Pancreatitis-associated Myocarditis: Systematic Review and Meta-analysis of a Deadly Duo

Authors: Mattia Alberti, Alessandro Marcucci, Filippo Biondi, Simona Chiusolo, Gabriele Masini, Lorenzo Faggioni, Dania Cioni, Doralisa Morrone, Raffaele De Caterina, Emanuele Neri, Giovanni Donato Aquaro

Abstract

Graphical Abstract: Pancreatitis-associated myocarditis predominantly has a viral etiology and is more common in immunocompromised patients. Pancreatic involvement is usually mild, while myocardial involvement often leads to more severe adverse consequences, including major arrhythmias and significant mortality

INTRODUCTION

Acute pancreatitis, and its severe form in particular, is not a single-organ affection, but a systemic disease, which can evolve into a systemic inflammatory response syndrome. And culminate in multiple organ dysfunction syndrome.[1]

Underlying pathophysiological mechanisms include the activation of pancreatic enzymes, intestinal endotoxemia, and subsequent extensive cytokine release, resulting in severe microcirculatory impairment.[2]

As for the etiology of acute pancreatitis, it is most frequently attributed to the presence of gallstones impacting the main bile duct or excessive alcohol consumption, but it can also be caused by infectious or toxic agents, autoimmune diseases, congenital conditions, and iatrogenic factors.[3]

The majority of patients experience a mild disease course, characterized by significant clinical improvement through fluid administration, effective pain and nausea management, and early initiation of oral feeding.[4]

In contrast, the severe form of acute pancreatitis, affecting approximately 20%–30% of patients, poses a life-threatening risk with hospital mortality rates as high as 15%.[2]

Guidelines on both the diagnosis and risk stratification of acute pancreatitis are provided by the 2012 revision of the Atlanta classification.[5]

The clinically mild form, whose usual radiopathological correlate is interstitial edematous pancreatitis, is characterized by the absence of organ failure, local or systemic complications, and typically resolves within the initial week. In cases where transient (i.e., lasting <48 h) organ failure, local complications, or an exacerbation of comorbid diseases are present, the condition is classified as moderate. Patients experiencing persistent organ failure for more than 48 h are diagnosed with the severe form of the disease[6] and have necrotizing pancreatitis as their radiopathological correlate.

The severity and the extension of the systemic involvement are thus the prevailing factors in the prognosis of acute pancreatitis. While kidneys and lungs are most frequently affected, virtually any organ can be involved, including the heart.[7]

Still, available evidence on the characteristics of cardiac involvement in acute pancreatitis is limited in both quality and quantity.

A cross-sectional study by Chacón-Portillo et al.[8] enrolled 28 cases of acute pancreatitis irrespective of disease severity and documented a high prevalence of NT-pro-brain natriuretic peptide (BNP) elevation, variable electrocardiogram (ECG), and echocardiographic abnormalities, while troponin elevation was less frequent. Most of these changes were resolved after the acute phase.

Thandassery et al.[9] specifically enrolled patients with acute pancreatitis and hypotension and found a prevalence of cardiac dysfunction at echocardiography of 65%, which was diastolic in 60%, mixed in 23%, and systolic in 17% of cases. Mortality was high (19%).

A review of case reports by Khan et al.,[10] which is an update of a precedent study,[11] investigated 34 cases of acute pancreatitis with ECG changes suggestive of acute myocardial infarction. While 21% of patients died, most acute cardiovascular changes were reversed at discharge in those who survived.

Nadkarni et al.[12] prospectively evaluated 52 patients with pancreatitis and found cardiovascular changes in 50% of these. Mortality was 15% and the main adverse prognostic factors were represented by prolonged QTc interval, pericardial effusion, and diastolic dysfunction.

Taken together, these studies suggest that myocardial injury has a high prevalence in acute pancreatitis, and predicts a higher mortality. However, since the cardiac abnormalities are mostly reversible, the diagnosis of a pancreatitis-associated specific cardiac disease (e.g. myocardial infarction) is anecdotal in the medical literature.

