Necrotic pericardial masses in tuberculous constrictive pericarditis: A rare presentation in a retroviral disease patient

INTRODUCTION

Tuberculosis (TB) is indeed a significant global health challenge, particularly in regions where healthcare access is limited or human immunodeficiency virus (HIV) prevalence is high.¹ The fact that a quarter of the world’s population is infected with Mycobacterium tuberculosis but may not display active disease highlights the complexity of managing and controlling TB transmission.² Early detection and appropriate treatment are crucial to prevent the development of active disease, especially considering the additional risks associated with HIV co-infection.

Extra-pulmonary TB, which can affect other organs beyond the lungs, presents additional diagnostic challenges. Although less common, its impact is critical because it can lead to severe complications and increase mortality rates, particularly when it involves organs such as the pericardium, as seen in tuberculous pericarditis (TP).

The high mortality rate associated with TP (17%-40%)³ reflects the difficulty in managing such cases, especially given the potential for rapid progression and the difficulty in diagnosing this condition early. Treatment typically involves a combination of anti-TB therapy and sometimes corticosteroids, but the response can vary depending on the timing of intervention and the individual’s overall health, especially if they are co-infected with HIV.

Pericarditis can stem from a range of different causes, such as infectious agents like viruses and bacteria, and non-infectious factors including systemic inflammatory conditions, cancer, and post-cardiac injury syndromes. In developing nations, TB is a major contributor to pericarditis, while in developed nations, it represents less than 5% of instances. Conversely, viral infections account for 80% to 90% of pericarditis occurrences in these areas.⁴ TB is implicated in around 4% of acute pericarditis instances, 7% of cardiac tamponade cases, and 6% of constrictive pericarditis cases.⁵ Contiguous dissemination from a lung lesion or hematogenous spread from a distant site is uncommon.⁶

TB can reach the pericardium through three primary routes: (1) retrograde lymphatic spread from mediastinal, peritracheal, or peribronchial lymph nodes; (2) hematogenous dissemination during primary TB infection; or (3) direct extension from adjacent pulmonary or pleural TB involvement.^7,8

In individuals with intact immune systems, the spread typically happens via the lymphatic system, while in those with HIV, immune suppression causes an increase in hematogenous dissemination.⁹ In HIV-negative individuals, TB pericarditis is often a paucibacillary condition, where the immune response plays a larger role in determining disease severity than the virulence of the pathogen itself.^10-12 Conversely, in HIV-positive patients, extra-pulmonary TB, including pericarditis, is more frequently part of a widespread infection, often linked with TB bacteremia, and tends to lead to more severe clinical outcomes.

Once mycobacteria reach the pericardium, viable mycobacterial proteins are presented to CD4⁺ T-cells by macrophages, triggering a cascade of immune responses involving the activation of lymphocytes, macrophages, and the production of complement-fixing antibodies. This results in pericardial inflammation, granuloma formation, and the release of a fibrinous exudate containing inflammatory cytokines.^11-14

HIV interferes with several of these crucial immune processes,¹⁵ leading to decreased CD4⁺ T-cell levels and impaired granuloma formation^14,16 both systemically and within the pericardium. Additionally, HIV can alter the function and phenotype of CD4⁺ memory T-cells in the pericardium,¹⁷ further exacerbating immune dysfunction. These immune system disruptions contribute to both an increased susceptibility to TB pericarditis and the altered clinical presentation of the disease in individuals with HIV.

The clinical manifestations of TB pericarditis and the impact of HIV.

There are four recognized stages of TB pericarditis and two general modes of clinical presentation [Table 1].¹

