Myocarditis is an inflammatory disease of the myocardium with a broad variability in clinical presentation, ranging from an asymptomatic course, palpitations, severe chest pain, to sudden cardiac death. There are typically three patterns of myocarditis presentation: pseudo-infarctual chest pain, heart failure, and arrhythmias [1]. Based on these different patterns of presentation, a risk stratification model has been proposed that categorizes patients with myocarditis into three different groups: low-risk, intermediate-risk, and high-risk. Each group requires different follow-up and has a distinct prognosis [2,3]. The etiology of myocarditis often remains undetermined. However, viral infections are responsible for the majority of myocarditis cases, but other infectious agents, drugs, toxins, and systemic diseases can also be incriminated [3,4]. Although endomyocardial biopsy remains the gold standard for diagnosing myocarditis, its limited routine use has led to an increased reliance on advanced cardiac imaging techniques, particularly cardiac magnetic resonance. Early and accurate identification is clinically important, as approximately 20% of patients with acute myocarditis progress to dilated cardiomyopathy, in which heart failure becomes the predominant clinical presentation [1,4]. Moreover, the risk of developing heart failure during follow-up appears to be influenced by patient age, with a higher incidence reported among individuals over 50 years compared to younger patients [5]. Given these considerations, the treatment approach for myocarditis should be guided by the pattern and severity of the clinical presentation, the immediate response to standard therapies, and any spontaneous or treatment-induced improvements [3]. In this context, the present paper reports the case of a 25-year-old patient with myocarditis who exhibited two characteristic clinical patterns of myocarditis, namely acute severe chest pain and subsequent heart failure, managed with standard therapy complemented by an SGLT2 inhibitor to support cardiac recovery.

This case report was prepared in adherence to institutional ethical regulations and the principles outlined in the Declaration of Helsinki. Written informed consent was obtained from the patient for diagnostic procedures, treatment, and the use of anonymized clinical information and imaging for publication. Clinical information was obtained throughout the patient’s admission to the Cardiology Department of Pius Brînzeu County Clinical Emergency Hospital, Timișoara. The diagnostic work-up comprised a comprehensive clinical assessment, including detailed medical history, physical examination, 12-lead electrocardiography (ECG), transthoracic echocardiography (TTE), serial quantification of cardiac biomarkers, invasive coronary angiography, and cardiac magnetic resonance imaging (CMR). Quantified biomarkers included high-sensitivity cardiac troponin I (hs-cTnI), creatine kinase (CK), CK-MB isoenzyme, C-reactive protein (CRP), and N-terminal pro-B-type natriuretic peptide (NT-proBNP), all processed using standardized laboratory methodologies. Echocardiographic evaluation was performed to assess global and regional ventricular systolic function, detect focal wall motion abnormalities, and exclude pericardial effusion. A coronary angiography was performed via radial access, employing standard contrast protocols, in order to exclude obstructive coronary artery disease. CMR was conducted using a 1.5-Tesla system with dedicated sequences for myocardial edema and late gadolinium enhancement. The imaging diagnosis of myocarditis was established according to the updated Lake Louise Criteria, integrating both T2-based edema markers and non-ischemic LGE distribution. Management strategies were aligned with contemporary European Society of Cardiology (ESC) clinical practice guidelines for myocarditis and heart failure, including evidence-based pharmacologic therapy aimed at optimizing cardiac function and preventing adverse remodeling.

A 25-year-old male with no prior history of cardiovascular disease or identifiable risk factors presented to the Emergency Department of Pius Brînzeu County Clinical Emergency Hospital, Timișoara, with acute-onset, severe retrosternal chest pain that had progressively worsened over the previous 12 h. The pain was associated with dyspnea, fatigability, and profuse diaphoresis. He reported mild, nonspecific symptoms suggestive of an upper respiratory tract infection approximately three days prior to presentation. On physical examination, the patient was diaphoretic and afebrile, with stable hemodynamics and no evidence of respiratory insufficiency. Cardiac auscultation revealed regular heart sounds without murmurs. Lung examination demonstrated normal, symmetrical vesicular breath sounds without adventitious sounds. All the other findings were within normal limits.

