Introduction
Myocarditis (MC) is the third most frequent cause of sudden cardiac death (SCD)
during physical activity in young sportsmen and women (≤35 years) in Germany
[1], and even at rest can trigger malignant
arrhythmias [2]. The exact incidence of acute MC
diseases is unclear since non-diagnosed and/or asymptomatic disease courses
make it difficult to compile valid statistics [3]
[4].
MC is an umbrella term for non-ischaemic myocardial inflammation, which can vary
widely regarding symptoms, course, and prognosis [5]
[6]. Initially there is a short acute
phase, during which the pathogens responsible for the inflammation reach the
myocardium, negatively impact the heart cells and trigger an immune reaction. In the
sub-acute phase, myocardial necrosis and fibrosis can then occur. Over the chronic
course, MC predominantly resolves, and in most cases the inflammation subsides.
Sometimes, however, small local non-ischaemic myocardial scars remain which can have
an arrhythmogenic impact [7]
[8]
[9].
Up to 20% of patients develop dilated cardiomyopathy (DCM) over the long-term
course, sometimes taking years to become clinically evident [4]
[5]
[7]
[8]
[10]
[11]
[12]
[13]. The main dangers associated with MC are reduced
systolic function of the myocardium, accompanied by comprehensive malperfusion of
the organism, as well as an increased susceptibility to malignant arrhythmias and
SCD [6]
[8].
Causes
The causes of MC are manifold [12] and can be
categorised as follows:
-
infectious (e. g. through viruses, bacteria, fungi, or
parasites)
-
toxic (e. g. through drug consumption, heavy metals, or
radiation) and
-
autoimmune (e. g. through rheumatic diseases, vaccination
reactions, or medication intolerance).
In Europe and North America, MC is chiefly attributable to viral pathogens, such
as a cold, influenza, or gastroenteritis [14]; but
bacterial infections, such as tonsillitis, scarlet fever, or borreliosis can
also be the cause [8].
In young patients and/or patients with sporting ambitions, it is also
conceivable that drugs or doping agents are involved. Likewise, genetic
predispositions can promote development of the disease [5]
[14]. In many MC patients it is
ultimately impossible to determine the exact aetiology of the disease at a later
stage. This can also be because no link is made between the cardiac problems
occurring (often with a delay of days or even weeks) and a previous (seemingly
harmless) infection [14].
Symptoms and diagnostics
Diagnosing MC is complex owing to its often heterogeneous course. Other
cardiovascular diseases, such as coronary artery disease (CAD) or valvular
vitia, must be excluded using differential diagnostics. The fact that sometimes
(particularly in women) symptoms are only mild/modified should also be
taken into account [5]. The following examinations
can be used to diagnose MC and produce a clearer picture when taken as a
synopsis [12]
[14]:
-
medical history/symptoms
-
electrocardiography (ECG)
-
transthoracic echocardiography (TTE)
-
biomarkers and/or inflammatory markers
-
cardiovascular magnetic resonance imaging (CMR)
-
endomyocardial biopsy (EMB).
Medical history/symptoms
Possible symptoms of MC can vary considerably in their manifestation. Degrees
of severity range from a complete lack of symptoms to cardiac
decompensation, cardiogenic shock or SCD [12].
Frequently, chest pain and/or classic symptoms of heart failure
(dyspnoea, performance drop) or arrhythmias (palpitations, dizziness,
syncope) are initially described [14]. In a
study including 670 cases of suspected MC, chest pain was the most common
symptom, at 52% [15]. In the ITAMY
study (n=386) [16], 95% of MC
patients with preserved left ventricular ejection fraction
(LVEF>50%) had chest pain symptoms.
Athletic patients additionally report restricted physical performance,
increased muscle soreness, as well as a slightly elevated heart rate both at
rest and during exercise (approx. 5–10 bpm). However, in a
differential diagnosis these symptoms can also point to
“overtraining syndrome”, and this needs to be excluded [3]
[17].
If the MC has an autoimmune cause, extra-cardiac symptoms can also occur
(e. g. in conjunction with sarcoidosis or systemic sclerosis) and
provide an indication of the underlying disease [14].
