J Med Cases

Journal of Medical Cases, ISSN 1923-4155 print, 1923-4163 online, Open Access

Article copyright, the authors; Journal compilation copyright, J Med Cases and Elmer Press Inc

Journal website https://jmc.elmerpub.com

Case Report

Volume 17, Number 11, November 2026, pages 670-684

Cardiac Magnetic Resonance-Supported Diagnosis of Acute Myocarditis Mimicking Acute Coronary Syndrome in a Patient With Sepsis Due to a Massive Perianal Abscess

↓ Figure 2. Chest X-ray indicated mild bilateral enlargement of the hilar region, and resolving basal pneumonia.

↓ Figure 3. Postoperative chest computed tomography demonstrated bilateral pleural effusions, pulmonary vascular congestion, diffuse ground-glass opacities, and interlobular septal thickening, findings consistent with pulmonary edema.

↓ Figure 4. ECG indicated tachycardia, atrial extrasystoles, ST-segment depression and T-inversion in leads V5–V6. ECG: electrocardiogram.

↓ Figure 5. Urgent coronary angiography demonstrated a non-obstructive 40% stenosis of the right coronary artery, while the left coronary arterial system was angiographically normal.

↓ Figure 6. Cardiac magnetic resonance imaging indicated: (a) Positive T2 map in septal region with LGE. (b) Positive T1 map in lateral wall region with LGE. (c) Positive T2 map in lateral wall region with LGE. (d) Late gadolinium enhancement. Non-ischemic epicardial in the lateral wall. LGE: Late gadolinium enhancement.

↓ **Table 1.** Clinical Parameters and Sequential Organ Failure Assessment Score at Admission
Parameter	Patient value	SOFA component	SOFA score
CNS: central nervous system; GCS: Glascow Comma Scale; MAP: mean arterial pressure; SOFA: Sequential Organ Failure Assessment.
Respiratory rate	26 breaths/min	Respiratory	-
PaO₂	69 mm Hg	Respiratory	-
Oxygen supplementation	10 L/min Venturi mask	Respiratory	-
Estimated FiO₂	∼0.40	Respiratory	-
PaO₂/FiO₂ ratio	∼173	Respiratory	2
Platelets	170 × 10³/µL	Coagulation	0
Bilirubin	1.2 mg/dL	Liver	0
Blood pressure	100/35 mm Hg	Cardiovascular	-
Estimated MAP	∼57 mm Hg	Cardiovascular	-
Norepinephrine	0.05 µg/kg/min	Cardiovascular	3
Heart rate	117 beats/min	-	-
GCS	15	CNS	0
Mental status	Slightly agitated	CNS	-
Creatinine	1.7 mg/dL	Renal	1
Lactate	3.6 mmol/L	-	-
SpO₂	95%	-	-
Infection	Massive perianal abscess	Clinical context	-
Total SOFA score			6

↓ Table 1. Clinical Parameters and Sequential Organ Failure Assessment Score at Admission

Parameter

Patient value

SOFA component

SOFA score

CNS: central nervous system; GCS: Glascow Comma Scale; MAP: mean arterial pressure; SOFA: Sequential Organ Failure Assessment.

Respiratory rate

26 breaths/min

Respiratory

PaO₂

69 mm Hg

Respiratory

Oxygen supplementation

10 L/min Venturi mask

Respiratory

Estimated FiO₂

∼0.40

Respiratory

PaO₂/FiO₂ ratio

∼173

Respiratory

Platelets

170 × 10³/µL

Coagulation

Bilirubin

1.2 mg/dL

Liver

Blood pressure

100/35 mm Hg

Cardiovascular

Estimated MAP

∼57 mm Hg

Cardiovascular

Norepinephrine

0.05 µg/kg/min

Cardiovascular

Heart rate

117 beats/min

GCS

CNS

Mental status

Slightly agitated

CNS

Creatinine

1.7 mg/dL

Renal

Lactate

3.6 mmol/L

SpO₂

95%

Infection

Massive perianal abscess

Clinical context

Total SOFA score

↓ **Table 2.** Inflammatory Markers, Microbiological Findings, and Intravenous Antibiotic Therapy
Parameter	Before treatment	After treatment	Reference range/interpretation
CRP: C-reactive protein.
Procalcitonin	2.28 ng/mL	0.41 ng/mL	0.5–2 ng/mL: suspected sepsis; > 2 ng/mL: sepsis
CRP	27.49 mg/dL	0.48 mg/dL	0–0.5 mg/dL
White blood cell count	25.38 × 10³/µL	19.45 × 10³/µL	4.0–10.5 × 10³/µL
Surgical-site microbiological cultures	Staphylococcus epidermidis; Enterococcus faecalis; Escherichia coli
Blood culture	Escherichia coli
Intravenous antibiotic regimen (10 days)	Piperacillin/tazobactam 4.5 g three times daily; levofloxacin 500 mg once daily; metronidazole 500 mg three times daily

↓ Table 2. Inflammatory Markers, Microbiological Findings, and Intravenous Antibiotic Therapy

Parameter

Before treatment

After treatment

Reference range/interpretation

CRP: C-reactive protein.

