strenuous exercise training or competition, and exercising in
extreme weather conditions). Initial clinical presentation is variable, but athletes characteristically express non-specific
symptoms of fatigue, muscle soreness, increased heart rate at rest, as well as during exercise and reduced overall
exercise capacity. Beyond resting electrocardiogram (ECG), cardiac biomarkers, echocardiography, and 24-hour
Holter ECG, diagnostic work-up should include cardiac magnetic resonance imaging (CMR) assessing inflammation,
oedema, and fibrosis by late gadolinium enhancement (LGE), respectively, as these measures are crucial for prognosis
and sports eligibility. For patients with insufficient cardiac recovery, endomyocardial biopsy is recommended to clarify
differential diagnoses and initiate specific treatment options. In uncomplicated cases with normal left ventricular function
during acute phase and absent LGE, eligibility for sports can be attested to three months after clinical recovery. In those
with persistent pathological findings, even after six months, the risk for SCD remains increased and resuming exercise
beyond recreational activities can only be recommended individually based on course of disease, left ventricular function,
arrhythmias, pattern of LGE in CMR, as well as intensity and volume of exercise performed during training and com-
petition. For all athletes, follow-up examination should be performed yearly.
Myocarditis, exercise, physical activity, return to play, sports eligibility
Received 8 December 2019; accepted 8 February 2020
Myocarditis is considered to be one of the most
common acquired causes of arrhythmias, myocardial
dysfunction, heart failure, and sudden cardiac death
(SCD) in young, otherwise healthy individuals.
Recommendations for preventative measures, as well
as advice for resuming physical activity and sports
after myocarditis, include assessment of exercise inten-
sity, establishing a stepwise training schedule, and
recommendations for eligibility in competitive sports.
These measures have only been discussed briefly in pre-
vious European and American recommendations.
Therefore, the aim of this clinical perspective is to sum-
marize the existing knowledge of exercise in the devel-
opment of acute myocarditis, and to extend the
Department of Preventive Sports Medicine and Sports Cardiology,
Technical University of Munich, Germany
DZHK (German Centre for Cardiovascular Research), partner site
Munich Heart Alliance, Germany
Department of Cardiology, Robert Bosch Medical Center, Stuttgart,
Department of Cardiology, Campus Virchow (CVK), Charite
¨tsmedizin Berlin, Germany
DZHK (German Centre for Cardiovascular Research), partner site
Berlin, Germany
Berlin Institute of Health/Center for Regenerative Therapy (BCRT),
Corresponding author:
Martin Halle, Department of Preventive Sports Medicine and Sports
Cardiology, School of Medicine, University Hospital Klinikum rechts der
Isar, Technical University of Munich, Georg-Brauchle-Ring 56, 80992
Munich, Germany.
European Journal of Preventive
0(00) 1–11
!The European Society of
Cardiology 2020
Article reuse guidelines:
DOI: 10.1177/2047487320909670
rationale for current recommendations for sports and
exercise training both during and after recovery. This
information applies to all individuals who perform
exercise, irrespective of whether they are involved in
competitive or recreational sports.
Potentially increased susceptibility for
myocarditis in athletes
The exact incidence of acute myocarditis in the general
population remains unclear, since undiagnosed and
asymptomatic cases defy a comprehensive statistical
In athletes, myocarditis accounts for up to
8% of deaths, but incidence rate varies significantly
depending on the investigated cohorts.
Elite athletes in particular have a unique lifestyle
characterized by frequent international travel, leading
to increased exposure to a variety of pathogens and
accompanied by factors that may potentially impair
the athlete’s immune system (e.g. extreme climate envir-
onmental or high altitudes during competition).
Moreover, their immunological competence may be
impaired by sleep deprivation, jet lag, climate shifts,
and exhaustive exertion during long tournaments,
although scientific evidence for this remains equivocal.
Continuing training or competition despite symptoms
of common cold infection may be an additional factor,
which, when combined (Figure 1), may pave the way
for various pathogens to trespass physical barriers,
spread systemically, and affect the myocardium.
Evidence from animal models
In the absence of data determining the effect of exercise
in the context of active myocarditis in humans, animal
studies have sought to illuminate immunological
features and clinical course of the condition. Mouse
models with CVB3 myocarditis have revealed an exer-
cise-induced increase of viral titers,
a threefold
increase in the number of cytotoxic T-cells when exer-
cise was initiated after 48 hours of viral infection,
an augmented myocardial necrosis,
by significantly increased mortality in most
not all studies.
Particularly strenuous exercise during
the early phase (within nine days of viral myocardial
infection) has shown to aggravate pathophysiological
mechanisms and significantly worsen clinical out-
The clinical course seems to be affected
to a lesser extent during the latter phase (>9 days),
when viral load diminishes.
These data, however,
Figure 1. Factors increasing susceptibility of infection and potential myocarditis in athletes.
2European Journal of Preventive Cardiology 0(00)
are limited to animal studies and may not be applicable
to humans.
Viral infections of the upper airways and of the
gastrointestinal tract are the most common pathogens
to cause acute myocarditis. Endomyocardial biopsy
(EMB) samples have revealed adenovirus (AV), enter-
oviruses (e.g. CVB3, cytomegalovirus), parvovirus B19
(B19V), and Human Herpesvirus 6 (HHV6) to be the
most frequent causes. Persisting cardiac B19V and
HHV6 virus may pose the potential for latent infection;
however, the mere presence of B19V specifically does
not automatically indicate a trigger for myocarditis,
since B19V DNA can also be found non-pathogenically
in nearly all organs, including in those of healthy indi-
viduals. Less prevalent causes include bacterial, fungal,
and protozoal infections.
In suspected cases of
myocarditis, a thorough travel history must be con-
ducted in order to assess for schistosomiasis (primarily
in Africa, but also in Japan, China, Middle East, South
America, the Caribbean; no direct infiltration of worms
into pulmonary artery or myocardium, but indirect
inflammatory or immune-reaction-induced vascular,
e.g. pulmonary artery or myocardial, manifestation),
Chagas disease (North America, Europe, Japan,
Australia), tuberculosis (Asia and Africa, Eastern
Europe), or hepatitis C (Japan). In athletes performing
outdoor sports, Lyme disease (borreliosis) is also a
common diagnosis. Non-infectious diseases, such as
inflammatory bowel disease, rheumatoid arthritis,
collagenosis, vasculitis, and idiopathic forms (e.g.
giant-cell myocarditis, sarcoidosis) should also be con-
Moreover, antibiotics, diuretics, tricyclic
anti-depressants, cocaine, or doping substances such
as amphetamines, dissociation curve modulators, and
anabolic agents can potentially induce myocardial
inflammation or cardiomyopathy (Figure 1).
