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Can You Train After Myocarditis? The Troponin-Door Audit: The Door Where the Gym's Two Default Scripts — a Virus Is Just a Virus, Train Through the Chest Weirdness, and Its Twin, Your Heart Is Permanently Fragile Now, Never Load It Again — Both Fail the Reader (the Definitions Column: the Inflamed Myocardium Named by Troponin and Imaged by CMR, the Leak That Opens the File and the Camera That Grades It; the Window Column: Kiel's Forced-Swimming Mice Where Exercise on Days 1–9 of Coxsackie Infection Took Mortality From 0–10% to 20–40% — the One Animal Result the Guidelines Never Overrode; the Rule Column: ESC 2023 — Three to Six Months Out of Competitive Sport, Re-Clearance Gated on Normal Ventricular Function, Normalized Biomarkers, No Arrhythmia on Holter and Exercise ECG, and a Quiet CMR; the Prognosis Column: Grün's 222 Biopsy-Proven Patients Where Late Gadolinium Enhancement Carried HR 8.4 for All-Cause Mortality — and Not One Patient Without It Died Suddenly, Even With an Enlarged Impaired Ventricle — Beside Gräni's 670 Where a Normal CMR Was Worth 0.8% Per Year of Major Events and 0.3% Per Year of Death; the Screening-Arc Column: the COVID Files — Rajpal's 26 College Athletes Where 4 Carried CMR Inflammation Behind a Clean Troponin, ECG and Echo, Then Martinez's 789 Professional Athletes at 0.6% With Zero Cardiac Events on Return, and Starekova's 145 at 1.4% Whose Own Conclusion Called Routine CMR Screening's Utility Questionable; the Denominator Column: Petek's NCAA 20 Years — Sudden Death 1:63,682 Athlete-Years and Falling, Myocarditis Adjudicated in 8 Deaths Across Two Decades; the Honesty Column: the 2024 Guideline Systematic Review Admitting Exercise-Restriction Advice Is Expert Opinion Rather Than Trial Data, and Claessen's Editorial Calling Time on One-Size-Fits-All) — the Answer Is After, Not Through: the Infection Owns the Acute File, the Cardiologist and the Calendar Own the Return, and the Cleared Heart Trains Again

By RightRep AI Assistant · · 24 min read

Myocarditis is the file where the internet's two default scripts — the push-through script: a virus is just a virus, chest weirdness is part of being sick, keep the streak alive and the fear script: your heart got inflamed, it is permanently compromised now, heavy training is a loaded gun, take up walking — both fail the reader at the exact door he walked in through, because this reader is one of two people: the one sitting on a diagnosis he barely understands — chest pain or a racing heart during a viral illness, a troponin blood test that came back high, a doctor who said the word "inflammation" and the word "rest" in the same sentence — or the cleared one holding a normal follow-up scan and asking whether the barbell is still dangerous. The push-through script dies on the mouse column, because during acute viral myocarditis exercise is not neutral: in the classic coxsackie model, mice forced to swim 60 minutes a day on days one through nine of infection ran cardiac viral titres up and mortality from 0–10% to 20–40% [4] — this is the one door in the whole condition wing where training during the illness measurably worsens the disease itself, which is why every guideline in the file mandates an exercise-free window [1][2][3]. The fear script dies on the prognosis column, because the scar is what matters and most readers don't have one: among 222 biopsy-proven patients, late gadolinium enhancement on the cardiac MRI carried a hazard ratio of 8.4 for all-cause mortality — and not one patient without it died suddenly, even with an enlarged, impaired ventricle [5], while a completely normal cardiac MRI was worth 0.8% per year of major events and 0.3% per year of death in the 670-patient outcome cohort [6]. So the fences come first. First: the emergency fence — chest pain, pressure or palpitations during a viral illness, or any unexplained breathlessness or fainting near one, is a same-day medical assessment with a troponin, not a training question [1][3]. Second: the window fence — no training at all while symptomatic and until biomarkers normalize; the mouse file is the reason the field treats this window as non-negotiable [2][4]. Third: the clearance fence — three to six months out of competitive sport after myocarditis, returning only through the full gate: normal ventricular function, normalized troponin and inflammatory markers, no arrhythmia on Holter and exercise ECG, and a quiet cardiac MRI [1][2][13]. Fourth: the permanence fence, inverted — residual scar is the variable that shapes follow-up, not a lifetime ban; shared decision-making with a sports cardiologist replaces the blanket rule [12][13][14]. With the fences standing, the file underneath is one of the cleanest exits in this library's condition wing: the door is real, it is time-limited, it is gated by tests that exist — and the cleared heart trains again, with 789 professional athletes returning through exactly this gate with zero cardiac events in the largest screening file the field owns [9].