Procalcitonin

2.28 ng/mL

0.41 ng/mL

0.5–2 ng/mL: suspected sepsis; > 2 ng/mL: sepsis

CRP

27.49 mg/dL

0.48 mg/dL

0–0.5 mg/dL

White blood cell count

25.38 × 10³/µL

19.45 × 10³/µL

4.0–10.5 × 10³/µL

Surgical-site microbiological cultures

Staphylococcus epidermidis; Enterococcus faecalis; Escherichia coli

Blood culture

Escherichia coli

Intravenous antibiotic regimen (10 days)

Piperacillin/tazobactam 4.5 g three times daily; levofloxacin 500 mg once daily; metronidazole 500 mg three times daily

↓ **Table 3.** Step-by-Step Diagnostic Evaluation and Establishment of the Final Diagnosis
Step	Diagnostic question/challenge	Examination/finding	Diagnostic conclusion/exclusion
ABG: arterial blood gas; ACS: acute coronary syndrome; CAD: coronary artery disease; CMR: cardiac magnetic resonance; CT: computed tomography; CK-MB: creatine kinase myocardial band; ECG: electrocardiogram; MINOCA: myocardial infarction with non-obstructive coronary arteries; MR: mitral regurgitation; LGE: late gadolinium enhancement; LV: left ventricular; LVEF: left ventricle ejection fraction; NT-proBNP: N-terminal pro-B-type natriuretic peptide; RCA: right coronary artery.
1. Respiratory deterioration	What caused the acute postoperative hypoxemia?	ABG showed PaO₂ of 51 mm Hg; chest CT showed pulmonary vascular congestion, bilateral pleural effusions, ground-glass opacities, and septal thickening	Pulmonary edema identified
2. Fluid overload	Could pulmonary edema be explained by excessive fluid administration?	1,100 mL intra-operative fluids; 1,800 mL urine output after furosemide; net fluid balance −700 mL	Simple fluid overload was less likely
3. New cardiac dysfunction	Was there acute deterioration in cardiac function?	Echocardiography: LVEF ∼35%, global hypokinesis, new moderate-to-severe functional MR, without significant regional wall-motion abnormalities	Acute myocardial dysfunction confirmed, with a predominantly global rather than regional pattern
4. Acute myocardial injury	Was the cardiac deterioration associated with myocardial injury?	Hs-troponin 1,950 ng/L and CK-MB 350 ng/mL; ECG showed ST depression and T-wave inversion in V5–V6	ACS was strongly suspected
5. Obstructive coronary disease	Was this an acute myocardial infarction due to coronary obstruction?	Urgent coronary angiography: only 40% non-obstructive RCA stenosis; normal left coronary system	Obstructive ACS excluded; MINOCA considered
6. Myocarditis vs. septic cardiomyopathy	What explained the myocardial injury in the setting of severe sepsis?	CMR: elevated T2 values indicating myocardial edema and LGE involving the interventricular septum and LV lateral wall	Active myocardial inflammation demonstrated, supporting acute myocarditis
7. Histological confirmation	Could myocarditis be confirmed by biopsy?	Endomyocardial biopsy was declined by the patient	Diagnosis was established non-invasively by clinical context, exclusion of obstructive CAD, and CMR findings
8. Diagnostic confirmation by outcome	Was the myocardial dysfunction reversible?	LVEF recovered to 55%, MR resolved, NT-proBNP decreased from 3,846 to 95 pg/mL, and cardiac enzymes normalized	Reversible inflammatory myocardial injury consistent with acute myocarditis

↓ Table 3. Step-by-Step Diagnostic Evaluation and Establishment of the Final Diagnosis

Step

Diagnostic question/challenge

Examination/finding

Diagnostic conclusion/exclusion

ABG: arterial blood gas; ACS: acute coronary syndrome; CAD: coronary artery disease; CMR: cardiac magnetic resonance; CT: computed tomography; CK-MB: creatine kinase myocardial band; ECG: electrocardiogram; MINOCA: myocardial infarction with non-obstructive coronary arteries; MR: mitral regurgitation; LGE: late gadolinium enhancement; LV: left ventricular; LVEF: left ventricle ejection fraction; NT-proBNP: N-terminal pro-B-type natriuretic peptide; RCA: right coronary artery.

1. Respiratory deterioration

What caused the acute postoperative hypoxemia?

ABG showed PaO₂ of 51 mm Hg; chest CT showed pulmonary vascular congestion, bilateral pleural effusions, ground-glass opacities, and septal thickening

Pulmonary edema identified

2. Fluid overload

Could pulmonary edema be explained by excessive fluid administration?

