Acute myocarditis in a young male after gastroenteritis: A case report
and literature review
Abstract
Gastroenteritis can be associated with life-threatening complications
like myocarditis. A 16-year-old male presented with acute myocarditis
mimicking STEMI after gastroenteritis. He made an uneventful recovery
after appropriate treatment. This case report highlights that clinicians
should be aware of this rare, but serious, cardiac complication when
treating patients with gastroenteritis.
Keywords: Myocarditis, Gastroenteritis, Electrocardiogram (ECG),
ST-elevation myocardial infarction (STEMI)
Introduction
Myocarditis is the inflammation of the myocardium and pericarditis is
the inflammation of the pericardium. When these two clinical conditions
co-exist, it is termed myopericarditis or perimyocarditis. The incidence
of myocarditis is under-recognized, with 1.8 million cases worldwide per
year. [1] Myocarditis and cardiomyopathy are the
third leading cause of death among young adults, accounting for 2-42%
of sudden cardiac deaths. [2] [3]
Case report
A 16-year-old male presented to the emergency department (ED) with
severe central chest pain, sweating, dyspnea, and palpitation. Before
that, he had a 3-day history of profuse, watery diarrhea, vomiting,
epigastric pain, and fever. He recalled eating some local street food.
He has been fully vaccinated against COVID-19 including a booster dose.
His last vaccine date was 3months ago. Upon arrival to ED, he was in
pain with blood pressure (BP) 130/80mmHg, heart rate (HR) 100 beats per
minute, temperature 100’F, and oxygen saturation (SpO2) 100% on room
air. Cardiac examination was unremarkable with no audible murmurs or
pericardial friction rub. Lungs were clear. Abdominal examination showed
mild tenderness in the epigastric area. There was no jaundice, bleeding
manifestations, or rashes.
Electrocardiogram (ECG) on admission showed T inversion in aVR and V1
with ST elevation in other leads without reciprocal ST depressions.
(Figure 1) Chest radiography (CXR) was unremarkable. (Figure 2) Initial
troponin-T was 351 pg/ml, and a repeat assay 6 hours later was 1176
pg/ml, with a maximum on the 3rd day (1573 pg/ml).
(Figure 3) Other laboratory results were as follows. (Table 1)
Salmonella typhi and Salmonella paratyphi A & B antigens were negative.
Stool culture did not show any pathogen. The COVID-19 antigen test was
negative. Serial ECG 12 hours later showed new morphological changes in
ST segments; ST elevation with upward concavity with notched and slurred
terminal QRS. (Figure 4) Transthoracic echocardiography (TTE) showed
mildly reduced left ventricular ejection fraction (LVEF) of
approximately 45% with no regional wall motion abnormalities or
pericardial effusion. (Figure 5/ video 1). Cardiac MRI and
endomyocardial biopsy (EMB) have not been done due to limited resources.
Based on clinical symptoms, laboratory parameters, and ECG findings,
post-gastroenteritis perimyocarditis was a provisional diagnosis. He was
initially treated with intravenous fluids, antibiotics, prophylaxis
subcutaneous low-molecular-weight heparin, low-dose β-blocker, and
angiotensin-converting enzyme inhibitor (ACEI). ECG on
3rd day showed evolutionary changes like ST elevation
falling back with diffuse T wave inversion. (Figure 6) He responded well
to treatment with troponin-T level decreasing to 46.12 pg/ml. He was
discharged on day 7. At follow-up, one month after discharge, he was
symptoms-free with normal LVEF and normal ECG.
Discussion
The etiologies of myocarditis are multifactorial: infections (viral,
bacterial, fungal, parasitic), systemic diseases (autoimmune,
malignancy), drug hypersensitivity, and toxins.[3] It occurs mostly in young males, without
conventional risk factors for atherosclerosis. Inflammation of the
myocardium due to direct invasion by pathogens, post-infectious immune
reaction, toxic injury, or ischemic insult stimulate innate, humoral
(autoreactive antibodies), and cell-mediated (T lymphocytes) immune
responses. This leads to myocytes necrosis and cell death. Chronic
myocarditis results in myocytes fibrosis, structural remodeling, and
cardiomyopathy. [4] [5] Myocarditis can
present with ACS-like presentation, heart blocks, ventricular
arrhythmia, cardiogenic shock, and sudden cardiac death.[3] Chest pain is usually due to immune-mediated
coronary vasospasm or co-existed pericarditis.
A standard 12-lead ECG is recommended in all patients.[3] Sinus tachycardia, non-specific ST/T changes,
and variable heart blocks are the most common. In 2012, a study by
Gaetano Nucifora et al. revealed that the sum of ST-elevation (sumSTE),
normalization of STE after 24 hours, and development of negative T wave,
have significant relation to the extent of myocardial damage. In
infarct-like myocarditis, STE is followed by gradual normalization of ST
segment, and occurrence of T wave inversion. [6]Perimyocarditis, should be suspected if ECG shows PR depression or STE
with upward concavity, with or without terminal QRS notching or
slurring. [7] In our case, diffuse STE with upward
concavity and both notched and slurred terminal QRS can be seen. (Figure
4) Thus, we suspect both pericarditis and infarct-like myocarditis
simultaneously occur.
In myocarditis, troponin levels gradually rise with a peak on the
2nd or 3rd day.[8] Troponins, erythrocyte sedimentation rate
(ESR), and CRP levels should be measured in all patients although
routine viral serology is not recommended. [3]N-terminal pro-BNP (NT- proBNP) may be useful prognostic markers.
Echocardiography (Echo) is recommended by ESC for serial non-invasive
monitoring of cardiac function. Cardiac MRI (CMR) has 100% sensitivity
and 90% specificity in detecting. [9] According
to the “Lake Louise Criteria”, the presence of mid-myocardial and
epicardial or patchy late gadolinium enhancement (LGE) indicates acute
myocarditis. [6] Cardiac computed tomography (CT)
may be used if CMR is not accessible. Endomyocardial biopsy (EMB) is the
gold standard to confirm the diagnosis and its etiology. However, its
use is limited because of invasiveness and low sensitivity. Thus, EMB is
not usually recommended except for some clinical settings.[3] [10]
Acute myocarditis resolves spontaneously in about 50% of cases.
Physical activity should be restricted for at least 6months. Aspirin
should be used with caution and other non-steroidal anti-inflammatory
drugs (NSAIDs) should be avoided. ACEIs or angiotensin-receptor blockers
(ARBs), β-blockers, diuretics, and aldosterone antagonists can be used
as heart failure therapy. Hemodynamically unstable patients may need
positive inotropic agents and mechanical circulatory support.
Anti-arrhythmic medications, implantable cardioverter defibrillators
(ICD), or temporary pacemakers may be required in patients with
arrhythmias or heart blocks. Role of anti-viral remains controversial.
Immunosuppressive therapy may be beneficial in some cases. Other
immunomodulatory therapies like high-dose intravenous immunoglobulin
(IVIG) and immunoadsorption (IA) have been shown to improve LV function
in some studies. However, larger randomized controlled clinical trials
are needed to determine their efficacy and safety.[3] All patients with myocarditis should undergo
regular monitoring at a cardiology clinic for long-term complications.
Conclusion
Myocarditis is not uncommon in clinical practice. It should be
considered an important differential diagnosis when a young patient,
with no significant cardiovascular risk factors, presents with acute
chest pain. A history of recent viral infection supports the diagnosis.
Timely diagnosis and management is the key to improve patient outcomes.
This case highlights that clinicians should be aware of this potentially
lethal cardiac manifestation when treating a patient with
gastroenteritis.