The short answer: yes — after, not through; and the door exits cleanly

Strip the file to its spine. The definition: myocarditis is inflammation of the heart muscle — usually viral, sometimes immune — diagnosed on a ladder of troponin (the leak that says the muscle is being injured), ECG, echocardiography, and cardiac magnetic resonance, the non-invasive gold standard, with biopsy as the definitive tissue call in selected cases [3][13]. The window: the field's oldest and least contested rule — no exercise during the acute illness, and a defined abstention period after it — born from animal data where exercise multiplied viral replication and mortality [4] and ratified by every guideline since [1][2][3]. The rule: ESC 2023 — competitive athletes with recent myocarditis sit out three to six months, the exact length individualized to the clinical course, and return through a four-part gate: normal ventricular function, normalized biomarkers, freedom from arrhythmia on ambulatory and exercise ECG, and resolved inflammation on CMR [1][13][14]. The prognosis: in 222 biopsy-proven patients followed a median 4.7 years, all-cause mortality was 19.2%, cardiac 15%, sudden 9.9% — concentrated almost entirely in patients whose MRI showed late gadolinium enhancement (HR 8.4 all-cause, 12.8 cardiac); zero patients without LGE suffered sudden death, even with enlarged impaired ventricles [5]; and in the 670-patient CMR outcome cohort, a normal study meant 0.8%/year MACE and 0.3%/year death [6]. The screening arc: the pandemic stress-tested the whole gate — Rajpal's small Ohio State series found 4 of 26 college athletes (15%) with CMR inflammation behind a completely clean troponin, ECG and echo [7]; the response era built triad-testing machines that then found, at scale, 789 professional athletes screened systematically → 30 abnormal first-line screens (3.8%) → 5 confirmed inflammatory heart disease (0.6%, three myocarditis, two pericarditis) → zero adverse cardiac events on return to play [9]; and Starekova's 145-athlete series at 1.4% ended with the field's own verdict that routine CMR screening's utility was "questionable" [8]. The denominator: NCAA's 20-year adjudicated file counts sudden cardiac death at 1:63,682 athlete-years — declining — with myocarditis adjudicated as the cause in 8 deaths across two full decades [10]. That is the audit in one paragraph: the acute file belongs to the infection and the emergency department, the return belongs to a calendar and a gate of named tests — and the gate opens [1][9].

What the condition actually is: inflammation of the pump, measured by its leaks

The mechanics in a paragraph: myocarditis is inflammatory injury to the heart-muscle cells, most often triggered by viruses (enteroviruses historically, SARS-CoV-2 more recently, and in tropical latitudes the arboviruses dengue and chikungunya [15]), sometimes by the immune system itself [3][13]. The heart handles injury the way skeletal muscle does — cells leak their contents — except here the leaked marker is troponin, which is why a "mild" case announces itself with a blood test that cardiologists reserve for heart attacks [3][11]. The injury disrupts the electrical grid as much as the pump: the inflammation makes the muscle irritable, which is where arrhythmias — the palpitations, the racing, in the worst case the arrest — come from, and why the clearance gate is built on rhythm monitoring as much as on pumping function [1][13]. The camera that grades all of this is cardiac MRI with late gadolinium enhancement: LGE is scar — replacement of muscle with fibrous tissue that neither contracts nor conducts properly — and its presence, location and extent turned out to be the single strongest predictor of who has a bad long-term outcome [5][6]. Two properties of the mechanism matter to the training reader. First, the illness is usually silent-to-mild and self-limiting: most viral myocarditis resolves, and the mortality files are dominated by the hospitalized and the biopsy-proven — selection at its most severe [5][6]. Second, the danger window is the inflamed window: an irritable, inflamed myocardium under adrenergic load — a hard session, a hot gym, a max attempt — is exactly the substrate for the arrhythmic catastrophe, which is why the abstention rule exists and why the mouse data still anchors it [1][2][4].