1,100 mL intra-operative fluids; 1,800 mL urine output after furosemide; net fluid balance −700 mL

Simple fluid overload was less likely

3. New cardiac dysfunction

Was there acute deterioration in cardiac function?

Echocardiography: LVEF ∼35%, global hypokinesis, new moderate-to-severe functional MR, without significant regional wall-motion abnormalities

Acute myocardial dysfunction confirmed, with a predominantly global rather than regional pattern

4. Acute myocardial injury

Was the cardiac deterioration associated with myocardial injury?

Hs-troponin 1,950 ng/L and CK-MB 350 ng/mL; ECG showed ST depression and T-wave inversion in V5–V6

ACS was strongly suspected

5. Obstructive coronary disease

Was this an acute myocardial infarction due to coronary obstruction?

Urgent coronary angiography: only 40% non-obstructive RCA stenosis; normal left coronary system

Obstructive ACS excluded; MINOCA considered

6. Myocarditis vs. septic cardiomyopathy

What explained the myocardial injury in the setting of severe sepsis?

CMR: elevated T2 values indicating myocardial edema and LGE involving the interventricular septum and LV lateral wall

Active myocardial inflammation demonstrated, supporting acute myocarditis

7. Histological confirmation

Could myocarditis be confirmed by biopsy?

Endomyocardial biopsy was declined by the patient

Diagnosis was established non-invasively by clinical context, exclusion of obstructive CAD, and CMR findings

8. Diagnostic confirmation by outcome

Was the myocardial dysfunction reversible?

LVEF recovered to 55%, MR resolved, NT-proBNP decreased from 3,846 to 95 pg/mL, and cardiac enzymes normalized

Reversible inflammatory myocardial injury consistent with acute myocarditis

↓ **Table 4.** Clinical Timeline of Symptom Onset, Peri-Operative Deterioration, Diagnostic Evaluation, Treatment, and Follow-Up
Time point	Clinical course/symptoms	Investigations and findings	Treatment/management	Outcome / diagnostic interpretation
ABG: arterial blood gas; ACE: angiotensin converting enzyme; BMI: body mass index; CT: computed tomography; CMR: cardiac magnetic resonance; CXR: chest X-ray; CK-MB: creatine kinase myocardial band; ECG: electrocardiogram; EMB: endomyocardial biopsy; hs-Tn: hs-troponin; ICU: intensive care unit; IV: intravenous; LGE: late gadolinium enhancement; LV: left ventricular; LVEF: left ventricle ejection fraction; MR: mitral regurgitation; RCA: right coronary artery; SOFA: Sequential Organ Failure Assessment.
Day 10	Fever (40 °C), right perianal pain/swelling, mild cough, and fatigue	Large perianal abscess identified	-	Severe local infection with systemic inflammatory response.
Day 5	Persistent symptoms with temporary improvement	-	Outpatient IV antibiotics	Subsequent clinical deterioration.
Day 0 – hospital admission	Fever 40 °C, tachypnea, diaphoresis; BMI 42.1 kg/m²	SOFA score 6; large perianal abscess	Broad-spectrum antibiotics; surgical consultation	Severe sepsis/septic shock secondary to perianal abscess.
Day 0 – pre-operative assessment	Large right perianal abscess extending into the gluteal region	CXR: hilar enlargement/resolving pneumonia; SpO₂ 95–96%. Echo: preserved LV function, mild-to-moderate MR	Emergency surgical drainage planned	Normal LV systolic baseline.
Day 0 – surgery	Emergency abscess drainage	Radial arterial monitoring; uncomplicated intubation	General anesthesia; propofol, fentanyl, vecuronium, sevoflurane, remifentanil	Surgery completed in ∼1 h.
Day 0 – emergence	Severe hypertension (201/77 mm Hg) and hypoxemia (SpO₂ 88–92%)	ABG: pH 7.33, PaO₂ 51, PaCO₂ 39 mm Hg	Furosemide 60 mg IV; net fluid balance −700 mL	Pulmonary edema initially suspected.
Early postoperative period	Persistent oxygen requirement, chest discomfort, and basal crackles	CT: bilateral pleural effusions, vascular congestion, ground-glass opacities, septal thickening	Cardiopulmonary monitoring and cardiac evaluation	Cardiac dysfunction increasingly suspected.
Early postoperative period – cardiac evaluation	New cardiac dysfunction	ECG: sinus tachycardia 119 bpm, ST depression/T-wave inversion V5–V6. Echo: LVEF 35%, moderate to severe MR. Hs-Tn 1,950 ng/L; CK-MB 350 ng/mL	Cardiology consultation	ACS/acute MI initially suspected.
Early postoperative ICU period	Hemodynamic instability requiring intensive monitoring	Adequate tissue perfusion maintained	Dobutamine 7.5 µg/kg/min + norepinephrine 0.05–0.1 µg/kg/min	Hemodynamic stabilization.
Early ICU period – coronary evaluation	Ongoing myocardial injury evaluation	40% non-obstructive RCA stenosis; normal left coronary tree	No coronary intervention	Obstructive ACS excluded; MINOCA/non-ischemic injury considered.
After hemodynamic stabilization – CMR	Persistent concern for myocarditis	CMR: elevated septal T2 values and LGE involving the interventricular septum/LV lateral wall	EMB declined	Findings supported acute myocarditis.
ICU days 1–6	Progressive cardiac and respiratory improvement	Stable tissue perfusion	Antibiotics, diuretics, oxygen, vasoactive/inotropic support	Transferred to cardiology after 6 days.
Day 6 – transfer from ICU	Continued improvement	-	Diuretics, ACE inhibitor, digitalis, oxygen, antibiotics, wound care	Continued recovery.
Day 10	Ongoing recovery	Echo: LVEF 45%, moderate residual MR	Conservative heart failure management	Improved LV function.
Three-month follow-up	Clinically recovered	Complete recovery of cardiac function; MR resolved	Follow-up	Complete healing of perianal wound/fistula and favorable outcome.