ECG
In 42% of patients with suspected MC (96% in the ITAMY study)
the resting ECG was conspicuous [15]
[16]. Non-specific changes which can occur
include [6]
[15]:
In many patients, however, no special changes are discovered in the resting
ECG. In elite endurance athletes, interpretation of the ECG signal can also
prove difficult since similar ECG changes can occur as typical and
non-pathological adaptations of the “athlete’s
heart”. If available, the findings should therefore be compared to
previous examinations in order to verify any changes. A 24-hour Holter ECG
can be considered. The monitored time period should then also include a
regular workout [3].
TTE
Imaging with TTE is a standard diagnostic procedure. The following phenomena
can provide indications of MC [3]
[6]
[7]:
-
pericardial effusion
-
left ventricular dilatation with thin myocardial walls
-
increase in myocardial wall thickness (due to myocardial oedema)
-
global or regional altered systolic function and wall motion
abnormalities
-
diastolic dysfunction.
Left ventricular ejection fraction (LVEF) can be slightly or considerably
reduced at rest, but not necessarily [6]. In
endurance athletes, the differentiation to physiological changes of
athlete’s heart can be difficult. In these cases, previous findings
should be taken as comparative images. A TTE can also be performed in a
semi-recumbent position on a bicycle ergometer in order to be able to
evaluate global systolic function and possible regional wall motion
abnormalities during exercise. In diseased athletes, the wall motion
abnormalities usually increase during physical exertion. In healthy
athletes, the systolic function increases significantly during exercise
[7].
Biomarkers and/or inflammatory markers
In case of suspected MC, the following laboratory values are relevant [14]:
These laboratory values are not specific MC markers, so that corresponding
concentration increases can also occur with other diseases or
non-pathological states. Nevertheless, the troponin T/I value in
particular has proved helpful. In approx. 63% of all cases of
suspected MC (100% in the ITAMY study), increased troponin values
can be found [9]
[15]. MC is thus the second most frequent reason (after myocardial
infarction) for an increased troponin value in patients below the age of 50
[18]. The time factor plays a crucial role
here: particularly in the initial phase following the first occurrence of
symptoms (<1 month), increased values can be observed which can
normalise again over the later course [14].
In athletes it should be taken into account that corresponding biomarkers can
also be physiologically increased following intense physical exercise and,
at least temporarily, be beyond the threshold range. However, the increase
in troponin caused by exercise is not quite as high and usually normalises
again within 48 h. A sports anamnesis and repeat tests can provide
the necessary information [3]
[7].
CMR
CMR has become established in the last few years as one of the primary
non-invasive diagnostic tools for patients with suspected MC [14]. Imaging provides information about global
systolic function, local wall motion abnormalities, as well as a qualitative
presentation of the tissue by visualising oedemas and fibroses [14]. Use of contrast medium and interpretation
of a possible “late gadolinium enhancement” (LGE) have
proved helpful [15]
[19].
The updated Lake Louise Criteria cite as the main criteria for radiological
proof of MC [19]:
-
myocardial oedema (T2-weighted, T2-mapping) and/or
-
myocardial injury (T1-weighted, T1-mapping, expanded extracellular
volume, LGE).
Secondary criteria focus on pericardial effusion and left ventricular
dysfunction [19].
In the current discussion, the valency and sensitivity of CMR in the chronic
phase of MC are controversial. For example, LGE is unable to differentiate
clearly whether the inflammation/scar is fresh, ongoing or already
healed. Estimating a patient’s sporting capability using this
parameter is therefore difficult. However, studies show the prognostic
significance of positive LGE for a major adverse cardiac event (MACE) [6]
[15]
[16].
EMB
EMB is the gold standard among diagnostic examinations for acute MC, and yet
it is not used routinely owing to its invasive nature [6]. It is used when standard treatment is not
successful and the genesis of the MC is highly significant for the treatment
[13]
[14].
With EMB, a distinction can be made between different pathogens using
histological, immunohistological and viral polymerase chain reaction tests.
In order to minimise potential false-negative findings, usually several
(≥5–7) tissue samples of sufficient size
(1–2 mm) are extracted from different cardiac areas [7]
[12]
[20].