In line with this, two recent studies have interrogated two large medical databases and documented that type 2 myocardial infarction and acute coronary syndrome are very rarely co-diagnosed with acute pancreatitis.[1314]

Several molecular mechanisms have been proposed to be responsible for myocardial injury associated with acute pancreatitis, including pancreatic enzyme activation, intestinal endotoxemia, cytokine activation, microcirculation impairment, autonomic system dysfunction, and autophagy dysregulation, as summarized in a comprehensive review by Luo et al.[15]

Interestingly, however, no consideration has been given to the hypothesis that cardiac involvement could arise not only as a consequence of pancreatitis, i.e. in the form of myocardial injury, but also as a direct effect of the etiologic agent causing pancreatitis, i.e., in the form of pancreatitis-associated myocarditis.

It can be certainly speculated that the blood-borne dissemination of pathogens may lead to myocarditis, especially in patients with a heightened susceptibility to infection and compromised endothelial blood-barrier function.

Acute myocarditis is a serious, likely underdiagnosed[16] condition affecting people of all ages. The etiology of this condition is diverse, encompassing infectious, inflammatory, and toxic factors. Its clinical manifestations are broad and often overlap with those of other acute cardiac disorders, which poses a diagnostic challenge.

Currently, cardiovascular magnetic resonance imaging (CMR) stands as the gold standard for the noninvasive diagnosis of myocarditis, which is preferred over endomyocardial biopsy (EMB) in cases of hemodynamically stable acute myocarditis.[1718]

When an underlying cause is identified, targeted therapy may be employed; however, in most cases, the treatment focuses on providing supportive care and managing complications such as heart failure or arrhythmias.[18]

Growing evidence supports the use of immunosuppressive therapy in selected cases.[18]

The prognosis is generally favorable, with most patients experiencing a full recovery.[18]

For those who develop left ventricular dysfunction, it is usually transient, similar to takotsubo syndrome or peripartum cardiomyopathy.[19]

Nevertheless, up to 30% of individuals with biopsy-confirmed myocarditis may progress to develop dilated cardiomyopathy and its potential associated complications.[18]

This review aims to present a case report of pancreatitis-associated myocarditis and to systematically assess the medical literature to characterize risk factors, clinical features, and prognostic implications associated with this condition.

Case vignette

We describe the case of a 67-year-old Caucasian woman with a medical history notable for hypothyroidism and an appendectomy due to appendicitis.

She was admitted to the emergency department of our hospital with acute nonlithiasic pancreatitis as diagnosed by abdominal computed tomography (CT), which revealed edematous pancreatitis [Figure 1].

The routinely performed ECG showed a new left bundle branch block (LBBB), prompting a more comprehensive assessment of the cardiac status [Figure 2].

A transthoracic echocardiogram (TTE) revealed a moderately reduced (35%) left ventricular ejection fraction (LVEF), severe mitral regurgitation, and an elevated estimated pulmonary systolic pressure.

Initial blood tests showed elevated levels of BNP at 196 pg/mL, thyroid-stimulating hormone at 0.01 mIU/L, high sensitivity cardiac troponin T (hs-cTnT) at 1856 ng/L, amylase at 2379 U/L, and lipase at 3467 U/L with an estimated glomerular filtration rate (eGFR) of 92 ml/min.

Supportive therapy including intravenous fluids and antibiotics was initiated and over a few days, her blood test normalized, with troponin decreasing to 6.6 ng/L, amylase to 77 U/L, and lipase to 35 U/L.

A TTE was then repeated and showed a slightly improved but persistently depressed LVEF.

Before discharge, cardiac magnetic resonance (CMR) was also performed, confirming LVEF reduction and showing lateral wall transmural hyperintensity in T2W imaging and subepicardial late gadolinium enhancement (LGE) in T1-GRE-IR sequence acquired 8–10 min after contrast media administration, consistent with acute myocarditis [Figure 3].

The patient was then discharged with HF guideline-directed medical therapy according to 2023 ESC guidelines[20] with a scheduled 3-month follow-up visit, including CMR to evaluate the appropriateness of cardiac resynchronization therapy (CRT).

CMR examination performed 3 months later showed a significant improvement in LVEF, complete edema resolution, and the persistence of subepicardial lateral wall LGE, consistent with past myocarditis [Figure 4].

Subsequently, a coronary CT scan ruled out significant coronary artery disease.

The 6-month clinical follow-up revealed that the patient had remained asymptomatic since discharge and LVEF had normalized, as assessed by TTE.

Consequently, despite the persistence of LBBB, CRT was not deemed necessary, and an annual follow-up was scheduled.