The electrocardiography showed sinus rhythm with ST-segment elevation in the inferolateral leads without arrhythmias (Figure 1). Transthoracic echocardiography revealed a left ventricle with preserved ejection fraction (55%), a discrete inferior wall motion abnormality, no significant valvular disease, and no pericardial effusion.

Laboratory investigations demonstrated marked elevation of cardiac biomarkers: hs-cTnI 9312 ng/L (reference < 30 ng/L), CK 529 U/L (reference < 170 U/L), and CK-MB 62 U/L (reference < 16 U/L). Inflammatory markers were elevated, with CRP at 80 mg/L. NT-proBNP was elevated to 923 pg/mL.

Due to the dynamic rise in myocardial injury biomarkers (Table 1) and localized ST-segment elevations as observed in Figure 1, a coronary angiography was performed to exclude acute coronary syndrome. The coronary arteries were normal, with no obstructive or structural lesions (Figure 2).

Cardiac MRI demonstrated positive late gadolinium enhancement with a non-ischemic intramyocardial and subepicardial pattern affecting the lateral, inferior, and septal walls. Increased T2 relaxation times (>60 ms) confirmed persistent myocardial edema, indicative of ongoing inflammation rather than fibrotic scar, consistent with active or subacute myocarditis—Figure 3.

The patient remained hemodynamically stable throughout hospitalization. At discharge, a six-month therapeutic regimen was prescribed, including dapagliflozin 10 mg once daily to alleviate heart failure symptoms, particularly in the context of elevated NT-proBNP, which reflects increased ventricular wall stress; Metoprolol 25 mg twice daily, a cardioselective beta-blocker, to improve heart failure–related symptoms and reduce the risk of potential post-myocarditis arrhythmias; and Ramipril 2.5 mg once daily, an ACE inhibitor to prevent adverse ventricular remodeling.

At one-month follow-up, the patient was asymptomatic and hemodynamically stable. Electrocardiography (Figure 4) and echocardiography were unremarkable, and NT-proBNP had decreased to 355 pg/mL. The clinical timeline of the present case was as showed in Table 2.

Acute myocarditis has a wide range of symptoms among patients. The most common symptom is chest pain, followed by dyspnea and syncope. Many patients diagnosed with myocarditis also report fever or prior respiratory or gastrointestinal infections [1]. Patients usually present with one of the three main patterns: severe chest pain, arrhythmias, or heart failure. Myocarditis should be suspected in any patient with these types of symptoms after exclusion of coronary artery disease, valvular heart disease, congenital heart disease, or hypertensive cardiomyopathy. It is crucial to rule out other possible causes, especially acute myocardial infarction, in these patients [3].