Prevention, impact of sport, and preventive training breaks
Prevention and impact of sport
The risk of contracting MC can be reduced by protection
from/minimisation of pathogen triggering (e. g. viral,
bacterial, toxic, parasitic). The use of suitable protective clothing and an
adequate level of vaccination appropriate to the country of residence is
recommended [3]. Triggering factors also
include drug and doping agent abuse, the significance of which should be
explained within the framework of primary prophylaxis [3]
[14].
Exposure to pathogens is not always avoidable. It is therefore crucial that
the body’s own immune system is functioning. With regard to
intensive sports activities, the following two problems arise in conjunction
with the emergence of MC [14]
[21]:
-
an assumed higher susceptibility to infection following intensive
exercising (“open window effect”)
-
a stronger MC development following intensive exercising in
conjunction with an already existing infection.
It is generally assumed that regular moderate physical training induces
multi-layer protective health effects and is concomitant with a stronger
immune system [7]
[22]. However, blood test results show a temporarily reduced
activation of the immune system following intensive physical exercise [23]. This phase can last for several hours and
is known as the “open window effect”. It is assumed that
pathogens can attack the organism more easily during this period [14]
[23], but the
significance of the “open window effect” is the subject of
controversial debate [22]
[24].
In professional athletes, the negative impact on the immune system of
additive factors should not be underestimated, e. g. increased
travelling, time differences, lack of sleep, extreme ambient conditions,
depression or an insufficient time for regeneration [3].
It is also assumed – in cases where an infection already exists
– that intensive physical training units can negatively impact the
emergence and course of MC. In animal experiments it could be proven that
intensive exertion in mice infected with Coxsackie B3 led to a significantly
increased mortality and more frequent pathological cardiac findings
(myocardial fibrosis, ventricular dilatation) compared to animals without
such physical training units [9]
[14]
[25]
[26]. In Swedish orienteers, the incidence of
SCD was considerably reduced after a preventive training break was
introduced for diseased athletes [27].
Preventive training breaks
The question of whether and when a preventive training break is necessary can
be difficult to answer in individual cases [3]
[14]. According to expert
opinion, it is recommended that in cases of mild disease with symptoms from
the neck upwards, such as a runny/blocked nose or a tickly throat,
sport can be continued as long as the athlete feels physically fit enough
[3]
[14]
[21]. The intensities should be within the
regenerative range. Preferable would be a short training break even with a
mild disease, or at least to shift the focus of the training to
tactical/technical elements without cardiovascular exertion [3].
Sport and competitive sport must be completely abandoned if the symptoms are
below the neck or if systemic complaints occur, such as [3]
[14]:
The relevance of this training break should be made sufficiently clear to
athletes since a high degree of motivation or a pressure to perform could
tempt them to maintain or prematurely resume their training programme.
Especially in the early days of the disease, the risk of pathophysiological
changes is higher [3]. Once the symptoms have
subsided, the break from training exertion should be upheld for at least
5–7 additional days, and resumption should start at a moderate level
and gradually increase in intensity [3]
[14].
MC and COVID-19
According to the current literature, a SARS-CoV-2 (COVID-19) infection can also
be concomitant with myocardial involvement [28]
[29]
[30]. In the early stages of the pandemic, the prevalence data were
vague and reason to fear a high level of danger (e. g. very high
prevalences of up to 78% [31]). Meanwhile,
many more studies have become available, and it is assumed that in approx.
1–3% of positively tested athletes, a myocardial involvement can
be shown in the CMR [32]
[33]. A correlation between a positive finding and possible COVID-19
symptoms is not necessarily given. It is also conspicuous that a fair number of
patients show pathological findings only in the CMR examination, whereas the
ECG, TTE and troponin values frequently remain inconspicuous [32]. Long-term investigations to evaluate
meaningfulness and prognosis are yet to become available.
Training break and diagnostics during/after COVID-19
infection
Different societies and authors have been fast to publish recommendations
regarding when and with which precautionary measures it is viable to restart
training and competitive sport after a COVID-19 infection [28]
[29]
[34]
[35]
[36]
[37]
[38]
[39].
Frequently (but not always), the severity of the COVID-19 symptoms is taken
as a criterion for the duration of the preventive training break and the
required screening instruments [38]
[40]
[41]. With an
asymptomatic course, sport should be abandoned for between 7 and 14 days
following a positive test. In symptomatic patients, sport should usually
only be resumed at least 7–14 days after the symptoms have
abated.