The window column: the one place exercise provably worsens the disease

Every condition door in this library eventually publishes a "training through it is fine, actually" column. This door never does, and the reason is a 1989 mouse experiment that forty years of guidelines never overrode: Kiel and colleagues inoculated inbred mice with coxsackievirus B3 and forced half of them to swim 60 minutes a day for the first nine days of infection [4]. The exercised animals carried significantly higher myocardial viral titres on days six and nine, larger hearts relative to body weight, more muscle-fibre necrosis — and overall mortality rose from 0–10% in the infected-rested group to 20–40% in the infected-exercised group [4]. The mechanism reads in gym terms: hard exercise during the viremic phase drives virus into the myocardium, suppresses the immune clearance that needs those days, and piles adrenergic load onto an electrically irritable muscle [2][4]. From that experiment descends the field's most durable instruction — Kindermann's 2012 review fixing the modern three-to-six-month exercise-abstention rule for confirmed myocarditis [2], Caforio's ESC position statement institutionalizing it [3], and ESC 2023 carrying it forward essentially unchanged in its numbers [1]. The honest caveat runs with it: no randomized human trial has ever tested exercise versus rest in acute myocarditis, for the obvious ethical reason — the guideline systematic review marks exercise restriction as expert opinion grounded in exactly this animal file [11]. For the training reader the translation is absolute and simple: during the acute illness and until biomarkers quiet, training is not a variable to manage — it is off [1][2][4].

The rule column: ESC 2023 and the four-part gate

The return rule the whole file converges on, stated in ESC 2023 for competitive athletes after myocarditis (and pericarditis): abstention from competitive sport for three to six months, the length individualized to severity — fulminant courses and impaired function sitting at the far end — followed by re-evaluation that must clear four gates: ventricular function back to normal on imaging; troponin and inflammatory markers normalized; no significant arrhythmias on 24-hour Holter and exercise ECG; and CMR free of active inflammation (oedema resolved — residual scar shifts the conversation to risk stratification rather than automatic exclusion) [1][13][14]. Recreational training follows the same ladder at gentler stakes: the recreational athlete's gate is the same four questions, asked with less machinery [13][14]. Two upgrades the modern rule carries over its ancestors. First, the gate is explicit rather than calendar-only: the old blanket six months has become a structured clearance, and the reviews now frame residual LGE as the variable that individualizes follow-up rather than ends careers [12][13][14]. Second, shared decision-making is now the named mode: Claessen's editorial — return to play after myocarditis, time to abandon the one-size-fits-all approach — argues the low-risk cleared majority deserves individualized risk pricing rather than a default ban, and the 2026 Portuguese review formalizes the same stance for the athlete consultation [12][13]. What the gate is not: permission to self-clear. Every column in this file routes the return through a cardiologist, because the tests that price the risk — the Holter, the exercise ECG, the CMR — are not gym instruments [1][13][14].

The prognosis column: the scar is the file — and most readers don't have one

The two outcome cohorts this door owns are German, large for the field, and complementary. Grün's 222 biopsy-proven patients, followed a median 4.7 years: all-cause mortality 19.2%, cardiac 15%, sudden cardiac death 9.9% — and the decisive gradient was imaging: LGE on the baseline CMR carried HR 8.4 for all-cause and 12.8 for cardiac mortality, outpredicting ejection fraction, ventricular volumes and symptoms; no patient without LGE suffered sudden death, even when the ventricle was enlarged and impaired [5]. Gräni's 670 patients with suspected myocarditis, same 4.7-year median follow-up: 44% carried LGE, which doubled-to-tripled major-event risk (HR 2.22; septal and midwall patterns HR 2.55 and 2.39, patchy distribution HR 2.93, each 10% of scarred muscle adding 79% to the hazard) — while a completely normal CMR meant 0.8%/year of major adverse events and 0.3%/year of death [6]. Read together, the two files reprice the fear script entirely: the mortality numbers that terrify a Google-searching reader come from biopsy-proven, hospitalized, scar-carrying cohorts [5]; the reader whose CMR has gone quiet carries event rates most gym populations would envy [6]. The scar column does not disappear — residual LGE is a real variable that shapes follow-up intensity and honest risk discussion [12][13] — but "inflamed once, fragile forever" is not what the file says. The file says: the MRI is the verdict, and its clean version is close to an acquittal [5][6].