Clinical presentation
Symptoms of acute myocarditis are highly variable and
rather non-specific, if not completely absent. Although
clinical findings in both physically active and sedentary
individuals with acute myocarditis are similar, athletes
are usually more alert to subtle disease symptoms that
are either commonly neglected or not perceived at all in
inactive subjects, due to their sedentary behaviour and
lower body awareness (Table 1). These symptoms
include increased fatigability, minor declines in physical
performance, myalgia, headache, mild depressive symp-
toms, or new onset of atrial or ventricular arrhythmias,
which may cause light-headedness, dizziness, or even
pre-syncopal symptoms, particularly in endurance
athletes with resting heart rates of 50 beats per
minute (BPM) or less. Peripheral muscle soreness unre-
lated to exercise training or overall body discomfort
may be present at rest or after training. An increase
in heart rate of 5–10 BPM at rest or during standar-
dized exercise may be recognized, indicating potential
subclinical infection. The more infrequent cases of
severe myocarditis initially present with dyspnoea on
exertion, post-viral-induced fatigue syndrome, signs of
heart failure, or cardiogenic shock, as well as rhythm
abnormalities or even aborted SCD.
Diagnostics in athletes
Typical electrocardiogram (ECG) findings are ventricu-
lar and supraventricular arrhythmias, multiple-lead ST-
elevation in associated pericarditis, T-wave inversions,
left-bundle branch block, ventricular ectopy, high-
grade AV block, and low voltage resulting from peri-
cardial effusion or myocardial oedema.
In some ath-
letes with acute myocarditis, however, the ECG
remains completely normal. Moreover, differential
diagnosis can be more complicated in elite endurance
athletes with ‘‘athlete’s heart’’, as characteristic ECG
findings of cardiac adaptation to long-term exercise
are similar to findings in myocarditis (e.g. low-grade
AV block, sinus bradycardia, or ST-elevations in pre-
cordial leads V2 and V3).
If a previous routine ECG
is available, a careful comparison with the present find-
ings should be made. A 24-hour Holter ECG may
reveal rhythm abnormalities that can reveal ventricular
arrhythmias uncommon for athletes in terms of morph-
ology and complexity. These abnormal arrhythmias
will have to be differentiated from those with primarily
benign prognosis (for detail, see Corrado et al.
Therefore, a 24-hour Holter ECG should be pursued
in the course of a complete cardiac work-up in athletes
when myocarditis is suspected, as well as in follow-up
examinations in confirmed cases.
Assessing cardiac biomarkers for establishing diag-
nosis and tracking recovery is generally regarded as
standard of care, particularly as the ECG may still
be normal. Laboratory findings include elevated tropo-
nin T/I and CK/CK-MB, as well as elevated inflam-
matory markers. In athletes, it is noteworthy that
high-intensity training or strenuous competition may
physiologically induce several-fold increases of cardiac
biomarkers such as CK, CK-MB, troponins, and myo-
globin and natriuretic peptide levels (even into the
pathological range). However, these should normalize
within 48 hours post exercise and stay prolonged
elevated in myocarditis.
Viral serology is currently
not recommended as part of the standard diagnostic
work-up due to prominently occurring false-negative
Halle et al. 3
Echocardiography is a key component of the stand-
ard diagnostic work-up for myocarditis. One of its
major advantages is the detection of pericardial effusion
as in (peri-)myocarditis or regional and global impair-
ment of left ventricular contractility (regional or global
dysfunction, or hypokinesia). Abnormal results from
strain analysis indicate cardiac inflammation with
oedema, especially when contractility is still pre-
However, dilation of the left ventricle in elite
endurance athletes should not be mistaken as a sign
of acute myocarditis or as a basis for the definitive
diagnosis of myocardial disease. In ‘‘athlete’s heart’’,
left ventricular end-diastolic diameters (LVEDD) of
up to 60–65 mm may still be physiological in highly
trained male elite endurance athletes.
In addition, in
athletes with significant bradycardia, resting echocardi-
ography may reveal mildly impaired left ventricular
ejection fraction (LVEF), which, in athletes, immedi-
ately resolves during a short bout of exercise. If myo-
cardial function of the right ventricle is impaired and
the right ventricle dilated, arrhythmogenic right ven-
tricular cardiomyopathy has to be included in the list
of differential diagnoses of myocarditis. Nonetheless, a
sound history of exercise volume over the last years,
adjustment of LVEDD for gender and body size, and
comparisons to previous echocardiographic assess-
ments are important to differentiate physiological
from pathological findings.
Beyond echocardiography, cardiac magnetic res-
onance imaging (CMR) is the gold standard in non-
invasive diagnostics to quantify tissue characteristics,
and is crucial in patients with suspected acute myocar-
Because of recent advances in relating CMR
findings to prognosis, the assessment of suspected
Table 1. Risk factors for increased risk for myocarditis and specific presentation of symptoms
in athletes.
Risk factors Stress factors by travelling
Jet lag
Time shift
Climate zone shift
Sleep deprivation
Increased exposure to pathogens
Frequent worldwide travel
Competition site with communal housing and canteens
Travel in buses between competition sites
Extreme environmental conditions
Cold (e.g. snow and ice sports)
Heat (e.g. high temperatures during the summer)
Extreme environments (e.g. desert runs)
Altitude (e.g. skiing and mountain climbing)
Low humidity (reduction of airway barrier)
High mental stress
High and repetitive intensive exercise strain
Reduced recovery time
Exercise despite early signs of infection
Illicit drugs (e.g. cocaine)
Doping agents (e.g. amphetamines and anabolic steroids)
Increased risk of depressive symptoms (e.g. tricyclic antidepressants)
Symptoms Increased body awareness
Perception of subtle disease symptoms
Subtle fatigability at rest and during exercise
Perception of arrhythmias
Presentation of uncommon symptoms
Exaggerated muscle soreness
Reduced submaximal and maximal exercise capacity
Prolonged presentation of unspecific symptoms after infection
Increased heart rate
at rest (e.g. 5 beats/min) and in 24-hour Holter ECG
during exercise (e.g. 5–10 beats/min)
4European Journal of Preventive Cardiology 0(00)
myocarditis by CMR has been proposed as a core diag-
nostic tool for clinical work-up as well as risk predic-
tion in athletes.
It is of particular value in patients
and athletes beyond echocardiography, as late gado-
linium enhancement (LGE) and tissue characterization
techniques provide prudent diagnostic information
characteristically for myocarditis.
Changes in
CMR are best detected at 7–14 days within the course
of disease, as depicted by myocardial oedema or LGE.
The sensitivity of LGE alone to detect myocarditis is
approximately 50–60%; in combination with the assess-
ment of cardiac morphology and function sensitivity,
however, the sensitivity increases to 83%.