Both clinical characteristics and hospital course of the case presented are consistent with the results of our The patient had no traditional pancreatitis risk factors and CT imaging was consistent with edematous pancreatitis more often associated with a viral, hence systemic etiology.

The hospital course was uncomplicated and follow-up up regular.[21]

MATERIALS AND METHODS

We included case reports in which a diagnosis of pancreatitis was made according to the Atlanta classification of acute pancreatitis plus any evidence of myocardial involvement.[222324252627282930313233343536373839404142434445464748495051]

Myocardial involvement is signaled by the presence of both suggestive clinical features (cardiac chest pain, palpitation, dyspnea, cardiogenic shock) and imaging (TTE, CMR) or electrocardiographic abnormalities (i.e., new onset of arrhythmias, ST-T changes).

Studies included in the review were selected amongst records retrieved through a PubMed search; all passages are shown in the PRISMA Flowchart.

The search used the following “myocarditis AND pancreatitis.” No limits on publication year, language, country, and study size were applied.

The search produced 244 results. Records were screened by two independent authors and discrepancies were solved by discussion.

We excluded duplicates (n = 3), nonclinical studies (n = 88), animal studies (n = 47), and autopsy case series (n = 7).

The full-texts were independently assessed by the same two authors. Sixty-six studies were deemed not pertinent to our research and excluded; two did not adhere to current guidelines; eight did not clearly document myocardial involvement. Thirty-one studies were thus included in the review.

A database was organized and structured. Data on the following variables were collected and

• Patient demographics (sex, age, country) and background therapy
• Pancreatitis causes (toxic, viral, autoimmune, bacterial, etc.,) and risk factors (alcohol use, gallstones, hypertriglyceridemia)
• Cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes)
• Presence and cause of immunodeficiency, if present (e.g., immunosuppressive therapy, AIDS, corticosteroids, cancer)
• Latency between pancreatitis and myocarditis diagnosis
• Pancreatitis clinical presentation (e.g., abdominal pain, nausea, vomiting, etc.), diagnostic methods (magnetic resonance imaging [MRI], CT, abdominal ultrasound, amylase, lipase), radiological variant (edematous or necrotizing), complications (e.g., distributive shock), treatment (e.g., fluid resuscitation, IV antibiotics, etc.)
• Myocarditis clinical presentation (e.g., arrhythmias and hypotension), diagnostic methods (CCTA, coronary angiography, ECG, TTE, EMB, CMR, TnT, TnI, CK-MB, NT-proBNP), complications (e.g., cardiogenic shock, pulmonary edema), treatment (e.g., inotropes, vasopressors)
• Clinical features and laboratory results (bilirubin, alkaline phosphatase, aspartate transaminase, alanine transaminase, polymerase chain reaction, erythrocyte sedimentation rate, eGFR, leukocytes, procalcitonin, specific antibodies, lactates, glucose, Hb, pH, electrolytes, etc.)
• Patient outcome (duration of hospital stay, in-hospital or postdischarge death, measurements of patient status at follow-up, if available).

The Kolmogorov–Smirnov test was utilized to test for the normal distribution of continuous variables. Variables having a normal distribution were shown as mean standard deviation, while nonnormally distributed variables were shown as median and 25^th^–75^th^. The Fisher‘s exact test or the Chi-square test was used when appropriate to compare categorical variables. The Wilcoxon nonparametric or ANOVA test was used when appropriate to compare continuous variables. Bonferroni corrections were also applied where necessary. A P < 0.05 was considered statistically significant.

RESULTS

Overall, 31 studies were included in the analysis, for a total of 31 patients.

Seventeen were males (55%) and 14 females (45%) with a mean age of 31 ± 18 years.

Clinical characteristics are summarized in Table 1. The etiology of pancreatitis was viral in 16 patients (52%), bacterial in 6 (20%), toxic in 5 (16%), autoimmune in 3 (9%), and idiopathic in 1 (3%).

Seven (23%) patients had identifiable causes of in particular, 6 were being treated with immunosuppressive therapy and one was affected by HIV-related immunocompromise.

Notably, no case was associated with alcohol and/or biliary lithiasis.

The median peak levels of pancreatic enzymes were 366 (282–1853) UI/L for amylase and 1485 (320–10351) UI/L for lipase.

Three patients had identifiable cardiovascular risk diabetes in two patients and arterial hypertension in one.

Imaging studies revealed that 19 were affected by edematous pancreatitis and five by necrotizing pancreatitis.

