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Case Report
9 (
3
); 183-187
doi:
10.25259/JCCC_8_2025

Beyond the Coronary-Enteric Myocarditis Masquerading as Acute Coronary Syndrome with Cardiogenic Shock: A Rare Case of Successful Management despite Initial Misdiagnosis

Department of Cardiology, Alluri Sita Ramaraju Academy of Medical Sciences, Eluru, Andhra Pradesh, India.
Department of General Medicine, Alluri Sita Ramaraju Academy of Medical Sciences, Eluru, Andhra Pradesh, India.
Department of Pathology, Alluri Sita Ramaraju Academy of Medical Sciences, Eluru, Andhra Pradesh, India.

*Corresponding author: Sravani Mallireddy, Department of General Medicine, Alluri Sita Ramaraju Academy of Medical Sciences, Eluru, Andhra Pradesh, India. sravsmallireddy@gmail.com

Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Tammiraju I, Mallireddy S, Dhurbesula AT, Meegada S, Vutukuru S. Beyond the Coronary-Enteric Myocarditis Masquerading as Acute Coronary Syndrome with Cardiogenic Shock: A Rare Case of Successful Management despite Initial Misdiagnosis. J Card Crit Care TSS. 2025;9:183-7. doi: 10.25259/JCCC_8_2025

Abstract

This case report presents a rare occurrence of enteric myocarditis caused by Salmonella Typhi, initially mistaken for acute coronary syndrome in a 33-year-old woman who presented with chest pain and fever. Despite the severity of her condition, characterized by atrioventricular dissociation and cardiogenic shock, coronary angiography revealed normal coronary arteries, prompting a revised diagnosis of myocarditis associated with enteric fever. The patient was managed with antibiotics, inotropic support, and temporary cardiac pacing. Her cardiac function steadily improved over several weeks, as confirmed by cardiac magnetic resonance imaging and normalization of her electrocardiogram (ECG). Although uncommon, enteric myocarditis can be difficult to diagnose due to its diverse symptoms and clinical similarities with other cardiac conditions, particularly in areas where typhoid fever is prevalent. Early detection through ECG, echocardiography, and biomarkers such as the Widal test is essential for prompt treatment and better outcomes. This case highlights the need to consider rare cardiac complications in febrile patients and emphasizes the value of thorough diagnostic workups and individualized treatment approaches to prevent serious complications.

Keywords

Atrioventricular dissociation
Cariogenic shock
Enteric fever
Misdiagnosis
Myocarditis

INTRODUCTION

Enteric fever, predominantly triggered by Salmonella enterica serotype Typhi, continues to pose a major health challenge, affecting nearly 17 million people annually, particularly in South and Southeast Asia.[1] It is a primary contributor to community-acquired bloodstream infections in these regions and is commonly transmitted through the fecal-oral route. The disease commonly presents with symptoms such as fever, general weakness, vomiting, and diarrhea, although severe gastrointestinal manifestations, including intestinal perforation and hemorrhage, are frequent complications.[2] Extraintestinal manifestations are not relatively common and may affect other organs including the nervous system, lungs, liver, and genitourinary tract. Among cardiovascular complications, myocarditis and endocarditis are the most prevalent, though pericarditis and arteritis may also occur, although less frequently.[3] Due to the widespread systemic involvement, timely identification and thorough management are essential to prevent the serious and potentially life-threatening complications of enteric fever.

CASE REPORT

A 33-year-old female with no significant medical history presented to the emergency department with sudden onset of chest pain, palpitations, fever, vomiting, and diarrhea. She described the chest pain as non-radiating and pricking, accompanied by shortness of breath and palpitations. The patient reported experiencing 10 episodes of vomiting and 10 episodes of loose stools. Upon arrival, she was febrile and hemodynamically unstable, with a blood pressure of <90/70 mm Hg. A systemic examination revealed muffled heart sounds during the cardiovascular assessment and bilateral decreased breath sounds, along with fine crepitations during the respiratory examination. An electrocardiogram (ECG) indicated diffuse ST-T changes and complete heart block [Figure 1]. Transthoracic echocardiography showed an enlarged left ventricle with significant left ventricular dysfunction (an ejection fraction of 30%) and regional wall motion abnormalities in the mid and distal interventricular septum, anterolateral wall, and apex [Figure 2]. A chest X-ray revealed pulmonary edema [Figure 3]. The initial diagnosis was acute coronary syndrome with cardiogenic shock. Due to her hemodynamic instability, the patient was intubated and received a temporary pacemaker along with inotropic support. A coronary angiogram was then performed, which surprisingly showed normal coronary arteries.