The screening-arc column: the COVID files and how the biggest gate in history ran

The pandemic handed this door its natural experiment, in three acts. Act one — the alarm: Rajpal's Ohio State series screened 26 competitive college athletes recovering from COVID-19 with CMR and found 4 (15%) meeting the Lake Louise criteria for myocarditis — every one with normal troponin, normal ECG and normal echocardiogram [7]. Fifteen percent, invisible to the standard triad — the number that paused college sport and launched the CMR-screening era [7]. Act two — the machine at scale: the North American professional leagues mandated the triad (troponin, ECG, echo) for every infected player, escalating to CMR only on abnormal screens — and Martinez's pooled file ran 789 professional athletes through it: 30 abnormal first-line screens (3.8%), of whom 5 (0.6%) had confirmed inflammatory heart disease — three myocarditis, two pericarditis — all restricted from play, and zero adverse cardiac events occurred in athletes who screened and returned [9]. Act three — the verdict: Starekova's Wisconsin series put 145 student athletes through CMR regardless of triad and found myocarditis in exactly 2 (1.4%) — concluding that CMR as a routine screening tool in mild or asymptomatic infection was of questionable utility [8]. The arc's teaching is the door's whole epistemology in miniature: the scary early estimate came from small, symptomatic-enriched samples; the machine at scale found the true prevalence low (0.6–1.4%) [8][9]; the events never came [9]; and the field walked back routine imaging while keeping the gate for the diagnosed [12][13]. For today's reader the arc's residue is practical: a positive troponin or symptomatic chest involvement gets the full workup and the calendar; a mild infection with a quiet triad does not need a panic MRI [8][9].

The denominator column: how big is the dragon, measured

The fear script needs a dragon, so the file prices the dragon: Petek's adjudicated 20-year NCAA study — four independent databases, expert-panel autopsy review, 2002 through 2022 — counted 143 sudden cardiac deaths across all NCAA athletes, an incidence of 1:63,682 athlete-years, and falling (five-year incidence rate ratio 0.71) [10]. The causes, where adjudicable: autopsy-negative sudden unexplained death first at 19.5%, idiopathic LVH or possible cardiomyopathy 16.9%, hypertrophic cardiomyopathy 12.7% — and myocarditis adjudicated in 8 deaths across the full two decades, one of them in the final pandemic window, none attributed to COVID infection [10]. Two readings for this reader. The sober one: half of all sudden cardiac deaths in the file were exertional, and myocarditis is one of the few causes where the exertion link is mechanistic — the inflamed, irritable muscle under load — which is precisely why the window fence leads this door [4][10]. The steadying one: eight deaths in twenty years, in a population of maximal-intensity competitive athletes, in a surveillance system this deep — myocarditis is a real cause of catastrophic events and a vanishingly rare event itself, concentrated in the undiagnosed [10]. The diagnosed reader holding this file is, by that fact, already outside the file's casualty column: the dragon mostly eats the ones who never knew they were in its territory [7][10].

The honesty column: what the guideline file cannot yet promise

This library's audits earn their keep on the nulls, and this door's biggest one is structural: the 2024 systematic review of acute-myocarditis clinical practice guidelines — multiple societies, rigour-assessed — concluded that the recommendations for exercise restriction, follow-up intervals and several treatment choices rest on expert opinion, not trial data; no randomized trial has ever assigned exercise [11]. The one-size-fits-all critique is the second null: Claessen's editorial and the 2026 athlete review both argue the blanket rule overprices risk for the clean-scan majority and underprices the individualization a scar-carrying athlete deserves [12][13]. The persistent-LGE question is the third: guidelines gate return on resolved inflammation, but what a permanent scar means for long-term training — the exact question the lifter asks — has no prospective trial, only the cohort gradients of Gräni and Grün [5][6][12][14]. The CMR-screening retraction is the fourth [8]. And the mouse column is the fifth, in the other direction: the abstention rule's strongest evidence base is an animal model, which is why it will likely never be randomized in humans — the ethics board is the fence [4][11]. What is not a null: the troponin-leak diagnosis itself, the CMR prognosis gradient, and the zero-event return file of the 789 — those are counted, and they are the spine of every practical rule below [5][6][9].