There is still no consensus among the societies regarding about which
cardiological diagnostics are necessary prior to return-to-play (RTP). A
compromise must be found between cost and benefit since the potential number
of positively tested athletes would considerably exceed screening capacity
(e. g. it is not practical to perform a CMR on every patient) [29]
[38]. [Table 1] shows a comparison between different
recommendations, especially for adult athletes in competitive sports.
Usually basic diagnostics (e. g. medical history, physical
examination, ECG) are recommended before RTP in conjunction with mild
symptoms (sometimes also if asymptomatic). Depending on the findings, and
with increasing severity and duration of the COVID-19 symptoms, more complex
screening instruments can then also be added. Special RTP algorithms exist
for athletes in competitive high school sports (<15 years) and for
recreational master athletes (>65 years) [29].
Table 1 Comparison of different return-to-play
recommendations in patients/athletes after COVID-19
infection. If abnormal findings are detected, extended
diagnostics are required. For detailed definitions and guidance,
please see specific recommendations.
|
Recommendation
|
COVID-19 symptoms
|
Time before return-to-play
|
Recommended diagnostics before return-to-play
|
|
Nieß et al. [39]
German Journal of Sport Medicine (May 2020)
|
Asymptomatic:
|
No intensive exercise for 2 weeks after positive test
|
Basic diagnostics: medical history and physical
examination, laboratory tests and ECG
|
|
Mild symptoms:
|
No exercise for 2–4 weeks after positive test
|
Basic diagnostics+extended diagnostics: stress
ECG with O2 saturation, echocardiography, spirometry
|
|
Severe symptoms:
|
No exercise for≥4 weeks after positive test
|
Basic diagnostics+extended
diagnostics+CPET with BGA and body
plethysmography
|
|
Phelan et al.[37]
JAMA Cardiology (May 2020)
|
Asymptomatic:
|
No exercise for≥2 weeks after positive test
|
No specific cardiovascular risk stratification. If
clinical and/or cardiac symptoms develop, follow
appropriate clinical pathway
|
|
Mild symptoms:
|
No exercise for≥2 weeks after symptom
resolution
|
Clinical evaluation including 12 lead
ECG+echocardiogram+laboratory test.
Consider additional symptom-guided testing
|
|
Severe symptoms:
|
No exercise for≥2 weeks after symptom
resolution
|
Consider cardiac imaging per local hospital protocols.
Consider repeated cardiac testing
|
|
Schellhorn et al.[36]
European Heart Journal (May 2020)
|
Asymptomatic:
|
No intensive exercise for 2 weeks after positive test
|
ECG
|
|
Symptomatic:
|
No exercise for≥2 to 4 weeks after positive
test
|
Diagnostics according to severity. Cardiological
follow-up (physical examination,
resting+exercise ECG, echocardiography) after 2
to 4 weeks to get full sports release
|
|
Baggish et al. [35]
British Journal of Sports Medicine (June 2020)
|
Asymptomatic:
|
N.A.
|
Focused medical history and physical examination.
Consider 12-lead ECG. If ECG is abnormal, then
additional evaluation with minimum echocardiogram and
exercise test is warranted in conjunction with a sports
cardiologist.
|
|
Mild symptoms:
|
N.A.
|
Same as asymptomatic+ECG as mandatory
|
|
Moderate to severe symptoms:
|
N.A.