Novel tools
in CMR technology (e.g. T1 and T2 mapping for
assessing relaxation times and detection of extracellular
volumes (ECVs)) are very sensitive markers beyond
classical LGE imaging. In these cases, T1 mapping
can detect and quantify even small areas of fibrosis,
whereas T2 mapping can quantitatively detect myocar-
dial oedema, enabling discrimination between acute
and chronic pathologies,
findings which may also be
a prognostic criterion.
Recent data have revealed that
ECV calculation by T1 mapping does not only yield
higher diagnostic accuracy, but also has a prognostic
value, even in LGE negative but clinically suspected
Moreover, the assessment of LGE visu-
ally or semi-quantitatively can both increase the accur-
acy of determining prognosis, although the predictive
value is limited (hazard ratio 1.05, 95% confidence
interval: 1.02–1.08, p¼0.001).
Healing of myocarditis
can be monitored by native myocardial T1 and T2
measurements, without the need for contrast media.
The association between the presence of LGE and
increased risk of cardiac mortality, as well as all-cause
mortality (including SCD), although only assessed in
few studies so far, makes CMR the key diagnostic
tool in the assessment of acute myocarditis.
Impairment of LVEF alone significantly increases mor-
tality. Positive LGE findings indicate increased cardiac
risk (MACE: death, heart failure decompensation,
heart transplantation, sustained ventricular arrhythmia
(>30 s), recurrent acute myocarditis) despite adequate
left ventricular (LV) function.
These findings also
indicate an increased MACE in patients with LVEF
40% from 1.1 to 2.6%, and in patients with LVEF
<40% from 6.4 to 10.5%. In those with mild impair-
ment (LVEF 40%) and absent LGE, mortality risk is
0.4% and increases to 1.2% with LGE, and further to
2.8–3.1% in those with LVEF <40%, depending on the
absence or presence of LGE.
Moreover, the negative
predictive potential of CMR, and especially LGE, is of
high clinical importance, as patients with biopsy-
proven myocarditis but normal CMR (LVEF >60%,
left ventricular end-diastolic volume <180 ml and no
LGE) have excellent prognoses.
Changes in the presence and size of LGE during the
first six months of disease also add to predicting clinical
outcomes. In a recent registry analysis (ITAMY:
ITAlian study in MYocarditis), compared to imaging
during the early phase of myocarditis, the number of
LGE segments decreased in 46%, remained unchanged
in 31% and increased in 14% of CMR, the latter being
associated with the worst prognosis.
Moreover, both
native myocardial T1 and T2 provide an excellent per-
formance for assessing the stage of myocarditis by
These findings indicate that the reassessment
of LGE after six months may be of additional value for
risk prediction.
Furthermore, the volume and character of the LGE
pattern seems to be of prognostic value, although a
more ‘‘benign’’ pattern does not exclude the potential
of life-threatening arrhythmias. LGE with a spotty pat-
tern at inferior insertion point of the right ventricular
free wall to the interventricular septum seems to be
rather benign in contrast to a stria pattern, which is
associated with increased life-threatening arrhythmias
and cardiac sudden death.
Moreover, the localization
of LGE within the myocardium is of prognostic signifi-
cance with an (antero)-septal mid-wall patchy LGE
pattern, which is associated with a less favourable clin-
ical outcome as compared to other LGE patterns (e.g.
infero-lateral location linear/diffuse epicardial pat-
Antero-septal mid-wall patchy LGE pat-
terns are also associated with a more than twofold
increase in a patient’s risk for clinical cardiac events.
A positive LGE in CMR in athletes is, however, not
pathognomonic for acute myocarditis, as myocardial
fibrosis is found in up to 12% of middle-aged, leisure
time, asymptomatic athletes.
In particular, long-term
endurance exercise may induce fibrosis at the hinge
points between the right ventricle and interventricular
septum. It is still unclear whether this fibrosis is due
either to (a) previous silent and/or de novo myocarditis,
(b) reactivation of virus activity after a primary infec-
tion in early childhood, or (c) repetitive and prolonged
myocardial strain and maladaptation due to lifelong
endurance training.
Under the view of the environ-
mental and immunological challenges of elite athletes
(Figure 1 and Table 1), the reactivation of viral infec-
tion and subsequent fibrosis in elite endurance athletes
may be a plausible, albeit unproven, explanation.
Overall acute myocarditis can be diagnosed with high
sensitivity (84–96%) using multiple diagnostic tools in
conjunction with one another.
These approaches are,
however, not sufficiently sensitive in chronic myocarditis
cases to exclude chronic inflammation via negative
results (sensitivity of T2 mapping 77%; native T1 map-
ping 54%).
Considering the high susceptibility and severe conse-
quences of undiagnosed myocarditis in elite athletes,
Halle et al. 5
the threshold for pursuing early diagnostic procedures
(including ECG, echocardiography, and laboratory
testing for cardiac markers and inflammation with
repetition after 72 hours of pausing exercise) should
be lower as compared to physically inactive subjects.
These diagnostics should be pursued even in athletes
with only subtle perception of general symptoms
regardless of whether these symptoms are acute or pro-
longed. Most importantly, for both diagnostic reasons
and for recommendations of eligibility for exercise
training or competition, the indication for CMR
should be broadly considered, even in patients with
normal LV function. This is especially important
since a normal CMR is indicative of a favourable prog-
nosis independent of clinical symptoms and other find-
In the chronic phase of the disease, a negative
CMR result cannot rule out the persistence of an
ongoing cardiac low-gradient inflammation, which
can have a prognostic impact over time. Furthermore,
chronic myocarditis should be included in the differential
diagnosis of ‘‘overtraining syndrome’’, a poorly defined
disease entity observed in athletes after overload of pro-
longed and intensive periods of exercise training, accom-
panied by reduced regeneration periods.
Therapy in athletes
The principles of myocarditis treatment in (elite) ath-
letes or those performing recreational exercise and
sports are not different from the general patient popu-
(Figure 2). They are rooted in general
approaches of heart failure and antiarrhythmic ther-
apy. In EMB virus-positive myocarditis specific anti-
viral therapy (e.g. HHV), immunomodulation (e.g.
AV and enterovirus) or immunosuppression (e.g.
B19V) may be considered. Immunosuppression is man-
datory for virus-negative giant-cell, eosinophilic,
lymphocytic or sarcoid myocarditis, or myocarditis
secondary to autoimmune disease. It is important to
recognize and treat giant-cell myocarditis promptly,
because its course is often fulminant and can be fatal.
In Lyme disease, which often induces AV block, anti-
biotic therapy can lead to full recovery. Therefore, the
implantation of pacemakers or defibrillators should be
deferred beyond the acute phase.