Electrocardiogram at presentation showing diffuse ST elevations in all leads with atrioventricular dissociation.
Figure 1:
Electrocardiogram at presentation showing diffuse ST elevations in all leads with atrioventricular dissociation.
Echocardiogram showing severe left ventricular dysfunction with an ejection fraction of 27% and decreased EDV and ESV. LVIDd-Left ventricular internal diameter in diastole; LVIDs-Left ventricular internal diameter in systole; EDV-End diastolic volume; ESV-End systolic volume; LVEF-Left ventricular ejection fraction; PWd-Posterior wall thickness in diastole; PWs-Posterior wall thickness in diastole; IVSd- Interventricular septum thickness in diastole; IVSs-Interventricular septum thickness in systole.
Figure 2:
Echocardiogram showing severe left ventricular dysfunction with an ejection fraction of 27% and decreased EDV and ESV. LVIDd-Left ventricular internal diameter in diastole; LVIDs-Left ventricular internal diameter in systole; EDV-End diastolic volume; ESV-End systolic volume; LVEF-Left ventricular ejection fraction; PWd-Posterior wall thickness in diastole; PWs-Posterior wall thickness in diastole; IVSd- Interventricular septum thickness in diastole; IVSs-Interventricular septum thickness in systole.
Chest X-ray showing features of pulmonary edema.
Figure 3:
Chest X-ray showing features of pulmonary edema.

Laboratory findings revealed a positive Widal test with a high titer of 1:320 that persisted for several months. In addition, elevated troponin T levels (>2000 ng/L) confirmed a diagnosis of enteric fever complicated by myocarditis (enteric myocarditis). The patient was started on intravenous antibiotics and oxygen supplementation. After 24 h, sinus rhythm was regained, although there was a prolonged QT interval, and thus, the temporary pacemaker was removed [Figure 4]. After 2 weeks of appropriate antibiotic therapy and supportive care, the patient’s ejection fraction improved to 37%. A cardiac magnetic resonance imaging (MRI) displayed features consistent with myocarditis. During follow-up, the ejection fraction returned to normal within 4 weeks, while the high titers from the Widal test normalized after 10 weeks.

Electrocardiogram showing sinus rhythm and no ST-T changes at the time of discharge.
Figure 4:
Electrocardiogram showing sinus rhythm and no ST-T changes at the time of discharge.

DISCUSSION

Myocarditis is characterized by inflammation of the heart and arises from exposure to various antigens, such as viruses, toxins, parasites, or drugs, as well as internal triggers such as autoimmune conditions.[4] Salmonella, a motile Gram-negative bacillus, spreads through the fecal-oral route, where it penetrates the intestinal epithelium and can reach systemic sites. The first documented association between myocarditis and Salmonella Typhi was noted in 1884.[5] Salmonella myocarditis is a rare yet significant complication of enteric fever, occurring in 1–5% of cases.[3] Despite its infrequency, the potential severity of this condition necessitates attention, especially among younger patients, who seem to be more vulnerable. Moreover, the condition is often underdiagnosed due to its non-specific symptoms and the overlap with other cardiac and systemic complications associated with typhoid fever.

Salmonella myocarditis typically arises in the 2nd week of enteric fever, with cardiovascular insufficiency being a major cause of mortality. Several factors influence its development, including the virulence of the Salmonella strain, the size of the initial bacterial inoculum, the host’s immune response, and any prior exposure history. Toxic myocarditis, which is associated with systemic Salmonella infections, plays a significant role in the cardiac inflammation and functional decline observed in affected patients. The cardiac manifestations are the result of direct bacterial invasion, systemic inflammatory responses, and immune-mediated injury, leading to complications such as systolic dysfunction, arrhythmias, and heart failure.[4]

Typhoid fever is characterized by severe systemic infection with a high-grade fever and abdominal pain. The severity of Salmonella myocarditis varies ranging from mild cases to life-threatening conditions.[6] Common symptoms include chest discomfort, dyspnea, and fatigue, often accompanied by signs of hypoxemia. Severe cases may present with hypotension, tachycardia, acute pulmonary edema, or features of congestive heart failure.[7] Myocarditis can be asymptomatic or present with a wide range of clinical features. Frequent ECG changes include QTc prolongation in approximately one-third of cases, followed by ST-T changes, bundle branch blocks, atrioventricular blocks (mostly first degree), and various arrhythmias. Other cardiovascular symptoms of enteric myocarditis are relative bradycardia and unusually, slow heart rate relative to the fever, a feature sometimes observed in typhoid fever and shock. Severe cases may lead to cardiovascular shock, particularly in untreated or late-diagnosed typhoid. Case reports have highlighted scenarios of sudden-onset chest pain and ischemic changes on ECG in travelers returning from endemic regions, emphasizing the diverse presentations of this condition.[8]

The diagnosis of enteric myocarditis is established through clinical presentation and a combination of diagnostic tests with a widal test positive and blood culture positive for Salmonella along with the following:

Clinical criteria

The patient may present with heart failure, fever, a viral prodrome, and complaints such as fatigue, dyspnea, or chest pain. ECG abnormalities are common, with QTc prolongation, ST-T changes, and bundle branch blocks frequently observed. Echocardiography is a valuable diagnostic tool, detecting impaired ventricular function and structural changes. Subclinical cases may reveal left ventricular dilation, altered geometry, and global systolic dysfunction.