|
Comprehensive evaluation prior return to sport, in
conjunction with a sports cardiologist, to include blood
biomarker assessment, 12-lead ECG, echocardiography,
exercise testing and ambulatory rhythm monitoring
|
|
Kim et al. [29]
JAMA Cardiology (October 2020)
|
Asymptomatic:
|
No exercise for 10 days after positive test
|
No specific cardiovascular risk stratification. If
clinical and/or cardiac symptoms develop, follow
appropriate clinical pathway
|
|
Mild symptoms:
|
No exercise for 10 days from symptom onset (but must have
full resolution of symptoms)
|
Specific cardiovascular risk stratification unnecessary,
but on individual basis reasonable, particularly for
protracted course of illness. If clinical and/or
cardiac symptoms develop, follow appropriate clinical
pathway
|
|
Moderate symptoms:
|
No exercise for 10 days after symptom resolution
|
Medical
evaluation+ECG+echocardiography+laboratory
test. If abnormal: consider repeated cardiac
testing+CMR+exercise test and extended
ambulatory rhythm monitoring
|
|
Severe symptoms:
|
No exercise for 14 days after symptom resolution
|
During hospitalisation: laboratory test+cardiac
imaging
|
|
McKinney et al. [38]
Canadian Journal of Cardiology (November 2020)
|
No evaluation stratified by COVID-19 symptoms
|
No≥moderate intensity exercise for≥7 days
after complete viral symptom resolution; If cardiac
symptoms are present: continued restriction from
exercise
|
Focused cardiac symptom history. If cardiac symptoms are
present after resolution of viral symptoms or a new
unexplained reduction in fitness is present, then
medical assessment is recommended, including history and
physical examination and considering ECG and laboratory
tests. In the presence of abnormal findings: referral to
cardiology with advanced cardiac imaging
(echocardiography and/or CMR) is recommended
|
Abbreviations: BGA, blood gas analysis; CMR, cardiovascular magnetic
resonance imaging; CPET, cardiopulmonary exercise testing; ECG,
electrocardiography; O2, oxygen.
RTP after COVID-19
RTP should be introduced with gradually increasing intensity. As a rule of
thumb, 2–3 days of graduated return can be planned per training unit
cancelled due to illness. This period should also serve to sufficiently
regenerate the non-cardiac systems (e. g. pulmonary tissue,
vasculature) [28]. In the training plan, first
the frequency should be increased, then the duration and only finally the
intensity [28]. Various graduated plans have
been published and can be used for orientation [42]
[43]
[44]. In this context the following is important: as soon as
cardiac symptoms (e. g. chest pain, palpitations) and/or an
unexplained reduction in fitness occur, extended MC diagnostics are
indicated [38]. Patients should be sensitised
to this and be informed about the potential risk of SCD. In patients with
ambiguous findings, the RTP strategy should be decided together with the
athlete (shared decision-making) [29]
[45]. In contrast, in cases of confirmed MC the
MC guidelines should be observed (see section RTP after MC).
MC after mRNA COVID-19 vaccination
Since mid-2021 there have been a growing number of reports that MC courses
have been more frequently observed following a COVID-19 mRNA vaccination
[46]
[47]
[48]. The mechanisms responsible
for this are not yet fully understood [47].
Numbers from Israel show a higher incidence by factor 5.34 after BNT162b2
vaccination (Comirnaty, BionTech/Pfizer), compared with before the
pandemic (factor 2.35 compared with an unvaccinated control group) [49]. The frequency of a vaccine-related MC is,
however, lower than after contracting COVID-19 [48]. Nevertheless, the risk was considerably increased following
the second vaccination, especially in young men (factor 13.6 compared to
pre-pandemic, factor 8.96 compared to unvaccinated control group) [49]. The observed course of the disease was
luckily usually mild, with the symptoms emerging 2–5 days after the
vaccination [47]
[49]
[50]
[51]. The German statistics also show a higher MC incidence rate
following mRNA vaccination, particularly in young male patients [46]. The Spikevax vaccine (Moderna) proved to
be the most risky and since mid-November has been recommended only for
people above the age of 30.
There are currently no generally recognised restrictions regarding the
interval between a COVID-19 vaccination and a return to sporting activity.
It does appear reasonable, however, to refrain from exertion in the first
few days, to await potential side-effects and to rest the body. The Ministry
of Health in Singapore recommends refraining from exertive sport for at
least 2 weeks following a COVID-19 vaccination [52].
Therapeutic options in conjunction with MC
In most cases, acute MC resolves favourably within a few weeks [20]. There are currently no controlled and
randomised studies available for the optimised treatment of MC. Treatment
involves a symptom-adjusted two-pillar approach, comprising [7]
[13]
[14]:
-
treatment of heart failure in accordance with the guidelines, and
-
treatment of arrhythmias in accordance with the guidelines.
In the case of acute symptoms, hospital admission and monitoring are necessary
[14]. The results of an EMB are required,
especially from patients in (pre-)cardiogenic shock or patients without
long-term improvement in their symptoms, in order to give their treatment a
specific direction [3]. Immunosuppressives are
administered in cases of proven giant cell MC or sarcoidosis, while a specific
antiviral therapy is commenced following a positive virus finding [3]
[5].