The only current diagnostic tool capable of verifying
the aetiology of myocarditis is EMB with tissue ana-
Histology and immune-histochemistry may be
applied, as well as polymerase chain reaction analysis to
directly detect viral genomes.
The procedure is recom-
mended in patients with acute myocarditis and (pre)car-
diogenic shock (class I recommendations
patients with arrhythmias and/or impaired LVEF, des-
pite conservative therapy for more than three months
(class II A recommendation
) to identify prognostically
relevant inflammation and aid in selecting treatment
options (e.g. giant-cell myocarditis). After exclusions
of the persistence of cardiotropic viruses, prednisone
plus azathioprine regimes are often used for up to six
months (e.g. methylprednisolone (initial dose 1 mg/kg,
after two weeks, decrease by 10 mg, and then another
10 mg every two weeks until 10 mg maintenance dose
(all together, six months) plus azathioprine (50–150 mg
for six months; accompanying treatment: proton
blocker, calcium 1 g/24 h)). In virus-positive patients,
treatment recommendations are not well established
(for a review, see Tschope et al.
). In these cases, the
differentiation between primarily cardiotropic viruses
3. Inflammation positive
Virus positive
2. Inflammation positive
Virus negative
Immunmodulation with
Interferons possible
1. Inflammation negative
Virus negative
EMB results Differential diagnosis Therapeutic options
Post MC
Dilated cardiomyopathy
Heart failure therapy
Risk-adjusted therapy
Lymphocytic MC
Giant Cell MC
Sarcoid MC
Eosinophilic MC
Immunosuppression according
to tailored protocols
Parvovirus B19
Immunoglobulins or antivirals
in selected cases
Immunglobulins or
immunosuppression in
selected cases
Figure 2. Treatment algorithm in acute myocarditis (MC) depending on endomyocardial biopsy (EMB).
6European Journal of Preventive Cardiology 0(00)
(e.g. entero- and adenoviruses) and bystander viruses
(e.g. B19V, HHV6) is important. Entero- and adeno-
virus-induced myocarditis can be treated by immune
globulins or interferons. Bystander-associated myocar-
ditis forms most probably do not a specific anti-viral
However, in selected no-option cases, anti-
viral therapy may be used.
Recommendations for exercise eligibility
Athletes with an uncomplicated course of acute myo-
carditis and complete recovery, including normal LV
function without LGE, have excellent prognosis.
In these cases, physical activity beyond moderate inten-
sity (as in cardiac rehabilitation or recreation, which
may be recommended as early as one month post-
acute phase with normal re-evaluation) can mostly be
resumed after three months
(Figure 3). This recom-
mendation also applies to pericarditis without signifi-
cant myocardial involvement.
Athletes with impaired LV function during the acute
phase, even with complete recovery, should be advised
to refrain from structured high-intensity training
or competitive sports for at least six months
(Figure 3), as long-term effects on myocardial function
remain uncertain depending on persistence of viral load
and chronic inflammation. Before starting exercise, a
thorough cardiological evaluation for example, echo-
cardiography and 24-hour Holter ECG, including
a maximal exercise test and, optimally, a cardio-
pulmonary exercise test with spirometry (CPET) has
to be performed to determine maximal exercise capacity
and exercise intensity thresholds. If results are normal,
athletes are eligible for sports, but, from our point
of view, should be advised to first start with moderate-
intensity (50–70% maximum oxygen uptake (VO
endurance exercise for 4–6 weeks before higher-
intensity exercise is resumed. If this is tolerated well
for two months, full eligibility for competitive sports
can be approved in most cases.
In athletes with persistently reduced LV function
beyond six months, despite optimal medical heart fail-
ure therapy, eligibility for competitive sports cannot
be attested to, but moderate-intensity exercise can be
safely resumed, according to recommendations based
on studies of exercise in heart failure patients.
Thereafter, depending on the subsequent course of
recovery and type of sports, eligibility may be attested
to, but only on an individual basis with close monitor-
ing (Figure 3). The reasons for this approach are based
on the findings that the combination of impaired EF
and positive LGE has the worst prognosis, with a
Normal Abnormal
Non-eligible for any competitive sports
and exercise of moderate to vigorous
intensity for 6 months. Restricted to low
to moderate intensity rehabilitation
exercise on an individual basis
LGE positive or EF impaired or both
No signs of inflammation,
LGE negative, normal EF
Cardiac MR Imaging (CMR)
Suspected diagnosis of myocarditis in an athlete
according to medical history and symptoms
Persisting symptoms
Complete recovery
cardiological work-up
including maximal
exercise test/CPET)
Eligible for any exercise and
competitive sport (start with
individually tailored recovery
Diagnosis of myocarditis confirmed.
(Consider endomycardial biopsy in case
of complications or signs of incomplete
Prognostically relevant myocarditis unlikely
Clinical diagnosis of (peri)myocarditis
(despite normal CMR)
Non-eligible for competitive sports
and exercise of vigorous intensity for
3 months (despite good prognosis).
Recreational exercise of moderate
intensity is allowed on an individual
Persisting symptoms
Complete recovery
cardiological work-
up including
maximal exercise
Exclusion of coronary artery disease
Complete recovery (symptoms, cardiological
work-up including maximal exercise
test/CPET). Advice on increased risk for
SCD in LGE+ (In uncertainty of risk of SCD,
CMR can be repeated after 6 months).
Incomplete recovery
Non-eligible for competitive sports
and exercise of vigorous intensity.
Restricted to low to moderate
intensity exercise. Reevaluation
every 3– 6 months.
Eligible for any exercise and
competitive sport depending
on risk for SCD (LGE)
Cardiological work-up: ECG, echocardiography, 24 h Holter ECG, inflammatory markers, cardiac biomarkers
Figure 3. Algorithm for sports and exercise eligibility in myocarditis.
SCD: sudden cardiac death; CMR: cardiac magnetic resonance imaging; CPET: cardio-pulmonary exercise testing; EF: left ventricular
ejection fraction; LGE: late gadolinium enhancement.
Halle et al. 7
MACE rate of 10.5% and mortality rate of 3.1% over
five years.
In patients with mildly impaired LV func-
tion, the presence of fibrosis also significantly increases
the risk for MACE and mortality.
However, clinically indicated recommendations are
not clear in those with completely normal LV function
with persistent LGE. Recent data from the ITAMY
registry indicate variability of LGE over six months
and an increased risk for cardiac events in LGE-
positive subjects.
Positive LGE may reflect post-
inflammatory scarring, but is also found in 12% of
asymptomatic athletes.
Until the pathophysiology,
differential diagnosis, and clinical significance of this
constellation is better understood, decision-making
will remain extremely difficult. However, from a current
perspective, eligibility for sports can mostly be recom-
mended, but only on an individual basis and close
follow-up examinations (Figure 3).