The return column: the graded ramp behind the gate

For the cleared athlete, the reviews converge on a ramp that will feel familiar from every rehab door in this library — because post-myocarditis programming is cardiac rehabilitation's cousin [13][14]. The sequence: clearance first — the four gates closed by a cardiologist, in writing, with the Holter and exercise ECG documenting rhythm under exactly the load the sport will impose [1][13]; a graded aerobic base first — weeks of easy, conversational work (the zone 2 register) rebuilding the aerobic chassis at a heart rate the exercise test has already covered [13][14]; intensity reintroduced before maximal work — tempo, then intervals, then anything resembling a max effort or a competition, each step held long enough to prove quiet [14]; resistance training in the same ladder — moderate loads, submaximal, breathing patterns that avoid long straining Valsalva in the earliest weeks, building back toward normal programming; and a symptom line that outranks the plan — any new chest symptom, palpitation at rest, unexplained breathlessness or near-faint steps back to the cardiologist, not to a deload [1][13]. The psychological column is the ramp's quiet half: the reviews name the fear-decondition spiral after myocarditis — athletes who self-ban long after clearance — and prescribe the same medicine as the cardiac-rehab literature, which is a programmed, progressive return rather than an open-ended "see how it feels" [14]. The calendar does the trusting; the plan does the ramping [13][14].

The program in gym terms: what stops, what waits, what ramps

Stops and refers, today: chest pain, pressure, palpitations or unexplained breathlessness during or after a viral illness — same-day medical assessment with a troponin; fainting or near-fainting during exertion is the emergency department, full stop [1][3].

Off, completely, through the window: from diagnosis, no training while symptomatic and none until biomarkers normalize — the mouse file is the reason this is not negotiable, and "just mobility work" still counts as load during viremia [2][4].

Waits on the calendar: three to six months out of competitive sport, the length set by the clinical course — fulminant courses and impaired function sit at the far end, quiet courses at the near end [1][13].

Ramps only through the gate: normal function, normalized troponin and CRP, quiet Holter and exercise ECG, resolved inflammation on CMR — a cardiologist closes each gate, and the ramp starts behind them: aerobic base, then intensity, then maximal work; moderate loads before maximal ones [1][13][14].

Never changes: the when-sick rules that would have kept most of this file's patients out of the acute ward in the first place — fever and chest symptoms are not training variables [1][4]; and the symptom line stays live for life, because a second inflammatory episode re-opens the door [3][13].

Keeps one dated ledger: symptoms, resting heart rate, sleep, session load — the columns the return ramp actually reads; a resting heart rate creeping 10 beats high with palpitations is a cardiology call, not a push-through test [13][14].

The Brazil anchors: the arbovirus heart, quantified

The pt-BR twin of this file exists for a Brazilian reader whose viral-illness landscape includes the arboviruses the temperate files treat as exotic — and both Brazil anchors are institution-led. The meta-analytic anchor: UNIVASF and Fiocruz's systematic review of heart disease in dengue, chikungunya and zika — 42 studies, 76,678 individuals — pooling cardiac involvement in dengue at 27.21% (with dengue myocarditis most frequent under age 20) and in chikungunya at 32.81% [15]. The autopsy anchor: the Fortaleza series that found lymphocytic myocarditis at autopsy in patients who died of dengue fever — the severe tail of exactly the involvement the meta-analysis prices [16]. For the Brazilian reader the practical splice runs through the existing dengue door: the phase rules there (nothing during the acute illness, the days around fever-defervescence the most dangerous of the infection) are, at the cardiac level, this door's window fence wearing mosquito-country clothes [4][15][16]. Chest symptoms or palpitations during dengue or chikungunya are the same-day troponin conversation this file leads with — in a country where the sickle-cell door and the heat columns already taught the same lesson: in tropical training conditions, the emergency fences are load-bearing year-round [15][16].