For the treatment of advanced heart failure, the temporary use of mechanical
circulatory support systems as a “bridge to recovery” can be
necessary in a small percentage of patients [4]
[13]. Heart transplantation as the
ultima ratio is not recommended until later, in order to allow time for
potential recovery of the myocardium [20].
In patients with arrhythmias, the danger of SCD can be minimised through the
temporary use of a wearable cardioverter defibrillator (WCD). A permanent
defibrillator system is implanted only later should symptoms persist [7]
[8]
[20].
Acute MC: training break and risk stratification
Training break
For patients with supposed or proven MC, the cardiological societies
recommend a break from training and competitions of at least 3–6
months [6]
[10].
The recommendations are equally valid for hobby, amateur, and professional
athletes, independent of their age, sex or global systolic function, and
they can be lengthened depending on the disease course.
Prior to RTP, a comprehensive cardiological diagnosis is necessary for risk
stratification. It includes the following examinations [3]
[6]
[7]
[10]:
Risk stratification
MC patients are at permanent increased risk of malign arrhythmias due to
possible myocardial scarring [6]
[8]
[14]. They also
display a risk of insidious maladaptive remodelling of the myocardium, with
a possible concomitant development of DCM [6]
[12]. A reliable test for whether
the inflammation is still present or has subsided meanwhile is not currently
available [2]
[6]. This is why current guidelines recommend annual check-ups
(including ECG and TTE) for a period of at least 4 years, in order to
observe the individual development [12].
Depending on the findings and the sporting ambition, the follow-up
observation phase can be significantly extended.
For risk stratification, evaluation of the LVEF and increasingly also the
change of a possible positive LGE finding are used. In asymptomatic patients
with an uncomplicated disease course, preserved systolic function and a
negative LGE finding, the prognosis is very good [3]
[15]. In a study with a total of
670 suspected MC cases [15], the annual event
rate in the first 5 years following onset of disease in patients with an
LVEF>40% and without an LGE finding was 1.1% for
MACE and 0.4% for mortality. In cases of a positive LGE finding
(LVEF still>40%), the annual event rates rose to 2.6 and
1.2%, respectively.
An isolated reduced LVEF was accompanied by a poorer prognosis (MACE:
6.4%; mortality 2.8%). The highest annual event rates were
observed in patients with restricted LVEF (<40%) and
positive LGE finding (MACE: 10.5%; mortality: 3.1%) [15].
The isolated interpretation and weighting of a positive LGE finding is
currently still being intensively researched and discussed [15]
[16].
RTP after MC
The precise scheduling of permitted resumption of sporting activity has to be
decided from case to case and in discussion with the patient [3]
[7]. In the acute
phase of MC, strict physical rest is indicated [53]
[54]
[55]. The relevance of the sports break and the risks of not adhering
to it should be expressly conveyed.
According to the current recommendations, a release for intensive sporting
activities and competitions can be issued 3–6 months after the acute
disease phase, provided that the following criteria are observed [6]
[10]:
-
ventricular systolic function within normal range
-
cardiac and inflammatory biomarkers within normal range
-
lack of clinically relevant arrhythmias in daily routines (24-hour Holter
ECG) and in stress situations (e. g. CPET).
The importance of re-assessments should be pointed out once again [6]
[12].
Two recent overviews provide additional pointers for a more differentiated
evaluation [3]
[7]:
constitutive physical training should be started at the earliest 1 month after
the acute disease phase, and only with light and moderate intensities (no
high-intensity interval training, HIIT), e. g. within the framework of
cardiac rehabilitation [3]
[53]
[55]. In stable patients with an
uncomplicated course, inconspicuous cardiac and inflammatory biomarkers,
preserved systolic function and no positive LGE indication, exertion levels can
be increased successively after 3 months into the intensive range [3]
[7] in conjunction
with prognostically low complication rates [56].
If during the acute phase of MC, in contrast, there was a restricted LVEF
and/or positive LGE indication of LGE, intensive physical exertion
(e. g. HIIT) and competitive sport should be avoided for at least 6
months, even if the systolic function has recovered in the meantime [3].