Overall, recommendations for eligibility for sports
should specify type and cardio-pulmonary intensity of
sports (e.g. marathon running vs golf), and also include
sports conditions at altitude or in water (e.g. climbing
or swimming) with high fatality risk during arrhyth-
mias and subsequent unconsciousness. An approach
of shared decision-making with well-informed athletes
is of utmost importance, as, from our experience, both
recreational and elite athletes continue their sports des-
pite restrictive advice from their attending medical pro-
fessional. Therefore, detailed documentation is also
mandatory for both forensic and legal reasons.
Exercise recommendations after recovery
from acute myocarditis
Before starting an exercise program, a CPET has to be
performed, which will yield maximal exercise capacity
as well as individual exercise intensity thresholds.
Initially, sessions are limited to regenerative intensity
levels (<50% VO
), which will then be gradually
increased in duration and, if tolerated well, also in
intensity (50–75% VO
). Dynamic resistance exer-
cise can also be included in this phase. Exercise tests
should be repeated after six and 12 weeks for assess-
ment of pathologies, and particularly before adaptation
of exercise of even higher intensity levels (>75%
). If maximal exercise is tolerated well and no
other pathologies for example, impaired LV function
or arrhythmias are present recommendation of full
eligibility can usually be given. In general, in recre-
ational as well as competitive athletes, a definition
and detailed prescription of mode, duration, as well
as definite exercise heart rate corridor is particularly
important, as these individuals often have a vastly dif-
ferent view and perception of training intensities or
optimal training schedule.
Preventative measures
For some of the above-mentioned microbial infections,
preventive measures are available in the form of vac-
cinations (Corynebacterium diphtheria, influenza virus,
tuberculosis (although less effective in the common
respiratory form)), general hygiene, and cautious con-
tact with animals and uncooked foods. Repellents and
appropriate clothing improve personal tick bite protec-
tion, particularly in athletes performing outdoor sports
and training (Lyme disease). Physicians caring for ath-
letes should frequently advise the athlete and coaches
against the use of illicit drugs. Moreover, lifestyle meas-
ures should be followed by athletes, including reduced
alcohol consumption, healthy food, regular sleep, and
avoidance of large groups of people with sufficient
recovery after travels, strenuous training sessions, and
competitions (Figure 1 and Table 1).
Recommendations for exercise training and compe-
tition in athletes with clinical symptoms of infection
are based on expert opinions only. In the presence
of common symptoms of upper airway and gastrointes-
tinal infections, particularly when accompanied by gen-
eral symptoms (e.g. fatigue), athletes should be very
cautious and significantly reduce exercise intensity
and prolong recovery periods after training sessions.
Optimally, endurance exercise should be stopped for a
minimum for 2–3 days when symptoms are present,
and may be fully resumed only after 3–4 days of com-
plete recovery. Exercise without cardio-pulmonary
strain, such as skill exercises, may be resumed earlier.
Athletes presenting with fever, general fatigue, periph-
eral muscle soreness, or even muscle pain are advised to
refrain from any exercise while symptoms persist. These
patients may resume exercise 5–7 days after symptoms
subside, but with reduced volume and intensity load.
Special counselling aspects in athletes
In acute myocarditis, the attending physician must
counsel the athlete and explain the generally prolonged
healing process, dangers of premature resumption of
exercise training, and potential of delayed disease
course, including potential lethal consequences. The
team physician and coach should be consulted and
advised on the risk associated with an athlete resuming
exercise too early. The diagnosis of myocarditis typic-
ally has a significant impact on an athlete’s career,
including cancellation of competitions, and potential
financial constraints. Therefore, early psychological
consultation may be advantageous. Team physicians
should take over the task to protect the athlete from
external psychological pressure of sponsors, coaches,
sports clubs, and league authorities. The collaboration
between a sports cardiologist and sports scientist is opti-
mal in defining an individually tailored training plan.
8European Journal of Preventive Cardiology 0(00)
Fortunately, most athletes with myocarditis undergo
complete recovery. Nonetheless, yearly cardiology con-
sultations remain important.
Clinical perspective and future research
Although (elite) athletes represent only a smaller group
within our society, the challenges for diagnosis, treat-
ment, and exercise recommendations are crucial for any
cardiologist in order to prevent an overall increased risk
of SCD. These also extend to recreational athletes a
group that is constantly increasing in numbers.
There is a clear demand for extending knowledge of
myocarditis in recreational as well as elite athletes
through both animal and human studies, especially
for studies which employ current state-of-the-art scien-
tific methods. From a clinical perspective, the long-term
effects of exercise during the post-acute phase
(<3 months) and the importance of LGE is unresolved.
To answer this, we currently lack an international stan-
dardized registry on myocarditis in recreational and
elite athlete populations,
which would considerably
help to improve future decision-making on initiation
of general exercise and recommendations of eligibility
for recreational and competitive sports.
Author contribution
LB and MaH drafted the manuscript. MeH, MS, KE, and CT
critically revised the manuscript. All authors gave final
approval and agree to be accountable for all aspects of
work ensuring integrity and accuracy.
We thank Rhys Isaac Beaudry, College of Nursing and
Health Innovation, The University of Texas Arlington,
USA, and Lennard Halle, University of Freiburg, Germany,
for their critical comments.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
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... While studies investigating the effects of exercise during active myocarditis in humans are lacking due to ethical reasons, mice models have shown strong deleterious cardiac effects such as adverse ventricular remodelling and an increase in ventricular tachyarrhythmias and mortality. 3 Consequently, athletes diagnosed with or suspected of active myocarditis are advised to refrain from sports for 3-6 months, 1 which can significantly impact an athlete's professional career. ...
Full-text available
Objective Longitudinal consequences and potential interactions of COVID-19 and elite-level sports and exercise are unclear. Therefore, we determined the long-term detrimental cardiac effects of the interaction between SARS-CoV-2 infection and the highest level of sports and exercise. Methods This prospective controlled study included elite athletes from the Evaluation of Lifetime participation in Intensive Top-level sports and Exercise cohort. Athletes infected with SARS-CoV-2were offered structured, additional cardiovascular screenings, including cardiovascular MRI (CMR). We compared ventricular volumes and function, late gadolinium enhancement (LGE) and T1 relaxation times, between infected and non-infected elite athletes, and collected follow-up data on cardiac adverse events, ventricular arrhythmia burden and the cessation of sports careers. Results We included 259 elite athletes (mean age 26±5 years; 40% women), of whom 123 were infected (9% cardiovascular symptoms) and 136 were controls. We found no differences in function and volumetric CMR parameters. Four infected athletes (3%) demonstrated LGE (one reversible), compared with none of the controls. During the 26.7 (±5.8) months follow-up, all four athletes resumed elite-level sports, without an increase in ventricular arrhythmias or adverse cardiac remodelling. None of the infected athletes reported new cardiac symptoms or events. The majority (n=118; 96%) still participated in elite-level sports; no sports careers were terminated due to SARS-CoV-2. Conclusions This prospective study demonstrates the safety of resuming elite-level sports after SARS-CoV-2 infection. The medium-term risks associated with SARS-CoV-2 infection and elite-level sports appear low, as the resumption of elite sports did not lead to detrimental cardiac effects or increases in clinical events, even in the four elite athletes with SARS-CoV-2 associated myocardial involvement.