So what do you actually do? The practical file

Six rules, every one sourced from the columns above:

  1. Route chest symptoms during any viral illness today. Chest pain, pressure, palpitations or unexplained breathlessness near an infection is a same-day troponin, not a training question — the troponin leak is how this file opens [1][3].
  2. Honor the window absolutely. No training while symptomatic, none until biomarkers normalize — exercised coxsackie mice died at 20–40% versus 0–10% rested, and no guideline in forty years has overruled the experiment [2][4].
  3. Run the calendar, then the gate. Three to six months out of competitive sport; return only through normal function, normalized troponin and CRP, a quiet Holter and exercise ECG, and a resolved CMR — closed by a cardiologist [1][13][14].
  4. Price the scar, not the history. LGE carried HR 8.4 for mortality and zero patients without it died suddenly [5]; a normal CMR is 0.8%/year MACE and 0.3%/year death [6] — the scan is the verdict, not the diagnosis letter.
  5. Ramp like it's rehab, because it is. Aerobic base first, intensity before maxima, moderate loads before maximal ones, symptoms outranking the plan — and treat the self-ban as the other complication; the programmed return is its antidote [13][14].
  6. Keep the screening perspective. The pandemic arc ended where your risk assessment should: 789 pros screened, 0.6% confirmed, zero events on return [9]; routine panic-imaging is not the lesson — the gate for the diagnosed is [8][12].

How RightRep fits into this

The myocarditis file is, at its core, a calendar-and-dose-management question disguised as a fragility question — a door where the program's structure (rest window, graded ramp, symptom vigilance) is the entire recovery column, and where the reader's own logged history is the best ramp instrument he owns:

  • The window made auditable. A training log with a rest window in it — sessions marked zero by design rather than by drift — is the difference between a medical rest and a vacation; the calendar owns this door, and the calendar is what RightRep keeps [1][13].
  • The ramp enforced by arithmetic. The graded return lives or dies on holding each dose step long enough — a program that counts load and progression is the difference between a ramp and a relapse-shaped spike [13][14].
  • The symptom line, dated. Resting heart rate, sleep, session loads and symptom flags in one dated ledger is exactly the monitoring the follow-up consultations ask for — the column that turns "see how it feels" into data [13][14].
  • The comeback steered, not guessed. Rebuilding from recorded pre-illness loads, at recorded fractions, on recorded dates — the same comeback machinery the heart-attack and stroke doors prescribe [13][14].
  • The habit the whole file prices. Trained, tracked, progressive programming — plus honest sick-day rules — is the column that keeps most readers from ever needing this door [4].

The bottom line

  • The definitions column: troponin names the leak, CMR grades the injury — LGE is scar, and the non-invasive gold standard plus biopsy anchor the diagnosis [3][13].
  • The window column: forced swimming on days 1–9 of coxsackie infection took mouse mortality from 0–10% to 20–40% — the animal result behind every abstention rule since [4].
  • The rule column: ESC 2023 — 3–6 months out of competitive sport; return through normal function, normalized biomarkers, quiet Holter and exercise ECG, resolved CMR [1][13][14].
  • The prognosis column: Grün's 222 biopsy-proven — LGE HR 8.4 all-cause / 12.8 cardiac mortality, zero sudden deaths without LGE [5]; Gräni's 670 — a normal CMR worth 0.8%/yr MACE and 0.3%/yr death [6].
  • The screening-arc column: Rajpal 4/26 = 15% on CMR behind a clean triad [7] → Martinez 789 pros: 3.8% abnormal screens, 0.6% confirmed, zero events on return [9] → Starekova 145 at 1.4%, routine CMR screening "questionable" [8].
  • The denominator column: NCAA 20 years — SCD 1:63,682 athlete-years and falling; myocarditis adjudicated in 8 deaths in two decades; half of SCD exertional [10].
  • The honesty column: exercise-restriction advice is expert opinion, not trials [11]; one-size-fits-all called time [12]; persistent-LGE meaning unknown by trial [5][12][14].
  • The Brazil anchors: UNIVASF/Fiocruz — dengue cardiac involvement 27.21% pooled, chikungunya 32.81% [15]; Fortaleza — lymphocytic myocarditis at autopsy in fatal dengue [16].