In MC patients with restored systolic function after 6 months yet still
displaying a positive (albeit not worse) LGE indication, there is a
theoretically an increased risk of ventricular arrhythmias linked to potential
SCD. In such cases, a release to sport can be granted only after thoroughly
informing the patient [3]
[6]
[7]. Shared decision-making between
the clinician and patient is encouraged, accompanied by annual routine check-ups
for long-term risk stratification [3]
[6]
[14].
A release to intensive sports and competitions cannot be granted if a lowered
LVEF or other indications of incomplete myocardial recovery are still present
after 6 months [3]. In such cases, a re-evaluation
should take place at 3- to 6-month intervals.
In cases where there is no improvement, not even in the long term, a decision
must be reached for the individual patient and together with that patient. The
decision process should include the nature of the envisaged sport with regard to
its cardiovascular impact (e. g. golf vs. football), as well as the
risks involved in losing consciousness (e. g. during motor sports or
diving) [3]. In some circumstances,
recommendations could extend to complete abstinence from extreme exertion and
competitive sport in the future [3]
[17]
[57]. Moderate
regular training at “rehabilitation level” is, however, possible
and also advisable [3].
Training design
In the training design a difference is made between healing and healed MC
[58]. In the healing phase, training may
take place only in conjunction with a stable clinical status and
significantly abating symptoms (e. g. 24-hour Holter ECG, TTE,
biomarkers) [53]
[55]. A maximal exercise test is still counter-indicated at this
stage and the training units should only have very low intensities (values
on rate of perceived exertion (RPE): 6–8, scale: 6–20) [53]
[55]
[58].
The training design following healed MC draws upon many years of experience
with heart failure patients, as well as the results of the individual
symptom-limited exercise test [7]
[53]
[55]
[59]
[60]. In the
first 4–6 weeks, the training should be performed with low to
moderate intensity (no maximum effort) to approx. 40–50% of
the maximal oxygen uptake (peak VO2) (RPE:<10–12)
[3]
[7]
[53]
[59]
[60]. Should conspicuities occur (e. g.
clinically relevant arrhythmias), training must be stopped immediately [53]
[58]. If the
patients tolerate the exertion well, more intensive units to approx.
50–60% (up to<75%) of peak VO2
(RPE: 12–14) can be performed over the course [58]. After approx. 6 and 12 weeks, as well as
before the implementation of highly intensive units (e. g. HIIT), a
new maximal exercise test should exclude possible conspicuities [3].
A moderate dynamic resistance training should start with low exertion
(30–50% of the 1 repetition maximum (1-RM), RPE:
12–13), with the intensity increasing gradually over the course
(40–60% of the 1-RM, RPE: 14–15) [53]
[59]
[60]. If intensive physical exertion is
tolerated well, and no other findings contradict it, a release for
competitive sport can be given in the long term [3].
Education and mental health
Adequate education of patients and their coaches or training partners is a
crucial aspect for reliable training design. Experience has shown that ideas
about moderate/regenerative training plans can diverge considerably,
and that consistent compliance is unfortunately not a given in all cases
[3]
[57].
Against this background, the recommended training ranges and intensities
should be clearly communicated and the information given should be
documented in writing, also in order to circumvent later liability issues
[3].
With regard to emergency prophylaxis, it is vital to instruct and educate
those with direct access to the patient/athlete since first aid is
crucial if a haemodynamically relevant arrhythmia should occur. Training in
groups, knowledge about adequate first aid measures, and the rapid
availability of an automated external defibrillator (AED) have all proven
favourable for the prognosis [1]
[61]. Education can and should therefore include
the following aspects:
-
training range and intensity during the first post-MC phase
-
possible consequences if ignored
-
symptoms of possible complications
-
first aid measures
-
relevance of regular check-ups
-
prevention of renewed MC.
Another significant point for RTP is the mental health of the patient: for
ambitious amateur or professional athletes, an uncertain long-term medical
prognosis, long training breaks, a lack of competitions and/or the
cancellation of sponsoring/prize money can represent a huge
psychological burden and tempt athletes to resume intensive physical
activities too soon. Potential anxieties can also restrict RTP following
resolved MC. The early integration of a psychological carer should therefore
be considered in relevant constellations [3].