↓ Table 4. Clinical Timeline of Symptom Onset, Peri-Operative Deterioration, Diagnostic Evaluation, Treatment, and Follow-Up

Time point

Clinical course/symptoms

Investigations and findings

Treatment/management

Outcome / diagnostic interpretation

ABG: arterial blood gas; ACE: angiotensin converting enzyme; BMI: body mass index; CT: computed tomography; CMR: cardiac magnetic resonance; CXR: chest X-ray; CK-MB: creatine kinase myocardial band; ECG: electrocardiogram; EMB: endomyocardial biopsy; hs-Tn: hs-troponin; ICU: intensive care unit; IV: intravenous; LGE: late gadolinium enhancement; LV: left ventricular; LVEF: left ventricle ejection fraction; MR: mitral regurgitation; RCA: right coronary artery; SOFA: Sequential Organ Failure Assessment.

Day 10

Fever (40 °C), right perianal pain/swelling, mild cough, and fatigue

Large perianal abscess identified

Severe local infection with systemic inflammatory response.

Day 5

Persistent symptoms with temporary improvement

Outpatient IV antibiotics

Subsequent clinical deterioration.

Day 0 – hospital admission

Fever 40 °C, tachypnea, diaphoresis; BMI 42.1 kg/m²

SOFA score 6; large perianal abscess

Broad-spectrum antibiotics; surgical consultation

Severe sepsis/septic shock secondary to perianal abscess.

Day 0 – pre-operative assessment

Large right perianal abscess extending into the gluteal region

CXR: hilar enlargement/resolving pneumonia; SpO₂ 95–96%. Echo: preserved LV function, mild-to-moderate MR

Emergency surgical drainage planned

Normal LV systolic baseline.

Day 0 – surgery

Emergency abscess drainage

Radial arterial monitoring; uncomplicated intubation

General anesthesia; propofol, fentanyl, vecuronium, sevoflurane, remifentanil

Surgery completed in ∼1 h.

Day 0 – emergence

Severe hypertension (201/77 mm Hg) and hypoxemia (SpO₂ 88–92%)

ABG: pH 7.33, PaO₂ 51, PaCO₂ 39 mm Hg

Furosemide 60 mg IV; net fluid balance −700 mL

Pulmonary edema initially suspected.

Early postoperative period

Persistent oxygen requirement, chest discomfort, and basal crackles

CT: bilateral pleural effusions, vascular congestion, ground-glass opacities, septal thickening

Cardiopulmonary monitoring and cardiac evaluation

Cardiac dysfunction increasingly suspected.

Early postoperative period – cardiac evaluation

New cardiac dysfunction

ECG: sinus tachycardia 119 bpm, ST depression/T-wave inversion V5–V6. Echo: LVEF 35%, moderate to severe MR. Hs-Tn 1,950 ng/L; CK-MB 350 ng/mL

Cardiology consultation

ACS/acute MI initially suspected.

Early postoperative ICU period

Hemodynamic instability requiring intensive monitoring

Adequate tissue perfusion maintained

Dobutamine 7.5 µg/kg/min + norepinephrine 0.05–0.1 µg/kg/min

Hemodynamic stabilization.

Early ICU period – coronary evaluation

Ongoing myocardial injury evaluation

40% non-obstructive RCA stenosis; normal left coronary tree

No coronary intervention

Obstructive ACS excluded; MINOCA/non-ischemic injury considered.

After hemodynamic stabilization – CMR

Persistent concern for myocarditis

CMR: elevated septal T2 values and LGE involving the interventricular septum/LV lateral wall

EMB declined

Findings supported acute myocarditis.

ICU days 1–6

Progressive cardiac and respiratory improvement

Stable tissue perfusion

Antibiotics, diuretics, oxygen, vasoactive/inotropic support

Transferred to cardiology after 6 days.

