Acute gastroenteritis is one of the most common infectious diseases worldwide. Its incidence is underestimated because not everyone with acute gastroenteritis seeks medical attention due to its self-limiting nature. Viruses (rotavirus, norovirus, enteroviruses) account for most cases of acute gastroenteritis. The other causes are bacteria (1-6%), medications, and toxins [1]. It usually presents with nausea, vomiting, watery diarrhea, abdominal pain, and fever, and usually resolves within 1 to 2 weeks.

Viral gastroenteritis can be associated with viral myocarditis. Direct invasion and replication of the virus itself and subsequent activation of immune response cause cytokines release, which results in myocyte inflammation and necrosis [2]. Cardiac electrical instability due to myocyte death, Viral-related ion channel impairment, and abnormal automaticity are supposed mechanisms for arrhythmogenicity in acute viral myocarditis [3]. Clinical features of acute myocarditis are variable: mild asymptomatic, chest pain mimicking myocardial infarction, palpitation due to brady-tachy arrhythmia, dyspnea, and in most severe forms, can present with life-threatening arrhythmia, acute heart failure, and sudden cardiac death [4].

The standard 12-lead ECG is the initial investigation although its sensitivity is low (47%) [5]. Sinus tachycardia with non-specific ST-T wave changes is the most common ECG finding. Conduction system disturbance can lead to various forms of brady-tachy arrhythmia. The most common bradyarrhythmias in acute myocarditis are sinus arrest, sick sinus syndrome, and AV blocks [6]. Apart from sinus tachycardia, acute myocarditis can also present with atrial fibrillation, atrial flutter, supraventricular tachycardia, and ventricular fibrillation [7]. ST segment changes, either elevation or depression can also be seen in ACS-like myocarditis [4].

Measurement of cardiac enzymes and biomarkers (Troponins and NT-proBNP) can also be used as indirect evidence of myocyte damage. Echocardiography is a valuable non-invasive imaging test and it can detect left ventricular systolic dysfunction, wall motion abnormalities, and chamber dilatation. Other advanced investigations include cardiac MRI (CMR), cardiac CT, and endomyocardial biopsy (EMB). Late gadolinium enhancement at CMR is a diagnosis of acute myocarditis and is associated with poor prognosis [8].

Management mainly depends on presenting symptoms. Acute myocarditis has a good prognosis with spontaneous recovery seen in about 50%. ACEI or angiotensin-receptor blockers (ARBs), β-blockers, diuretics, and aldosterone antagonists are first-line medications for heart failure treatment. Circulatory support (either inotropic agents or mechanical) may be required in fulminant myocarditis. Bradyarrhythmia needs close cardiac monitoring because it can progress to high-grade atrioventricular block, sinus arrest, and asystole. Temporary pacing may be a consideration. Pharmacological or mechanical cardioversion should be considered in patients with atrial or ventricular fibrillation with hemodynamic compromise. Anticoagulation may be needed and beneficial if there is a risk of arterial and venous thromboembolism associated with atrial fibrillation or concomitant myocardial ischemia cannot be excluded [9]. Long-term antiarrhythmic medications, implantable cardioverter defibrillators (ICD), or permanent pacemaker insertion may be warranted if tachy or brady arrhythmia persists after acute illness subsides. The role of anti-viral is unclear. Immunosuppressive therapy, immunomodulatory therapies like high-dose intravenous immunoglobulin, and immunoadsorption (IA) may be used in special cases. All patients with acute myocarditis should limit physical activity for at least 6months [10]. Regular ECG and echocardiographic monitoring are essential for the early detection of complications due to chronic myocarditis.