The etiology of myocarditis can vary, ranging from viral, bacterial, fungal, or parasite infections to drugs, toxic substances, hypersensitivity, and high catecholamine states. In many situations, the etiology of the disease cannot be determined, especially in the advanced stage—3 to 4 weeks after the infection—when the immune system already cleared out the pathogen that caused the infection [3]. Diagnosis is supported by clinical presentation and symptoms, widespread ST-segment elevation, and elevated cardiac biomarkers such as high-sensitivity Troponin I. If the pericardium is involved, there could be some PR depression on the electrocardiogram along with the widespread ST-segment changes. Echocardiography plays a crucial role in assessing the presence of other causes for the symptoms, such as valvular disease or hypertensive cardiomyopathy, and also to assess biventricular size and function [1,4]. Histopathological analysis of myocardial tissue through endomyocardial biopsy is the gold standard for the definite diagnosis of myocarditis, but it is associated with a low rate of major complications (such as cardiac perforation, tamponade, valvular trauma, etc.) even if performed by experienced operators [6]. The current guidelines of the European Society of Cardiology recommend endomyocardial biopsy in high-risk patients and in some intermediate cases. Due to the advancement in technology and imaging techniques, cardiac magnetic resonance has been widely used to diagnose myocarditis successfully [7]. One large-scale epidemiological study reports that 12.2% of myocarditis patients aged 50 or older develop heart failure or dilated cardiomyopathy (DCM) within the first year after hospitalization compared to just 3.1% among those under 50 years [5]. Among children, the incidence rate of heart failure after myocarditis is relatively low, but the disease burden and risk for severe outcomes are high because of their immature immune systems [8]. Even though myocarditis can present in various forms, each form (chest pain, arrhythmias, and heart failure) should be treated accordingly. Angiotensin-converting enzyme (ACE) inhibitors are used routinely in patients with heart failure to reduce morbidity and mortality and to improve symptoms [9]. Discontinuation of ACE inhibitors after left ventricular improvement in patients with myocarditis could cause another heart failure episode in up to one-third of these patients [10]. Because sympathetic activation can aid in the progression of left ventricular dysfunction, beta-blockers have been extremely useful in patients with heart failure, improving morbidity and mortality with better clinical outcomes [11]. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are one of the pillars of heart failure treatment. Across reduced, mildly reduced, and preserved ejection fraction, SGLT2 inhibitors have a strong indication for use in patients with heart failure [9,12]. Data from this retrospective cohort study indicate that treatment with SGLT2 inhibitors is associated with lower all-cause mortality and a reduced risk of progression to end-stage kidney disease in patients with heart failure with preserved ejection fraction, independent of diabetic status. These findings support the use of SGLT2 inhibitors as a beneficial therapeutic option in HFpEF, suggesting clinically meaningful cardioprotective and renoprotective effects in this population [13]. An experimental study demonstrated that SGLT2 inhibitors, such as canagliflozin, ameliorate cardiac inflammation in animal models of myocarditis, indicating a possible therapeutic benefit for myocarditis through anti-inflammatory mechanisms [14]. In a murine model of Coxsackievirus B3-induced myocarditis, dapagliflozin reduced disease severity, improved survival, and enhanced cardiac function. Its effects were linked to Stat3 pathway activation, promoting macrophage polarization toward the anti-inflammatory M2 phenotype over the pro-inflammatory M1 type. Treatment also lowered levels of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α [15]. In a myocardial ischemia–reperfusion model, dapagliflozin inhibited NLRP3 inflammasome activation, lowering IL-1β levels and caspase-1 activity. It also restored autophagic flux, enabling selective degradation of inflammasome components and improving lysosomal function. Additionally, by influencing Na⁺ and Ca²⁺ handling via NHE1 and NCX, dapagliflozin may directly modulate cardiomyocyte stress and autophagy [16]. Overall, these data indicate that dapagliflozin may mitigate myocardial injury by modulating innate immune responses. Multiple systematic reviews and meta-analyses confirm significant reductions in hospitalization for heart failure and cardiovascular death with SGLT2 inhibitors in patients with heart failure of diverse etiologies, suggesting possible benefit if extended to myocarditis populations [17,18]. Although clinical data in young patients with myocarditis remain limited, preclinical and mechanistic studies indicate that SGLT2 inhibitors may offer a promising therapeutic approach. These agents appear to exert anti-inflammatory, anti-apoptotic, and cardioprotective effects, in part by modulating NLRP3 inflammasome activity, suppressing pro-inflammatory cytokine production, and preserving cardiomyocyte viability. Further clinical trials are warranted to confirm these benefits in humans [13]. Arrhythmias are a recognized complication of myocarditis, especially in cases accompanied by signs of heart failure. Cytokines modify myocardial ion channel function, prolonging action potentials and disrupting repolarization, thereby creating a proarrhythmic environment, especially in patients with underlying cardiovascular issues or severe viral infections [19]. Recent studies suggest that SGLT2 inhibitors possess antiarrhythmic properties, though the precise mechanisms have yet to be fully clarified. Direct effects seem to involve changes in myocardial function, circulation, ion regulation, and cardiac electrical activity, while indirect effects include improvements in blood pressure, body weight, sympathetic tone, and cardiac loading conditions in patients with heart failure [20]. The positive impact of SGLT2 inhibitors on cardiac remodeling and inflammation found in preclinical studies supports further research in the context of myocarditis.

This case illustrates the variable presentation of acute myocarditis in a young, previously healthy patient, manifesting with severe chest pain and early heart failure. Multimodal assessment, including cardiac biomarkers, electrocardiography, echocardiography, coronary angiography, and cardiac MRI, was essential for diagnosis, differential diagnosis with acute coronary syndrome, and evaluation of myocardial inflammation. Early initiation of guideline-directed therapy with an SGLT2 inhibitor, beta-blocker, and angiotensin-converting enzyme (ACE) inhibitor led to symptomatic improvement and prevention of adverse ventricular remodeling, underscoring the importance of prompt and comprehensive management in myocarditis.