Day 6 – transfer from ICU

Continued improvement

Diuretics, ACE inhibitor, digitalis, oxygen, antibiotics, wound care

Continued recovery.

Day 10

Ongoing recovery

Echo: LVEF 45%, moderate residual MR

Conservative heart failure management

Improved LV function.

Three-month follow-up

Clinically recovered

Complete recovery of cardiac function; MR resolved

Follow-up

Complete healing of perianal wound/fistula and favorable outcome.

↓ **Table 5.** Differential Diagnosis Between Sepsis-Induced Cardiomyopathy and Myocarditis
Feature	Sepsis-induced cardiomyopathy	Myocarditis
BNP: B-type natriuretic peptide; CRP: C-reactive protein; ECG: electrocardiogram; ESR: erythrocyte sedimentation rate; GLS: global longitudinal strain; LGE: late gadolinium enhancement; NT-proBNP: N-terminal pro-B-type natriuretic peptide.
Underlying cause	Systemic inflammatory response to sepsis causing reversible myocardial dysfunction	Inflammatory injury of the myocardium, most commonly viral, autoimmune, toxic, or immune-mediated
Clinical context	Occurs during severe sepsis or septic shock	May occur following a viral prodrome, autoimmune disease, drug exposure, or independently of sepsis
Typical onset	Concurrent with septic illness	Acute, subacute, or chronic; may precede or occur without systemic infection
Symptoms	Signs of sepsis with circulatory failure; heart failure symptoms may be masked	Chest pain, dyspnea, palpitations, fatigue, syncope, heart failure
Fever	Common due to sepsis	May be present if infectious; absent in autoimmune forms
Hemodynamics	Vasodilatory shock with reduced systemic vascular resistance; myocardial depression contributes to hypotension	Variable; may range from stable hemodynamics to cardiogenic shock (fulminant myocarditis)
ECG findings	Sinus tachycardia; non-specific ST-T changes; occasional arrhythmias	ST-segment and T-wave abnormalities, PR depression, conduction disturbances, ventricular arrhythmias
Cardiac biomarkers	Troponin mildly to moderately elevated; BNP/NT-proBNP frequently elevated	Troponin often markedly elevated; BNP/NT-proBNP elevated with ventricular dysfunction
Inflammatory markers	Markedly elevated (CRP, procalcitonin, leukocytosis) reflecting sepsis	Elevated CRP and ESR; procalcitonin usually normal unless concomitant bacterial infection
Echocardiography	Global biventricular systolic dysfunction, ventricular dilatation, reduced ejection fraction, usually without regional wall motion abnormalities	Regional or global ventricular dysfunction; increased wall thickness (edema), pericardial effusion may be present
Speckle-tracking echocardiography	Reduced global longitudinal strain, usually diffuse	Reduced GLS with regional abnormalities corresponding to inflamed myocardium
Cardiac magnetic resonance	Usually non-specific; myocardial edema may occur, but late gadolinium enhancement is uncommon	Diagnostic modality of choice; demonstrates myocardial edema and non-ischemic LGE according to updated Lake Louise criteria
Coronary angiography	Usually normal if performed	Usually normal unless concomitant coronary artery disease
Endomyocardial biopsy	Not indicated	Gold standard for definitive diagnosis in selected patients, particularly fulminant or unexplained cases
Treatment	Source control, antibiotics, hemodynamic support, vasopressors/inotropes, management of septic shock	Guideline-directed heart failure therapy, treatment of underlying cause, immunosuppression in selected cases, mechanical circulatory support if required
Recovery	Usually reversible within 7–10 days after resolution of sepsis	Variable; complete recovery, persistent ventricular dysfunction, dilated cardiomyopathy, or death
Prognosis	Primarily determined by severity of sepsis rather than cardiac dysfunction alone	Depends on etiology and severity; fulminant myocarditis has high early mortality, but survivors often recover well

↓ Table 5. Differential Diagnosis Between Sepsis-Induced Cardiomyopathy and Myocarditis

Feature

Sepsis-induced cardiomyopathy

Myocarditis

BNP: B-type natriuretic peptide; CRP: C-reactive protein; ECG: electrocardiogram; ESR: erythrocyte sedimentation rate; GLS: global longitudinal strain; LGE: late gadolinium enhancement; NT-proBNP: N-terminal pro-B-type natriuretic peptide.