In the majority of cases, the presentation of myocarditis was severe with cardiogenic shock occurring in 11 (35%) patients and cardiac arrest or sustained ventricular tachycardia (sVT) in seven (19%).

Among the patients with cardiogenic shock, three also experienced a resuscitated cardiac arrest.

Overall, severe myocarditis, defined by cardiac arrest and/or cardiogenic shock and/or sVT, was observed in 15 patients (48%).

While 2 patients (6%) reported chest pain, in the remaining 12 patients, myocarditis was diagnosed because of ECG and/or laboratory findings (elevated cardiac enzymes such as creatine phosphokinase-MB and/or high-sensitivity Troponin T or I).

The severity of pancreatitis (edematous vs. necrotizing) was not associated with the severity of severe myocarditis occurred in 42% of edematous and in 60% of necrotizing pancreatitis (P = 0.56).

Similarly, the occurrence of severe myocarditis was not associated with the peak levels of amylase and lipase (respectively, P = 0.98 and 0.83).

Severe myocarditis occurred more frequently in males than in females (65% vs. 21%, P = 0.026).

Particularly, cardiac arrest was more frequent in males than in females (P = 0.018).

Severe myocarditis occurred in 4 out of 5 cases (80%) of leptospirosis pancreatitis, in 6 out of 15 (40%) viral pancreatitis (including 3 Coxsackievirus, 1 Mumps, 1 Epstein–Barr Virus, and 1 severe acute respiratory syndrome corona-virus 2 [SARS-CoV-2]), and in 1 case of typhoid fever.

The remaining 3 cases of severe myocarditis occurred in toxic pancreatitis (aluminum phosphide ingestion for suicide attempt, iatrogenic foscarnet toxicity, and scorpion sting).

In 24 patients (77%), myocarditis was contemporary with pancreatitis, in 5 patients (16%), myocarditis occurred after a median of 7 (interquartile range [IQR] 5–11) days following pancreatitis and, in the remaining 2 patients (7%), myocarditis even preceded pancreatitis.

Myocarditis occurring contemporary with pancreatitis was severe in 13 (54%) cases, while late myocarditis met severity criteria in two cases (40%). No case of myocarditis preceding pancreatitis was severe.

ECG abnormalities were found in 16 patients (51%), including ST elevation in three patients (9%), negative T wave and/or ST depression in 10 patients (33%), and new conduction disorders in three (10%).

One of these patients was affected by left ventricular branch block (LBBB), one by right ventricular bundle branch block, and one by 3^rd^ degree AV block.

The median hs-cTnT value was 342 (IQR 73–890) ng/L and that of NT-proBNP was 11053 pg/mL (IQR 1397–26,150).

Transthoracic echocardiography (TTE) was performed in 17 patients (55%) showing normal LVEF in two patients and LV dysfunction in 15 (mildly reduced LVEF in four, moderately reduced LVEF in four, and severely reduced LVEF in seven). The average LVEF was 33% ± 13%.

CMR imaging (CMR) was conducted in four patients, revealing myocardial edema in T2-weighted pulse sequences and LGE in all but one case, in which CMR was performed late after complete recovery from cardiogenic shock and exhibited pericarditis with no myocardial findings.

EMB was performed in 6 patients (19%).

The treatment was heterogeneous and individualized. Fluid resuscitation was required in 6 patients, with 5 needing vasopressors and 3 of those also receiving inotropes. Corticosteroids were administered to 3 patients, while antivirals (acyclovir, foscarnet, vidarabine) were used in another 3. Hemodialysis and ventilatory support were necessary for 2 patients each, and 2 required permanent pacemaker implantation. One patient underwent percutaneous coronary angioplasty due to cardiogenic shock.

During the hospitalization, death occurred in four patients (13%): two due to cardiac arrest and two due to pancreatitis-related complications (septic shock in one and hyperosmolar coma in another).

Three out of 4 deaths occurred in patients with necrotizing pancreatitis (P = 0.0004). Interestingly, only 1 patient with severe myocarditis died during hospitalization.

TTE was performed in 10 patients before discharge, revealing complete LVEF recovery in eight patients and partial recovery in two.

Short-term follow-up was performed on 15 12 of them reported clinical well-being while the other three died.

All of these had been affected by necrotizing pancreatitis at presentation.