Train like the file reads: window shut, gate closed, then ramp counted — and let the camera count the reps of the comeback at rightrep.app.

This post was written by the RightRep AI Assistant — the same AI that counts and scores your reps at rightrep.app.

Sources

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  2. Kindermann I, Barth C, Mahfoud F, et al. Update on myocarditis. Journal of the American College of Cardiology, 2012;59(9):779–792. pubmed.ncbi.nlm.nih.gov
  3. Caforio AL, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. European Heart Journal, 2013;34(33):2636–2648. pubmed.ncbi.nlm.nih.gov
  4. Kiel RJ, Smith FE, Chason J, Khatib R, Reyes MP. Coxsackievirus B3 myocarditis in C3H/HeJ mice: description of an inbred model and the effect of exercise on virulence. European Journal of Epidemiology, 1989;5(3):348–350. pubmed.ncbi.nlm.nih.gov
  5. Grün S, Schumm J, Greulich S, et al. Long-term follow-up of biopsy-proven viral myocarditis: predictors of mortality and incomplete recovery. Journal of the American College of Cardiology, 2012;59(18):1604–1615. pubmed.ncbi.nlm.nih.gov
  6. Gräni C, Eichhorn C, Bière L, et al. Prognostic value of cardiac magnetic resonance tissue characterization in risk stratifying patients with suspected myocarditis. Journal of the American College of Cardiology, 2017;70(16):1964–1976. pubmed.ncbi.nlm.nih.gov
  7. Rajpal S, Tong MS, Borchers J, et al. Cardiovascular magnetic resonance findings in competitive athletes recovering from COVID-19 infection. JAMA Cardiology, 2021;6(1):116–118. pubmed.ncbi.nlm.nih.gov
  8. Starekova J, Bluemke DA, Bradham WS, et al. Evaluation for myocarditis in competitive student athletes recovering from coronavirus disease 2019 with cardiac magnetic resonance imaging. JAMA Cardiology, 2021;6(8):945–950. pubmed.ncbi.nlm.nih.gov
  9. Martinez MW, Tucker AM, Bloom OJ, et al. Prevalence of inflammatory heart disease among professional athletes with prior COVID-19 infection who received systematic return-to-play cardiac screening. JAMA Cardiology, 2021;6(7):745–752. pubmed.ncbi.nlm.nih.gov
  10. Petek BJ, Churchill TW, Moulson N, et al. Sudden cardiac death in National Collegiate Athletic Association athletes: a 20-year study. Circulation, 2024;149(2):80–90. pubmed.ncbi.nlm.nih.gov
  11. Shyam-Sundar V, Mahmood A, Slabaugh G, et al. Management of acute myocarditis: a systematic review of clinical practice guidelines and recommendations. European Heart Journal – Quality of Care and Clinical Outcomes, 2024;10(8):658–668. pubmed.ncbi.nlm.nih.gov
  12. Claessen G, La Gerche A, De Bosscher R. Return to play after myocarditis: time to abandon the one-size-fits-all approach? British Journal of Sports Medicine, 2023;57(20):1282–1283. pubmed.ncbi.nlm.nih.gov
  13. Dores H, Dinis P, Puga L, Freitas A, Cardim N. Myocarditis in athletes: challenges for return to play. Revista Portuguesa de Cardiologia, 2026;45(6):307–317. pubmed.ncbi.nlm.nih.gov
  14. Yamagata K, Malhotra A. Return-to-play post-myocarditis for athletes: to play or not to play? Diagnostics, 2024;14(19):2236. pubmed.ncbi.nlm.nih.gov
  15. Nicacio JM, Gomes OV, Carmo RFD, et al. Heart disease and arboviruses: a systematic review and meta-analysis. Viruses, 2022;14(9):1988. pubmed.ncbi.nlm.nih.gov
  16. Torres AF, Braga DN, Muniz F, et al. Lymphocytic myocarditis at autopsy in patients with dengue fever. Brazilian Journal of Infectious Diseases, 2013;17(5):619–621. pubmed.ncbi.nlm.nih.gov