... For instance, the incidence of cardiac complications such as myocarditis after COVID-19 ranges internationally from 1.1%-2.3% among competitive athletes (Halle et al., 2021). Myocarditis is difficult to diagnose as symptoms are nonspecific (Daniels et al., 2021). ...
Full-text available
Guidelines for medical clearing after SARS-CoV-2 infection in elite athletes do not include T-cell immunity aspects despite its relevance in the course of COVID-19 disease. Therefore, we aimed to analyze T-cell-related cytokines before and after in-vitro activation of CD4+ T-cells. We sampled professional indoor sports athletes at medical clearing after SARS-CoV-2 infection obtaining clinical, fitness data, and serological data including CD4+ T-cell cytokines. All data were analyzed by principal component analysis and 2 × 2 repeated measures ANOVA. CD4+ T-cells were sampled for cell culture activation with anti-CD3/anti-CD28 tetramers. At medical clearing, CD4+ T-cells from convalescent athletes secreted increased levels of TNF-α 72 h after in-vitro activation compared to vaccinated athletes. IL-18 levels in plasma were elevated and a cluster of parameters differentiated convalescent from vaccinated athletes by 13 parameters at the timepoint of medical clearing. All clinical data indicate infection is resolved, while increased TNF-α may reflect altered proportions of peripheral T-cells as a hangover of infection.
... Dicha alteración está relacionada con las fibras de calcio tipo L. Además, tanto la disminución del período refractario inducida por el nervio vago como la conducción más lenta, acortan la longitud de onda de excitación y, por lo tanto, facilitan la reentrada, lo que induce la aparición de FA.(26) En relación a la presencia de ectopia auricular, en particular la ectopia de la vena pulmonar, este se comporta como un desencadenante de la mayoría de los episodios de FA paroxística en la población general,(27) queda por demostrar su participación real en la FA asociada a la actividad física extenuante, por lo que se necesita más investigación. La ectopia auricular y ventricular puede aumentar como consecuencia de la práctica regular del ejercicio físico extenuante.(28) En relación a la remodelación eléctrica del nódulo sinoauricular en deportistas, para probar la hipótesis de que la bradicardia inducida por el entrenamiento de resistencia puede ser causada por un cambio intrínseco en el nódulo sino auricular, que a su vez sería el resultado de una remodelación de los canales iónicos que gobiernan el marcapasos, D'Souza et al.,(29) recientemente realizaron un estudio en animales en el que compararon ratas entrenadas en cinta rodante frente a sedentarias, ratones sedentarios frente a entrenados (natación) y controles sedentarios; estos utilizaron análisis in vivo, in vitro y transcriptómicos, así como enfoques mecánicos que incluyeron el bloqueo con ivabradina del componente más importante del reloj de membrana, la corriente graciosa (If). ...
... He stayed as an in-patient for two days and was discharged after arrhythmias were ruled out and troponin levels decreased. Medical treatment with ACE inhibitor was initiated and the patient was advised to abstain from moderate to high-intensity sports and exercise for 3-6 months according to European Society of Cardiology (ESC) guidelines and current consensus documents (1,2,5). During the first 3 months, the patient was advised to strictly abstain from any exercise training, afterwards he slowly resumed low-intensity exercise training. ...
Full-text available
We report the case of a young professional soccer player who underwent cardiac MRI (CMR) for work-up of discrete intermittent chest pain and subtle ST segment elevations in the ECG after having been tested positive for SARS-CoV-2 type B.1.1.529 despite full vaccination including recent mRNA booster. Troponin levels were significantly increased and myocarditis was suspected. Comprehensive CMR including CINE and late gadolinium enhancement as well as multi-parametric T1/T2 mapping techniques revealed local hypokinesia and swelling of the posterolateral wall with non-ischemic late gadolinium enhancement and increased T2 relaxation time compatible with acute viral myocarditis. The patient was admitted to a cardiology ward for rhythm and troponin monitoring and was discharged after two days of uneventful rhythm monitoring and with decreased troponin levels. Adhering to current recommendations the patient was advised to abstain from moderate- to high-intensity sports and exercise for 3-6 months. After 6 months of exercise avoidance, follow-up ECG showed regression of prior ST segment elevations, and Holter ECG as well as a treadmill exercise stress test did not reveal any abnormalities. Follow-up CMR was performed before return-to-sports which revealed persisting myocardial fibrosis but complete regression of myocardial edemam and excluded ongoing inflammation. This example underscores the value of multi-parametric CMR tissue characterization for the work-up of suspected SARS-CoV-2 associated myocarditis, as well as for follow-up before return-to-sports.
... Despite the fact that all current subjects reported no cardiovascular disease clinically silent or unrecognized myocarditis cannot be excluded per se. In fact, previous work pointed out that elite athletes seem to have an increased risk of viral infection and subsequent myocarditis due to increased exposure to pathogens related to worldwide traveling and international competition or impaired immune system related to continuing training during infections or resuming training early thereafter, strenuous exercise training or competition, and exercising in extreme weather conditions [25]. This assumption for elite athletes could also be true for non-elite athletes. ...