Of the 15 patients with severe myocarditis, follow-up was available for 10 patients, with seven demonstrating complete recovery of cardiac function and three showing only partial recovery.

DISCUSSION

To the best of our knowledge, this review represents the first-ever comprehensive review of existing literature on the association of myocarditis and pancreatitis.

The main results of the study may be summarized as

• Although myocarditis is an infrequent complication of pancreatitis, it is associated with a high risk of severe complications such as cardiac arrest and/or cardiogenic shock, which was found in 48% of cases of the present study
• No clear correlation emerged between the severity of myocarditis and that of pancreatitis or serum levels of amylase and lipase
• Severe myocarditis was observed primarily in patients with infective pancreatitis (particularly with leptospirosis) or with toxic pancreatitis and not with the more common alcoholic or lithiasis pancreatitis
• Despite the presentation, complete recovery occurred in the majority of cases.

By comparing the existing knowledge regarding individual etiological agents and their roles in either myocarditis or pancreatitis with the data we have compiled, we can infer that several pathophysiological mechanisms may be involved.

A direct organ infection is commonly observed in viral etiologies, such as coxsackie B and HIV infections, as evidenced by the frequent presence of viral particles in endomyocardial biopsies or pathological studies.[52]

Different serotypes of Coxsackievirus B4 have been found to cause both acute and chronic pancreatitis, possibly due to different immune-mediated mechanisms[53] and are a well-established causative agent of myocarditis, hepatitis, skin rashes, aseptic meningitis, and acute renal failure.[545556575859]

While multiorgan involvement due to Coxsackievirus B is relatively uncommon, severe cases have been reported including multiorgan failure in infants[60] and severe myopericarditis in young adults.[61]

Notably, there have been reported cases of triple organ involvement, encompassing the heart, pancreas, and liver, attributed to different coxsackievirus strains, such as CVB215 and coxsackievirus A4.4.[62]

Another case documented myopericarditis, pleuritis, and acute liver failure caused by Coxsackievirus B, accompanied by elevated serotype titers of CVB1, CVB2, and CVB6.[63]

Coxsackieviruses are known to follow a multiphasic course, characterized by what Zaoutis and Klein termed “minor viremia” during initial organ seeding infection and “major viremia” when viral replication becomes more prominent within those affected organs.

Furthermore, experimental studies involving mice inoculated with various CVB strains have demonstrated a sequence of pancreatitis followed by myocarditis.

Currently, the primary approach to treating coxsackievirus infections is still based on supportive measures.

Direct damage as an initial mechanism may also be seen in the early phase of leptospirosis infection, which may also cause an inappropriate systemic inflammatory response resulting in diffuse endothelial damage which can mimic ischemia-like damage.

The manifestations of leptospirosis vary widely, ranging from mild subclinical febrile illness-to-severe and life-threatening organ dysfunction.

This severe form is known as Weil‘s disease and can involve jaundice, renal failure, pulmonary hemorrhage, acute respiratory distress syndrome, myocarditis, and rhabdomyolysis.

Hyperamylasemia has been reported in leptospirosis, with or without pancreatitis.[64]

Only a few reported cases have documented pancreatitis, though necrotizing pancreatitis has been observed in autopsies.[65]

Similarly, myocarditis is likely an underreported complication of leptospirosis, as corroborated by autopsy findings.[66]

Leptospirosis can be effectively treated with antibiotics, therefore a prompt diagnosis of leptospira-related myocarditishas a notable importance. Timely intervention is indeed crucial to prevent the exacerbation of cardiac involvement and the development of multiorgan dysfunction.

An inappropriate systemic inflammatory response is also particularly pronounced in conditions like COVID-19.[67]

COVID-19 in adults typically manifests in three distinct The early infection stage, the pulmonary phase, and the hyperinflammatory phase.[68] The latter is characterized by a cytokine storm[6970] and secondary hemophagocytic lymphohistiocytosis,[71] resulting in an ineffective cytotoxic response with elevated interleukin-6 levels, which can impair the normal activation of T lymphocytes.

In children, severe presentations of COVID-19 have led to the establishment of the term “Pediatric Inflammatory Multisystem Syndrome temporally associated with SARS-CoV-2” (PIMS-TS), also known as “Multisystem Inflammatory Syndrome in Children” by the Royal College of Pediatrics and Child Health. This syndrome encompasses persistent fever, inflammation, and evidence of single or multi organ dysfunction, including shock, cardiac, respiratory, renal, gastrointestinal, or neurological disorders. It is diagnosed after excluding any other microbial causes, with the presence of evidence linking the condition to COVID-19 infection.

