When Ventricular Tachycardia Hides a Deeper Cause: A Case of Cardiac Sarcoidosis

INTRODUCTION

Sarcoidosis is a multisystem granulomatous disease which is not much thought of as a diagnosis in the emergency department, especially when a patient presents with a life-threatening arrhythmia. Cardiac sarcoidosis (CS) refers to granulomatous inflammation involving the heart, either in isolation or as a component of systemic sarcoidosis. Cardiac involvement is one of the less common manifestations of sarcoidosis, occurring in approximately 5% of patients with confirmed disease.¹ We present to you a case that had two different presentations, one with heart failure and another with monomorphic ventricular tachycardia within a gap of 2 months. Although the initial clinical suspicion pointed towards a malignant aetiology, subsequent investigations established the diagnosis of chronic granulomatous disease.

Case report

A 71-year-old gentleman presented to the emergency department at Aster Whitefield Hospital, Bengaluru, on 18/02/2025 with complaints of palpitations lasting for a few hours, associated with mild chest discomfort. He reported a history of high-grade fever and productive cough for the preceding three days, for which he was started on oral antibiotics. There was no history of chest pain, breathlessness, sweating, or giddiness.

He had a prior episode of palpitations a few months ago, during which he was diagnosed with shortness of breath and was diagnosed to have heart failure with preserved ejection fraction and non-STEMI at a local hospital. His past medical history included community-acquired pneumonia, non-ST elevation myocardial infarction (NSTEMI), type 2 diabetes mellitus with diabetic nephropathy (baseline serum creatinine 1.0–2.0 mg/ dL), hypertension, and obstructive sleep apnea for which he used continuous positive airway pressure (CPAP). His regular medications included antihypertensives, a single antiplatelet agent, a low-dose diuretic, a statin, and oral hypoglycemic drugs.

On arrival, he was fully conscious and oriented, with a Glasgow Coma Scale score of 15/15. His vital signs were: heart rate 160 bpm, blood pressure 110/90 mmHg, oxygen saturation 95% on room air, and respiratory rate 21 breaths per minute. Peripheral pulses were palpable and equal in all four limbs, with no radio-radial or radio-femoral delay. General and systemic examination findings were unremarkable.

An Electrocardiogram (ECG) revealed monomorphic ventricular tachycardia [Figure 1]. The patient was initially managed with a bolus dose of amiodarone, which failed to terminate the arrhythmia. He developed hypotension and underwent synchronised cardioversion with 150 joules under sedation, following which sinus rhythm was restored with heart rate reducing to 100 bpm. A screening echocardiogram post cardioversion showed a normal-sized right ventricle, adequate left ventricular function with a scar in the basal septum, mild hypokinesia, right ventricular systolic pressure of 50 mmHg, severe mitral regurgitation, and preserved ejection fraction. Chest X-ray revealed mild haziness in the left lower zone, likely of infective aetiology. Laboratory investigations showed a normal complete blood count and a serum creatinine of 1.7 mg/dL.

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Figure 1:

A 71-year-old male with sarcoidosis presenting with ventricular tachycardia (VT), ECG showing ventricular tachycardia

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He was started on an amiodarone infusion, minimal vasopressors, a broad-spectrum antibiotic and admitted to the cardiac care unit.

Patient improved symptomatically and was off vasopressors on the second day. Amiodarone was started as an oral dose, and infusion was stopped. Coronary angiography was planned, which revealed minor coronary artery disease. In view of recurrent infections and heart related complications, possible malignancy, infiltrative or granulomatous cardiac disease was provisionally thought and hence a whole-body fluorodeoxyglucose-positron emission tomography (FDGPET) scan was performed, which demonstrated a perfusion defect in the basal inferio-septum and basal inferior wall, focal FDG uptake in the apex and basal inferolateral wall [Figure 2A, B], an FDG-avid right level II cervical lymph node, patchy areas of consolidation and ground-glass opacities in both lungs, and multiple low-grade FDG-avid peri-broncho vascular nodules and mediastinal/hilar lymphadenopathy [Figure 3A, B].

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Figure 2A, B:

(2A) Coronal view of PET-FDG focal increased uptake near apex and basal inferolateral wall. (2B) Axial view of PET-FDG focal increased uptake near apex and basal inferolateral wall.

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Figure 3A, B:

(3A)Axial view of PET-FDG showing right cervical level II lymph node. (3B) Axial view of PET-FDG showing lung nodule uptake.