Underlying cause

Systemic inflammatory response to sepsis causing reversible myocardial dysfunction

Inflammatory injury of the myocardium, most commonly viral, autoimmune, toxic, or immune-mediated

Clinical context

Occurs during severe sepsis or septic shock

May occur following a viral prodrome, autoimmune disease, drug exposure, or independently of sepsis

Typical onset

Concurrent with septic illness

Acute, subacute, or chronic; may precede or occur without systemic infection

Symptoms

Signs of sepsis with circulatory failure; heart failure symptoms may be masked

Chest pain, dyspnea, palpitations, fatigue, syncope, heart failure

Fever

Common due to sepsis

May be present if infectious; absent in autoimmune forms

Hemodynamics

Vasodilatory shock with reduced systemic vascular resistance; myocardial depression contributes to hypotension

Variable; may range from stable hemodynamics to cardiogenic shock (fulminant myocarditis)

ECG findings

Sinus tachycardia; non-specific ST-T changes; occasional arrhythmias

ST-segment and T-wave abnormalities, PR depression, conduction disturbances, ventricular arrhythmias

Cardiac biomarkers

Troponin mildly to moderately elevated; BNP/NT-proBNP frequently elevated

Troponin often markedly elevated; BNP/NT-proBNP elevated with ventricular dysfunction

Inflammatory markers

Markedly elevated (CRP, procalcitonin, leukocytosis) reflecting sepsis

Elevated CRP and ESR; procalcitonin usually normal unless concomitant bacterial infection

Echocardiography

Global biventricular systolic dysfunction, ventricular dilatation, reduced ejection fraction, usually without regional wall motion abnormalities

Regional or global ventricular dysfunction; increased wall thickness (edema), pericardial effusion may be present

Speckle-tracking echocardiography

Reduced global longitudinal strain, usually diffuse

Reduced GLS with regional abnormalities corresponding to inflamed myocardium

Cardiac magnetic resonance

Usually non-specific; myocardial edema may occur, but late gadolinium enhancement is uncommon

Diagnostic modality of choice; demonstrates myocardial edema and non-ischemic LGE according to updated Lake Louise criteria

Coronary angiography

Usually normal if performed

Usually normal unless concomitant coronary artery disease

Endomyocardial biopsy

Not indicated

Gold standard for definitive diagnosis in selected patients, particularly fulminant or unexplained cases

Treatment

Source control, antibiotics, hemodynamic support, vasopressors/inotropes, management of septic shock

Guideline-directed heart failure therapy, treatment of underlying cause, immunosuppression in selected cases, mechanical circulatory support if required

Recovery

Usually reversible within 7–10 days after resolution of sepsis

Variable; complete recovery, persistent ventricular dysfunction, dilated cardiomyopathy, or death

Prognosis

Primarily determined by severity of sepsis rather than cardiac dysfunction alone

Depends on etiology and severity; fulminant myocarditis has high early mortality, but survivors often recover well

↓ **Table 6.** Key Diagnostic Elements for Myocarditis
Diagnostic modality	Key findings	Diagnostic value
AV: atrioventricular; BNP: B-type natriuretic peptide; CK-MB: creatine kinase myocardial band; CMR: cardiac magnetic resonance; CT: computed tomography; EF: ejection fraction; EMB: endomyocardial biopsy; NT-proBNP: N-terminal pro-B-type natriuretic peptide; PCR: polymerase chain reaction.
Clinical presentation	Chest pain, dyspnea, palpitations, syncope, fatigue, acute or chronic heart failure; recent viral illness or autoimmune disease may be present	Raises clinical suspicion but is not diagnostic
Electrocardiogram	Sinus tachycardia, ST-segment elevation or depression, T-wave inversion, PR depression, AV block, bundle branch block, ventricular arrhythmias	Non-specific; useful for identifying conduction abnormalities and arrhythmias
Cardiac biomarkers	Elevated cardiac troponin (I or T); elevated CK-MB; elevated BNP or NT-proBNP if ventricular dysfunction is present	Indicates myocardial injury but does not establish the cause
Inflammatory markers	Elevated C-reactive protein, erythrocyte sedimentation rate, leukocytosis; procalcitonin may help identify concomitant bacterial infection	Supports inflammatory process but lacks specificity
Transthoracic echocardiography	Regional or global left ventricular dysfunction, reduced ejection fraction, increased wall thickness due to edema, diastolic dysfunction, pericardial effusion	First-line imaging to assess cardiac function and exclude alternative diagnoses
Speckle-tracking echocardiography	Reduced global longitudinal strain, often with regional impairment	Detects subtle myocardial dysfunction before EF declines
Cardiac magnetic resonance	Myocardial edema (T2-weighted imaging or T2 mapping), non-ischemic late gadolinium enhancement, increased native T1 and extracellular volume	Preferred non-invasive diagnostic test; diagnosis based on the updated Lake Louise Criteria
Coronary angiography or CT coronary angiography	Normal coronary arteries	Excludes acute coronary syndrome in appropriate patients
Endomyocardial biopsy	Histological evidence of inflammatory infiltrates with myocyte necrosis; immunohistochemistry and molecular testing can identify inflammatory cell type and viral genome	Gold standard for definitive diagnosis; recommended in selected patients (e.g., fulminant, unexplained, or treatment-resistant myocarditis)
Virological and autoimmune testing	Viral PCR, serology (limited role), autoimmune antibodies, eosinophil count when clinically indicated	Identifies underlying etiology and guides management in selected cases
Diagnostic criteria	Combination of compatible clinical presentation with CMR findings and/or histological confirmation by EMB	Diagnosis should integrate clinical, imaging, laboratory, and histopathological findings