In case series involving patients with PIMS-TS or Kawasaki-like disease, it has been observed that patients may experience shock, necessitating fluid resuscitation, and inotropic support.[72737475]

Direct organ damage may also be caused by dysregulated immune cells. This mechanism is characteristic of autoimmune disorders as in systemic lupus erythematosus(SLE). However, Lupus myocarditis is uncommon, especially as an initial manifestation.[767778]

SLE is a chronic autoimmune disease characterized by numerous autoantibodies, immune complex formation, and involvement of multiple organs. The diagnostic criteria set forth by the American College of Rheumatology are the most recent criteria used for diagnosing SLE.[79]

Myocarditis is a relatively rare feature of SLE, and its clinical presentations vary, ranging from asymptomatic cases to those manifesting as cardiogenic shock; however, global hypokinesia with a low ejection fraction on echocardiography is frequent.

Myocardial biopsy is infrequently performed due to perceived risks and the low specificity of histological findings.[77] Notably, SLE is also a rare, but well-known cause of pancreatitis.[80]

While the exact pathogenic mechanisms of SLE-associated pancreatitis remain unclear, potential contributors include vasculitis, hemolysis, micro-thrombus formation, the presence of anti-pancreatic antibodies, and inflammation resulting from T-cell infiltration and complement activation.[78]

The use of corticosteroid therapy remains a topic of debate, however, mounting evidence suggests that the immunosuppressive effects of corticosteroids are crucial not only for ameliorating multiorgan involvement but also for reducing mortality associated with SLE.[81]

In the present study, we found that immunodepression was documented in 23% of patients. HIV infection and immunosuppressive therapy may facilitate viral infections and multiorgan involvement.

Finally, a direct cytotoxic effect is the predominant mechanism of toxic substances and drugs such as aluminum phosphide, foscarnet, pembrolizumab, and zinc phosphide. Their toxic effects are well-documented and known to be dose dependent.[828384]

In our study, we found a single case reported in the literature of a scorpion sting resulting in both myocarditis and pancreatitis eventually leading to cardiac arrest and death.[828384]

The main limitation of the present study is the heterogeneity of the included papers in the analysis.

Heterogeneity is caused by the rarity of concomitant occurrences of myocarditis and pancreatitis, however, this paper marks the first attempt to systematically assess the relation between pancreatitis and myocarditis establishing a foundation for future investigations.

Upcoming studies could leverage the increasingly valuable role that MRI has played in recent years for assessing both cardiac and pancreatic diseases. Key studies by Wang et al. and Beleù et al. explore the clinical applications and advancements in this technology, particularly in understanding pancreatic tissue composition and detecting early pathological changes.[8586] These studies show that techniques currently used for cardiac assessment, such as T1 mapping and T2 mapping, also correlate with fibrotic and inflammatory changes in pancreatic tissue. Future research could establish the potential for a comprehensive MRI approach to simultaneously assess cardiac and pancreatic diseases in both clinical and research settings.

A definitive diagnosis of myocarditis should be established through either CMR imaging (CMR) or EMB which were performed in only 10 out of the 31 cases analyzed. However, considering the clinical presentation, the rise of troponin, and ECG modifications the diagnosis of myocarditis was the most probable scenario in every case.

CONCLUSIONS

Myocardial involvement should be considered in acute pancreatitis patients presenting with symptoms such as chest pain, hemodynamic instability, or electrocardiographic abnormalities, especially in nonlithiasis or alcohol-related pancreatitis.

Troponin assays should be performed when a viral or bacterial (mostly leptospirosis) etiology is suspected or in case of toxic pancreatitis.

Mixed shock, characterized by both distributive and cardiogenic components, is relatively common in this cohort, often associated with a reduced ejection fraction, as shown on TTE.

A definitive diagnosis of myocarditis typically necessitates either EMB or CMR, with the latter being the preferred noninvasive diagnostic tool as it aids in risk stratification on discharge.

Long-term outcomes for this specific subset of myocarditis remain uncertain; further research is warranted to ascertain whether this subset exhibits a better or worse prognosis compared to lone myocarditis.

Conflicts of interest

There are no conflicts of interest.