Full-text available
Objectives This study analyzed the prevalence and pattern of focal and potential diffuse myocardial fibrosis detected by late gadolinium enhancement (LGE) and extracellular volume (ECV) imaging in male and female marathon runners using cardiac magnetic resonance (CMR). Methods Seventy-four marathon runners were studied including 55 males (44 ± 8 years) and 19 females (36 ± 7 years) and compared to 36 controls with similar age and sex using contrast-enhanced CMR, exercise testing, and blood samples. Results Contrast-enhanced CMR revealed focal myocardial fibrosis in 8 of 74 runners (11%). The majority of runners were male (7 of 8, 88%). LGE was typically non-ischemic in 7 of 8 runners (88%) and ischemic in one runner. ECV was higher in remote myocardium without LGE in male runners (25.5 ± 2.3%) compared to male controls (24.0 ± 3.0%, p < 0.05), indicating the potential presence of diffuse myocardial fibrosis. LV mass was higher in LGE + males (86 ± 18 g/m ² ) compared to LGE- males (73 ± 14 g/m ² , p < 0.05). Furthermore, LGE + males had lower weight (69 ± 9 vs 77 ± 9 kg, p < 0.05) and shorter best marathon finishing times (3.2 ± 0.3 h) compared to LGE- males (3.6 ± 0.4 h, p < 0.05) suggesting higher training load in these runners to accomplish the marathon in a short time. Conclusion The high frequency of non-ischemic myocardial fibrosis in LGE + male runners can be related to increased LV mass in these runners. Furthermore, a higher training load could explain the higher LV mass and could be one additional cofactor in the genesis of myocardial fibrosis in marathon runners. Key Points • A high frequency of myocardial fibrosis was found in marathon runners. • Myocardial fibrosis occurred typically in male runners and was typically non-ischemic. • Higher training load could be one cofactor in the genesis of myocardial fibrosis in marathon runners.
... In short, the perception of fatigue is equivalent to less exercise, which implies a worsening of the quality of life and an increase in health problems and comorbidities, especially in the elderly population (Egerton et al., 2015;Puetz, 2006). Halle et al. (2020) in their study showed that factors such as an impaired immune system, sleep deprivation or exhausting efforts can cause myocarditis. In addition, continuous physical training coupled with symptoms of common cold infection can be an additional factor that, when combined, can cause different pathogens to break through physical barriers, spread systemically, and affect the myocardium . ...
... Elite athletes, representing the category of the highest level of competitiveness [3], have an increased risk of virus infection, with the consequences that follow, due to increased exposure to pathogens (worldwide travel/international competitions) or an impaired immune system (training continues during infection/training starts immediately after infection, stressful training or competition and exercise in extreme climatic conditions) [4]. ...
Full-text available
During the COVID-19 pandemic, many athletes from several sporting disciplines were infected with the SARS-CoV-2. The aim of this systematic review is to summarize the current scientific evidence on the psychological sequelae and mental health of elite athletes who have been infected by the virus. The review was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Statement; three databases were searched: PubMed, ISI Web of Knowledge, and Scopus. The initial search resulted in 2420 studies; after duplicate removal and screening by title and abstract, 41 articles were screened by full-text. A total of four eligible articles were included in the review. All included articles measured depression and anxiety in athletes who had suffered from COVID-19, while in three papers levels of stress were measured. Overall, the only two questionnaires used in more than one study were the DASS-21 and the APSQ. In our systematic review, we highlighted that mental and psychological health in elite athletes has the same importance as physical health. This statement suggests that these examinations should be introduced and performed during the competitive sports’ medical examinations conducted at the start of the sporting season, which currently consists only of the examination of physical parameters. Due to lack of studies on the topic, the results of our review show that mental health in athletes with a history of SARS-CoV-2 infection is an issue that requires more investigation, considering the evidence of clinical consequences. The importance of post-infection psychological sequelae is significant in assessing possible repercussions on the athletes’ sporting performance.
Cardiac-related deaths are the leading nontraumatic cause of death in the young athlete. Although there are multiple causes for cardiac arrest in athletes, sideline evaluation and management does not vary. Recognition, immediate high-quality chest compressions, and time to defibrillation are the greatest factors affecting survival. This article reviews the approach to the collapsed athlete, causes for select cardiac emergencies in athletes, preparedness for cardiac emergencies, and return to play considerations and recommendations.
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The clinical manifestations of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection responsible for coronavirus disease 2019 (COVID-19) commonly include dyspnoea and fatigue, and they primarily involve the lungs. However, extra-pulmonary organ dysfunctions, particularly affecting the cardiovascular system, have also been observed following COVID-19 infection. In this context, several cardiac complications have been reported, including hypertension, thromboembolism, arrythmia and heart failure, with myocardial injury and myocarditis being the most frequent. These secondary myocardial inflammatory responses appear to be associated with a poorer disease course and increased mortality in patients with severe COVID-19. In addition, numerous episodes of myocarditis have been reported as a complication of COVID-19 mRNA vaccinations, especially in young adult males. Changes in the cell surface expression of angiotensin-converting enzyme 2 (ACE2) and direct injury to cardiomyocytes resulting from exaggerated immune responses to COVID-19 are just some of the mechanisms that may explain the pathogenesis of COVID-19-induced myocarditis. Here, we review the pathophysiological mechanisms underlying myocarditis associated with COVID-19 infection, with a particular focus on the involvement of ACE2 and Toll-like receptors (TLRs).
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Although premature ventricular beats (PVBs) in young people and athletes are usually benign, they may rarely mark underlying heart disease and risk of sudden cardiac death during sport. This review addresses the prevalence, clinical meaning and diagnostic/prognostic assessment of PVBs in the athlete. The article focuses on the characteristics of PVBs, such as the morphological pattern of the ectopic QRS and the response to exercise, which accurately stratify risk. We propose an algorithm to help the sport and exercise physician manage the athlete with PVBs. We also address (1) which athletes need more indepth investigation, including cardiac MRI to exclude an underlying pathological myocardial substrate, and (2) which athletes can remain eligible to competitive sports and who needs to be excluded.
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Purpose of Review In this review, our aim is to summarize the evidence of exercise interventions in heart failure. Addressing pathophysiology, we discuss training modalities and optimal dose finding in exercising patients with reduced (HFrEF) and preserved ejection fraction (HFpEF). Recent Findings While smaller studies showed a trend towards improved exercise capacity by high-intensity interval training in comparison with moderate continuous training in HFrEF, recent multicenter randomized trials were unable to confirm these findings. Considering the lack of effective drug therapies in HFpEF, exercise training plays an even more important role in this particular population. Summary Exercise training in heart failure is beneficial in addition to medical and device therapy. Data are still mostly limited to HFrEF. Intensity should primarily be moderate at a daily base. The concept of “the higher the better” could not be confirmed for HFrEF. The overall concept of training is to maximally strain the periphery without straining the myocardium.
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Myocarditis is generally a mild and self-limited consequence of systemic infection of cardiotropic viruses. However, patients can develop a temporary or permanent impairment of cardiac function including acute cardiomyopathy with hemodynamic compromise or severe arrhythmias. In this setting, specific causes of inflammation are associated with variable risks of death and transplantation. Recent translational studies suggest that treatments tailored to specific causes of myocarditis may impact clinical outcomes when added to guideline-directed medical care. This review summarizes recent advances in translational research that influence the utility of endomyocardial biopsy for the management of inflammatory cardiomyopathies. Emerging therapies for myocarditis based on these mechanistic hypotheses are entering clinical trials and may add to the benefits of established heart failure treatment.