↓ Table 6. Key Diagnostic Elements for Myocarditis

Diagnostic modality

Key findings

Diagnostic value

AV: atrioventricular; BNP: B-type natriuretic peptide; CK-MB: creatine kinase myocardial band; CMR: cardiac magnetic resonance; CT: computed tomography; EF: ejection fraction; EMB: endomyocardial biopsy; NT-proBNP: N-terminal pro-B-type natriuretic peptide; PCR: polymerase chain reaction.

Clinical presentation

Chest pain, dyspnea, palpitations, syncope, fatigue, acute or chronic heart failure; recent viral illness or autoimmune disease may be present

Raises clinical suspicion but is not diagnostic

Electrocardiogram

Sinus tachycardia, ST-segment elevation or depression, T-wave inversion, PR depression, AV block, bundle branch block, ventricular arrhythmias

Non-specific; useful for identifying conduction abnormalities and arrhythmias

Cardiac biomarkers

Elevated cardiac troponin (I or T); elevated CK-MB; elevated BNP or NT-proBNP if ventricular dysfunction is present

Indicates myocardial injury but does not establish the cause

Inflammatory markers

Elevated C-reactive protein, erythrocyte sedimentation rate, leukocytosis; procalcitonin may help identify concomitant bacterial infection

Supports inflammatory process but lacks specificity

Transthoracic echocardiography

Regional or global left ventricular dysfunction, reduced ejection fraction, increased wall thickness due to edema, diastolic dysfunction, pericardial effusion

First-line imaging to assess cardiac function and exclude alternative diagnoses

Speckle-tracking echocardiography

Reduced global longitudinal strain, often with regional impairment

Detects subtle myocardial dysfunction before EF declines

Cardiac magnetic resonance

Myocardial edema (T2-weighted imaging or T2 mapping), non-ischemic late gadolinium enhancement, increased native T1 and extracellular volume

Preferred non-invasive diagnostic test; diagnosis based on the updated Lake Louise Criteria

Coronary angiography or CT coronary angiography

Normal coronary arteries

Excludes acute coronary syndrome in appropriate patients

Endomyocardial biopsy

Histological evidence of inflammatory infiltrates with myocyte necrosis; immunohistochemistry and molecular testing can identify inflammatory cell type and viral genome

Gold standard for definitive diagnosis; recommended in selected patients (e.g., fulminant, unexplained, or treatment-resistant myocarditis)

Virological and autoimmune testing

Viral PCR, serology (limited role), autoimmune antibodies, eosinophil count when clinically indicated

Identifies underlying etiology and guides management in selected cases

Diagnostic criteria

Combination of compatible clinical presentation with CMR findings and/or histological confirmation by EMB

Diagnosis should integrate clinical, imaging, laboratory, and histopathological findings

↓ **Table 7.** Comparison of the Present Case With the Clinically Relevant Evidence
Reference	Focus of the cited study/recommendation	Relevance to the present case	Present case: corresponding finding	Contribution to diagnostic reasoning
ACS: acute coronary syndrome; CAD: coronary artery disease; CMR: cardiac magnetic resonance; ECG: electrocardiogram; LGE: late gadolinium enhancement; LV: left ventricular; LVEF: left ventricle ejection fraction; SICM: sepsis-induced cardiomyopathy.
Beesley et al [4]	Sepsis-induced cardiomyopathy and its clinical recognition	Establishes SICM as an important alternative explanation for myocardial dysfunction during sepsis	New global LV dysfunction developed during severe bacterial sepsis	SICM had to be considered before attributing the dysfunction to myocarditis
Romero-Bermejo et al [7]	Sepsis-induced cardiomyopathy	Describes reversible myocardial dysfunction associated with sepsis	LVEF decreased from preserved pre-operatively to 35% postoperatively	Demonstrates why septic cardiomyopathy was an important differential diagnosis
Borkowski et al [8]	Clinical complexity of sepsis-induced cardiomyopathy	Highlights diagnostic overlap between sepsis and cardiac dysfunction	Marked troponin elevation, LV dysfunction and hemodynamic instability occurred in the setting of sepsis	Supports the need for systematic cardiac evaluation rather than assuming SICM
Aissaoui et al [9]	Contemporary understanding, diagnosis, and assessment of SICM	Provides the framework for evaluating myocardial dysfunction in sepsis	Echocardiography demonstrated new global LV dysfunction without significant regional abnormalities	Global dysfunction supported SICM as a differential but did not establish it
Sato et al [12]	SICM as a heterogeneous syndrome and role of echocardiography	Emphasizes multimodal assessment of septic cardiac dysfunction	Serial echocardiography demonstrated marked deterioration followed by recovery	Serial cardiac imaging helped establish the evolution and reversibility of dysfunction
Martin et al [15]	Mechanisms and clinical implications of the septic heart	Explains inflammatory myocardial injury during severe sepsis	Severe bacterial sepsis coincided with marked myocardial injury	Provides biological plausibility for sepsis-associated inflammatory myocardial injury
Lampejo et al [18]	Diagnosis and management of acute myocarditis	Defines the clinical and diagnostic spectrum of myocarditis	Troponin elevation, ECG abnormalities, and new LV dysfunction	Demonstrates that the patient’s presentation was compatible with acute myocarditis but non-specific
Ammirati and Moslehi [19]	Diagnosis and treatment of acute myocarditis	Supports multimodal diagnostic assessment	CMR was performed after coronary angiography excluded obstructive CAD	Supports the stepwise transition from suspected ACS to myocarditis
Domínguez et al [20]	Consensus approach to myocarditis and inflammatory cardiomyopathy	Supports integration of clinical, laboratory, and imaging findings	Clinical context + biomarkers + echocardiography + coronary angiography + CMR	Reinforces the multimodal diagnostic approach used in this case
Ferreira et al [26]	CMR evaluation of non-ischemic myocardial inflammation	Directly relevant to the decisive investigation	Elevated T2 values and non-ischemic LGE in the septum/LV lateral wall	CMR provided the principal non-invasive evidence supporting acute myocarditis

