European Journal of Cardiovascular Medicine

Sarcoidosis is a systemic granulomatous disorder that primarily affects the lungs but can involve multiple extrapulmonary organs, including the heart. Cardiac sarcoidosis (CS) is a serious manifestation, with clinically overt  disease  found in  approximately 5% of sarcoidosis patients, whereas subclinical myocardial involvement is reported in up to 25% of cases in autopsy studies (1,2). The diagnosis of CS is often delayed due to its nonspecific symptoms, which can mimic other cardiac conditions, particularly in TB-endemic regions where latent or active tuberculosis is prevalent (3).

Tuberculosis, caused by Mycobacterium tuberculosis, remains a major global health concern, particularly in regions like South Asia, where it is endemic. Both sarcoidosis and TB share granulomatous inflammation as a hallmark feature, however, this distinction is not always evident in cases of latent or paucibacillary tuberculosis (4,5), making their differentiation complex. Also, the two entities have different management and prognosis. While sarcoidosis is characterized by non-caseating granulomas, and requires long-term immunosuppression with steroids, TB typically presents with caseating necrosis and demands anti-tubercular therapy; thus, misclassification may worsen outcomes. This diagnostic challenge necessitates a combination of clinical evaluation, imaging modalities, and histopathological examination.

The advent of FDG-PET and cardiac MRI has significantly improved the diagnostic accuracy of CS. FDG-PET is highly sensitive in detecting active myocardial inflammation, whereas cardiac MRI remains the gold standard for identifying myocardial fibrosis and late gadolinium enhancement (LGE), which are characteristic of CS (6,7). EBUS-TBNA has emerged as a minimally invasive tool for evaluating mediastinal lymphadenopathy and differentiating sarcoidosis from TB, providing histological confirmation in suspected cases (8).

This report details a case of CS with concurrent latent tuberculosis, illustrating the role of multimodal imaging, histopathology, and microbiological testing in diagnosis and management

A 37 year-old male with type 2 diabetes mellitus on regular oral hypoglycemics presented with acute-onset palpitations, chest pain, dizziness, and profuse sweating. The chest pain was sharp, non-radiating, and associated with a sense of impending doom. He denied fever, weight loss, cough, or night sweats. There was no history of tuberculosis or cardiac illness. He was a non-smoker and did not consume alcohol.

On general examination, the patient was anxious and diaphoretic. Systemic exam: Cardiovascular examination revealed tachycardia with a regular rhythm, normal S1 and S2, no additional heart sounds, murmurs, rubs, or gallops, and no evidence of jugular venous distension, pedal edema, or peripheral cyanosis. Peripheral pulses were palpable and symmetrical.; respiratory exam was clear bilaterally; abdomen and CNS were normal.  Vitals: BP 90/60 mmHg, HR 180 bpm, SpO₂ 96% RA, Temp 98.4°F.  Electrocardiography Was done which demonstrated wide- complex tachycardia, consistent with ventricular tachycardia (VT) (Figure 1). Chest Xray was  unremarkable . The Laboratory Investigations are as follows

The patient was stabilized (Figure 2) with intravenous adenosine (6 mg, stat), diltiazem (5 mg, stat), heparin (5000 IU, stat), and cordarone (150 mg bolus followed by infusion). Echocardiography revealed concentric left ventricular hypertrophy with preserved left ventricular ejection fraction (LVEF 55%) and mild regional wall motion abnormalities. Coronary angiography ruled out ischemic heart disease.

Given the absence of coronary pathology, further evaluation with cardiac MRI revealed mid-myocardial and subepicardial Late gadolinium enhancement in the basal septal and apical segments, indicative of granulomatous myocardial disease (Figure 3).  Fluorodeoxyglucose Positron Emission Tomography demonstrated hypermetabolic activity in the myocardium and mediastinal lymph nodes, suggestive of active inflammation (Figure 6).Endobronchial Ultrasound – Transbronchial Needle Aspiration

Was performed, targeting the subcarinal and right paratracheal lymph nodes (Figure 5), and histopathological examination showed non-caseating granulomas, consistent with sarcoidosis. TB-PCR testing of biopsy samples detected low-burden Mycobacterium tuberculosis DNA, confirming latent tuberculosis. No acid-fast bacilli were identified, and rifampicin resistance was absent.

The patient was diagnosed with cardiac sarcoidosis and latent tuberculosis. Anti-tubercular therapy (AKT-4) was initiated with isoniazid (300 mg/day), rifampicin (600 mg/day), ethambutol (800 mg/day), and pyrazinamide (1500 mg/day) for an intensive phase of two months, followed by a continuation phase of isoniazid and rifampicin for four months. Prednisolone (40 mg/day) was introduced to control myocardial inflammation and was tapered over ten months. Anti-arrhythmic therapy with amiodarone (200 mg/day) and metoprolol (50 mg/day) was prescribed to prevent VT recurrence.

Follow-up imaging at ten months showed complete resolution of subcarinal lymphadenopathy (Figure 4,7) and significant reduction in right paratracheal nodes. Persistent mid-myocardial LGE in the basal septal and apical regions suggested stable fibrosis without new involvement. LVEF remained preserved at 55%, and the patient remained asymptomatic without recurrent VT.

The coexistence of cardiac sarcoidosis and latent tuberculosis presents a unique diagnostic challenge, particularly in TB-endemic regions where differentiating between these two granulomatous diseases is critical for appropriate management. Both diseases share overlapping clinical features, including systemic inflammation and granuloma formation, making histopathology a key diagnostic tool (9,10).

FDG-PET and cardiac MRI have revolutionized the diagnosis of CS, allowing for accurate identification of myocardial inflammation and fibrosis. In this case, FDG-PET highlighted hypermetabolic activity in the myocardium and mediastinal lymph nodes, prompting further histopathological confirmation via EBUS-TBNA (11,12). The presence of non-caseating granulomas was consistent with sarcoidosis, while TB-PCR detected Mycobacterium tuberculosis, confirming latent TB. Studies have reported that EBUS-TBNA has a high diagnostic yield exceeding 80% in differentiating sarcoidosis from TB (13,14).

Management of CS requires a delicate balance between immunosuppression and TB control. Corticosteroids remain the mainstay of CS treatment, effectively reducing myocardial inflammation and stabilizing arrhythmias. However, in TB-endemic regions, corticosteroid use necessitates concurrent ATT to prevent TB reactivation (15,16). In this case, the patient tolerated corticosteroid therapy well without evidence of TB activation.

Anti-arrhythmic therapy with amiodarone and beta-blockers played a critical role in preventing VT recurrence. The patient’s long-term stability and absence of new myocardial involvement on follow-up MRI further support the efficacy of this tailored approach (17).

This case illustrates the complexities of diagnosing and managing cardiac sarcoidosis in a tuberculosis-endemic setting. The integration of advanced imaging, histopathology, and microbiological testing was crucial in differentiating sarcoidosis from latent TB, allowing for appropriate treatment. The patient’s favorable clinical outcome highlights the importance of a multidisciplinary approach in managing overlapping granulomatous diseases. Long-term follow-up with cardiac MRI and clinical assessments is essential to monitor disease progression and optimize treatment strategies

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