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Background Although the presence of late gadolinium enhancement (LGE) using cardiovascular magnetic resonance imaging (CMR) is a significant discriminator of events in patients with suspected myocarditis, no data are available on the optimal LGE quantification method. Methods Six hundred seventy consecutive patients (48 ± 16 years, 59% male) with suspected myocarditis were enrolled between 2002 and 2015. We performed LGE quantitation using seven different signal intensity thresholding methods based either on 2, 3, 4, 5, 6, 7 standard deviations (SD) above remote myocardium or full width at half maximum (FWHM). In addition, a LGE visual presence score (LGE-VPS) (LGE present/absent in each segment) was assessed. For each of these methods, the strength of association of LGE results with major adverse cardiac events (MACE) was determined. Inter-and intra-rater variability using intraclass-correlation coefficient (ICC) was performed for all methods. Results Ninety-eight (15%) patients experienced a MACE at a medium follow-up of 4.7 years. LGE quantification by FWHM, 2- and 3-SD demonstrated univariable association with MACE (hazard ratio [HR] 1.05, 95% confidence interval [CI]:1.02–1.08, p = 0.001; HR 1.02, 95%CI:1.00–1.04; p = 0.001; HR 1.02, 95%CI: 1.00–1.05, p = 0.035, respectively), whereas 4-SD through 7-SD methods did not reach significant association. LGE-VPS also demonstrated association with MACE (HR 1.09, 95%CI: 1.04–1.15, p < 0.001). In the multivariable model, FWHM, 2-SD methods, and LGE-VPS each demonstrated significant association with MACE adjusted to age, sex, BMI and LVEF (adjusted HR of 1.04, 1.02, and 1.07; p = 0.009, p = 0.035; and p = 0.005, respectively). In these, FWHM and LGE-VPS had the highest degrees of inter and intra-rater reproducibility based on their high ICC values. Conclusions FWHM is the optimal semi-automated quantification method in risk-stratifying patients with suspected myocarditis, demonstrating the strongest association with MACE and the highest technical consistency. Visual LGE scoring is a reliable alternative method and is associated with a comparable association with MACE and reproducibility in these patients. Trial registration number NCT03470571. Registered 13th March 2018. Retrospectively registered.
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Cardiovascular magnetic resonance imaging (CMR) has become a key investigative tool in patients with suspected myocarditis. However, the prognostic implications of T1 mapping, including extracellular volume (ECV) calculation, is less clear. Patients with suspected myocarditis who underwent CMR evaluation, including T1 mapping at our institution were included. CMR findings including late gadolinium enhancement (LGE), left ventricular ejection fraction (LVEF), native T1 mapping, and ECV calculation were associated with first major adverse cardiac events (MACE). MACE included a composite of all-cause death, heart failure hospitalization, heart transplantation, documented sustained ventricular arrhythmia, and recurrent myocarditis. One hundred seventy-nine patients with a mean age of 49 ± 15 years were identified. Seventy nine individuals (44%) were female. Mean LVEF was 48 ± 16. At a median follow-up of 4.1 [interquartile-range (IQR) 2.2–6.1] years, 22 (12%) patients experienced a MACE. Mean ECV (per 10%) was significantly associated with MACE (HR 2.09, 95% CI 1.07–4.08, p = 0.031). Presence of ECV ≥ 35% demonstrated significant univariable association with MACE (HR 3.3, 95% CI 1.43–7.97, p = 0.005) and such association was maintained when adjusted to LVEF (HR 3.42, 95% CI 1.42–7.94, p = 0.006). ECV ≥ 35% portended a greater than threefold increased hazards to MACE adjusted to LGE presence (HR 3.14, 95% CI 1.29–7.36, p = 0.012). In patients without LGE, ECV ≥ 35% portended a greater than sixfold increased hazards (HR 6.6, p = 0.010). In the multivariable model including age, LVEF and LGE size, only ECV ≥ 35% maintained its significant association with outcome. ECV calculation by CMR is a useful tool in the risk stratification of patients with clinically suspected myocarditis, incremental to LGE and LVEF.
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Myocardial diseases are associated with an increased risk of potentially fatal cardiac arrhythmias and sudden cardiac death/cardiac arrest during exercise, including hypertrophic cardiomyopathy, dilated cardiomyopathy, left ventricular non-compaction, arrhythmogenic cardiomyopathy, and myo-pericarditis. Practicing cardiologists and sport physicians are required to identify high-risk individuals harbouring these cardiac diseases in a timely fashion in the setting of preparticipation screening or medical consultation and provide appropriate advice regarding the participation in competitive sport activities and/or regular exercise programmes. Many asymptomatic (or mildly symptomatic) patients with cardiomyopathies aspire to participate in leisure-time and amateur sport activities to take advantage of the multiple benefits of a physically active lifestyle. In 2005, The European Society of Cardiology (ESC) published recommendations for participation in competitive sport in athletes with cardiomyopathies and myo-pericarditis. One decade on, these recommendations are partly obsolete given the evolving knowledge of the diagnosis, management and treatment of cardiomyopathies and myo-pericarditis. The present document, therefore, aims to offer a comprehensive overview of the most updated recommendations for practicing cardiologists and sport physicians managing athletes with cardiomyopathies and myo-pericarditis and provides pragmatic advice for safe participation in competitive sport at professional and amateur level, as well as in a variety of recreational physical activities.
Presentation of myocarditis in athletes is heterogeneous and establishing the diagnosis is challenging with no current uniform clinical gold standard. The combined information from symptoms, electrocardiography, laboratory testing, echocardiography, cardiac magnetic resonance imaging, and in certain cases endomyocardial biopsy helps to establish the diagnosis. Most patients with myocarditis recover spontaneously; however, athletes may be at higher risk of adverse cardiac events. Based on scarce evidence and mainly autopsy studies and expert's opinions, current recommendations generally advise abstinence from competitive sports ranging from a minimum of 3 to 6 months. However, the dilemma poses that (un)necessary prolonged disqualification of athletes to avoid adverse cardiac events can cause considerable disruption to training schedules and tournament preparation and lead to a decline in performance and ability to compete. Therefore, better risk stratification tools are imperatively needed. Using latest available data, this review contrasts existing recommendations and presents a new proposed diagnostic flowchart putting a greater focus on the use of cardiac magnetic resonance imaging in athletes with suspected myocarditis. This may enable cardiac caregivers to counsel athletes with suspected myocarditis more systematically and furthermore allow for pooling of more unified data. To modify recommendations regarding sports behavior in athletes with myocarditis, evidence, based on large multicenter registries including cardiac magnetic resonance imaging and endomyocardial biopsy, is needed. In the future, physicians might rely on combined novel risk stratification methods, by implementing both noninvasive and invasive tissue characterization methods.