↓ Table 7. Comparison of the Present Case With the Clinically Relevant Evidence

Reference

Focus of the cited study/recommendation

Relevance to the present case

Present case: corresponding finding

Contribution to diagnostic reasoning

ACS: acute coronary syndrome; CAD: coronary artery disease; CMR: cardiac magnetic resonance; ECG: electrocardiogram; LGE: late gadolinium enhancement; LV: left ventricular; LVEF: left ventricle ejection fraction; SICM: sepsis-induced cardiomyopathy.

Beesley et al [4]

Sepsis-induced cardiomyopathy and its clinical recognition

Establishes SICM as an important alternative explanation for myocardial dysfunction during sepsis

New global LV dysfunction developed during severe bacterial sepsis

SICM had to be considered before attributing the dysfunction to myocarditis

Romero-Bermejo et al [7]

Sepsis-induced cardiomyopathy

Describes reversible myocardial dysfunction associated with sepsis

LVEF decreased from preserved pre-operatively to 35% postoperatively

Demonstrates why septic cardiomyopathy was an important differential diagnosis

Borkowski et al [8]

Clinical complexity of sepsis-induced cardiomyopathy

Highlights diagnostic overlap between sepsis and cardiac dysfunction

Marked troponin elevation, LV dysfunction and hemodynamic instability occurred in the setting of sepsis

Supports the need for systematic cardiac evaluation rather than assuming SICM

Aissaoui et al [9]

Contemporary understanding, diagnosis, and assessment of SICM

Provides the framework for evaluating myocardial dysfunction in sepsis

Echocardiography demonstrated new global LV dysfunction without significant regional abnormalities

Global dysfunction supported SICM as a differential but did not establish it

Sato et al [12]

SICM as a heterogeneous syndrome and role of echocardiography

Emphasizes multimodal assessment of septic cardiac dysfunction

Serial echocardiography demonstrated marked deterioration followed by recovery

Serial cardiac imaging helped establish the evolution and reversibility of dysfunction

Martin et al [15]

Mechanisms and clinical implications of the septic heart

Explains inflammatory myocardial injury during severe sepsis

Severe bacterial sepsis coincided with marked myocardial injury

Provides biological plausibility for sepsis-associated inflammatory myocardial injury

Lampejo et al [18]

Diagnosis and management of acute myocarditis

Defines the clinical and diagnostic spectrum of myocarditis

Troponin elevation, ECG abnormalities, and new LV dysfunction

Demonstrates that the patient’s presentation was compatible with acute myocarditis but non-specific

Ammirati and Moslehi [19]

Diagnosis and treatment of acute myocarditis

Supports multimodal diagnostic assessment

CMR was performed after coronary angiography excluded obstructive CAD

Supports the stepwise transition from suspected ACS to myocarditis

Domínguez et al [20]

Consensus approach to myocarditis and inflammatory cardiomyopathy

Supports integration of clinical, laboratory, and imaging findings

Clinical context + biomarkers + echocardiography + coronary angiography + CMR

Reinforces the multimodal diagnostic approach used in this case

Ferreira et al [26]

CMR evaluation of non-ischemic myocardial inflammation

Directly relevant to the decisive investigation

Elevated T2 values and non-ischemic LGE in the septum/LV lateral wall

CMR provided the principal non-invasive evidence supporting acute myocarditis