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A cervical lymph node biopsy showed granulomatous inflammation, and GeneXpert testing for Mycobacterium tuberculosis detected a very low level. Rheumatology consultation was obtained, and the patient was started on corticosteroids and methotrexate. He was discharged in stable condition with advice for follow-up regarding implantable cardioverter-defibrillator (ICD) placement. On subsequent follow-up, he underwent successful implantation of a dual-chamber automatic implantable cardioverter defibrillator (AICD) and continues regular follow-up.

DISCUSSION

Sarcoidosis is a multisystem granulomatous disease of unknown cause, characterised by the formation of noncaseating inflammatory granulomas in various organs such as the lungs, eyes, skin, lymph nodes, and heart. Cardiac sarcoidosis (CS) refers to granulomatous inflammation affecting the myocardium, either as an isolated finding or as part of systemic disease. Although less common than pulmonary or cutaneous involvement, cardiac manifestations are clinically significant and occur in about 5% of patients with confirmed sarcoidosis.¹ The prevalence and incidence of sarcoidosis vary widely across different geographic regions, sexes, and ethnic groups.

In cardiac sarcoidosis, granulomas typically involve the myocardium, especially the left ventricular free wall.² The main manifestations are conduction abnormalities, ventricular arrhythmias, and heart failure, though symptoms such as chest discomfort, dyspnoea, syncope, fatigue, or palpitations are often nonspecific. Our patient developed both heart failure and monomorphic VT within a few months. ECG may show conduction blocks, QRS (complex of electrocardiogram) widening, Q waves, or tachyarrhythmias,³ while echocardiography can reveal hypertrophy, wall motion abnormalities, dysfunction, septal thinning, or aneurysms. Because these findings overlap with cardiomyopathies and ischemic disease, misdiagnosis is frequent.

The American Thoracic Society currently recommends screening for cardiac involvement in sarcoidosis based on clinical symptoms or suggestive signs. When cardiac sarcoidosis is suspected, cardiac MRI cardiac magnetic resonance (CMR) and/or FDG-PET scans are advised as initial imaging modalities to support diagnosis and assess prognosis.⁴ FDG-PET helps detect active myocardial inflammation and, when combined with CMR, is useful for assessing disease activity and monitoring treatment response. According to the 2017 society of nuclear medicine and molecular imaging-American society of nuclear cardiology (SNMMI–ASNC) guidelines, cardiac PET/CT should be considered in patients with systemic sarcoidosis and abnormal cardiac findings, new-onset atrioventricular (AV) block before age 60, sustained idiopathic ventricular tachycardia, or in established cardiac sarcoidosis requiring serial imaging for therapy monitoring.⁵ We did PET-CT as he fits into the above criteria.

There are two generally accepted diagnostic pathways for cardiac sarcoidosis. One approach requires histological confirmation of noncaseating granulomas in myocardial tissue with no alternative explanation. Alternatively, a diagnosis can be made through a combination of clinical, imaging, and pathological criteria. However, imaging alone is not considered definitive.

Cardiac sarcoidosis, often termed the “great masquerader,” can mimic myocarditis, cardiomyopathies, and other granulomatous diseases.⁶ Diagnosis is particularly difficult in isolated cases and usually requires a multidisciplinary team involving sarcoidosis, heart failure, imaging, electrophysiology, pathology, and genetics specialists.

Corticosteroids are the mainstay of treatment for cardiac sarcoidosis, aiming to reduce myocardial inflammation and prevent fibrosis.⁷ They may improve conduction abnormalities but have uncertain effects on arrhythmias, ventricular function, and mortality.⁸ Patients with persistent or relapsing disease often require additional immunosuppressants such as methotrexate, azathioprine, mycophenolate, or leflunomide, while refractory cases may benefit from TNF-α inhibitors. Treatment response is assessed through symptom improvement and imaging, with FDG-PET uptake serving as a useful marker of disease activity.⁹

Adjunctive care includes guideline-directed therapy for heart failure, with pacemaker or ICD placement for advanced AV block. While ICDs are standard for left ventricular ejection fraction (LVEF) ≤35%, patients with preserved function may still face arrhythmic risk.¹⁰ Given its multisystem nature, management of sarcoidosis requires a multidisciplinary approach. Severe or refractory cases—especially with pulmonary or neurologic involvement—carry high morbidity and should be referred to specialised centres for advanced therapy and management of complications such as recurrent VT or end-stage heart failure.¹⁰

CONCLUSION

This case highlights the need for thorough evaluation of ventricular tachycardia, especially with atypical features or systemic symptoms. Though often overlooked in the emergency setting, sarcoidosis should be considered in such presentations. In this patient, further workup revealed cardiac sarcoidosis, guiding disease-modifying therapy and long-term rhythm management with AICD. As a clinical mimicker, cardiac sarcoidosis requires high suspicion and a multidisciplinary approach for timely diagnosis and optimal outcomes.