Speckle tracking echocardiography (STE)

Myocarditis is often hard to detect early due to its wide range of symptoms. STE has proven effective in identifying subtle heart muscle dysfunction and may offer both diagnostic and prognostic insights. Two-dimensional STE correlates well with myocardial edema seen on cardiac MRI in acute myocarditis. Global longitudinal strain measures from both 2D and 3D STE outperform traditional metrics such as left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume in detecting myocarditis. While 2D STE is time-consuming and operator-dependent, 3D STE provides faster, more consistent results and offers detailed regional wall motion analysis through 3D radial strain. However, 3D STE is limited by its dependence on image quality, difficulty in defining heart borders, and lower temporal resolution.

Cardiac MRI

It provides greater diagnostic accuracy, utilizing the Lake Louise Criteria to confirm myocarditis by identifying inflammation, edema, and fibrosis within the myocardium.[7]

Endomyocardial biopsy

While rarely performed due to its invasive nature and associated risks, biopsy can provide direct evidence of myocarditis and the specific pathogen involved based on Dallas criteria.[9]

The primary approach to treating Salmonella myocarditis involves antibiotics tailored to local resistance patterns, alongside conventional heart failure therapies including beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and diuretics. The World Health Organization Essential Medicines Expert Committee recommends a 7–10-day course of ciprofloxacin, ceftriaxone, or azithromycin as the first-line treatment for both adults and children. Supportive care, including inotropes for hemodynamic compromise, plays a critical role in stabilizing patients. Dexamethasone has shown promise in some studies, particularly in adults, though data for pediatric patients remain limited.[10] Intravenous immunoglobulin has also demonstrated potential benefits, with meta-analyses suggesting improved LVEF and survival in children and adults with acute myocarditis.[11] However, these therapies require further investigation in the context of Salmonella myocarditis. Our patient has improved with inotropic support initially for 2 days along with IV antibiotic ceftriaxone and sulbactam for 7 days followed by oral cefixime, antiplatelets, and diuretics. Early recognition and appropriate management are crucial, as most patients recover normal cardiac function with timely intervention. However, persistent complications such as bundle branch blocks may occur in severe cases.

The prognosis for Salmonella myocarditis is generally favorable when diagnosed and treated promptly even in patients with severe hemodynamic collapse with a survival rate of 93% over an 11-year follow-up period.[10] ECG abnormalities generally return to normal within 1–2 months after appropriate treatment, though bundle branch block may persist for several years in some cases. The salient features of enteric myocarditis are summarized in Table 1.

Table 1: Salient features of enteric myocarditis.
Enteric myocarditis
Incidence In endemic areas, enteric fever incidence is more than 270/100,000 persons/year. The prevalence of cardiovascular complications is reported as 1–5%
Clinical features Fever, malaise, diarrhea, vomiting, fatigue, dyspnea, and chest pain at rest, severe hypotension, tachycardia, shock, and heart failure
ECG QTc prolongation, ST-T changes, bundle branch block, and arrhythmias
Echocardiography Global hypokinesia of left ventricle, reduced ejection fraction, multiple wall motion abnormalities, pericardial effusion, and valve dysfunction
Angiogram Normal
Management Third-generation cephalosporins or fluoroquinolones, diuretics for underlying enteric fever
No specific treatment for myocarditis

ECG: Electrocardiogram

CONCLUSION

Salmonella myocarditis is a rare yet serious complication of enteric fever, presenting with a range of cardiac issues from mild impairment to severe arrhythmias and heart failure. Prompt diagnosis using ECG, echocardiography, and advanced imaging techniques, coupled with effective antibiotic therapy and supportive care, significantly improves outcomes. Routine ECG screening in all cases of enteric fever is strongly recommended, particularly in endemic regions or among travelers returning from such areas. Identifying high-risk patients through systematic evaluation allows for timely intervention, reducing the likelihood of severe complications and mortality. If not diagnosed and treated in a timely manner, enteric myocarditis can be life-threatening. Further research is needed to refine diagnostic criteria and therapeutic strategies, ensuring optimal management of this underrecognized condition.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Financial support and sponsorship: Nil.

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