CASE REPORT

A 30-year-old male patient presented with complaints of chest pain and cough in October 2023. Initial chest radiograph [Figure 1a] revealed bilateral hilar opacities and prominent broncho-vascular markings. Sputum analysis revealed growth of acid-fast bacilli; hence, the patient was started on anti-tuberculous therapy (ATT) for 6 months. On 6-month follow-up, the patient had complaints of dyspnea on exertion grade I-II and palpitations. Follow-up chest radiograph [Figure 1b] suggested well-defined radiopacities obscuring the bilateral heart borders and a few ill-defined radiopacities in the right middle zone. Physical examination was unremarkable. 2D echocardiography (April 2024) revealed evidence of septal bounce, annulus reversus, mitral E/A ratio = 1.6, mitral septal annular e’ more than the lateral wall; these features suggested constrictive pericarditis other findings were myxomatous affection of the mitral valve, mild mitral regurgitation (MR), trivial tricuspid regurgitation (TR), and 60% ejection fraction (EF). Also incidentally detected as HIV positive and on First-line line probe assay (FL-LPA) and Second-line line probe assay (SL-LPA) revealed resistance to isoniazid and fluoroquinolones during further clinical workup, treatment was started based on MDR-TB regimen and ART along with steroids.

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Figure 1:

(a) Chest radiograph (October 2023) revealed bilateral hilar opacities and prominent broncho-vascular markings (yellow arrows), (b) Chest radiograph (dated April 2024) suggestive of well-defined radiopacities noted obscuring the bilateral heart borders (white arrows) and a few ill-defined radiopacities noted in the right middle zone (white star).

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Subsequent cardiac CT [Figure 2] was performed (18.04.2024), There was an ill-defined heterogeneously enhancing soft tissue with central necrosis involving the pericardium along the left ventricular border, right atrial border, aorto-pulmonary window, subaortic, and subpulmonary regions. There was a loss of the pericardial fat plane along the left ventricular border. The soft tissue along the right atrial border was seen to likely extend into the right atrial appendage. The component on the right measured approximately 4.3 × 4.9 × 5.2 cm (AP × TRA × CC), while on the left measured 7.4 × 6 × 4.2 cm (AP × TRA × CC). The thickness of the uninvolved pericardium along the left ventricular apex was less than 2 mm. No pericardial effusion or calcification was seen. Few heterogeneously enhancing subcarinal lymph nodes were seen, the largest of size approximately 14 mm (short axis diameter).

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Figure 2:

(a) Plain axial CT cardiac shows ill-defined hypodense soft tissue in the pericardial recesses (yellow arrows). Image (b to f) shows contrast axial and coronal multidetector CT cardiac with maximum intensity projection images (e and f) shows ill-defined heterogeneously enhancing soft tissue with central necrosis along the heart borders and pericardial recesses (white arrows) in a 30-year-old male patient known case of multidrug-resistant tuberculosis (MDR TB) and retroviral disease (RVD) on treatment. CT: Computed tomography.

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High resolution computed tomography (HRCT) [Figure 3] showed multiple centrilobular nodules with linear branching opacities giving tree in bud appearance were seen in the medial segment of right middle lobe and inferior lingular segment of the left upper lobe.

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Figure 3:

Plain axial lung window MIP image show multiple centrilobular nodules with linear brandling opacities are seen in the medial segment of right middle lobe (white arrow). MIP: Maximum intensity projection.

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Histopathology report with sample collected from the mediastinal mass suggestive of granulomatous inflammation.

Subsequent cardiac MRI [Figure 4] was performed (dated 17.07.2024), which revealed cardiomegaly, mild biatrial enlargement, septal bounce of the interventricular septum with 50% left ventricular ejection fraction (LVEF). The pericardium was thickened, measuring 5.5 mm, but no pericardial effusion was present.

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Figure 4:

(a to d) Cardiac MRIT2 hyperintense heterogeneously enhancing partially necrotic pericardial masses (white arrows) seen along right atrium, left ventricular pericardium, extending superiorly up to the pulmonary trunk.

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T2 hyperintense heterogeneously enhancing partially necrotic pericardial mass measuring 4 × 3.6 cm was seen indenting on the right atrium.

Another similar morphology mass with conglomerate appearance measuring 5 × 4 cm was seen along the left ventricular pericardium, extending superiorly up to the pulmonary trunk.

Treatment with MDR-TB and an ART regimen with low-dose steroids was continued.

A follow-up (after 5 months) MRI [Figure 5] was performed (dated 07.01.2025), which showed similar findings as the prior MRI, except there was an increase in necrosis of the pericardial lesions. Additionally, T1 and T2 mapping were performed, which showed raised T2 values, suggestive of edema.

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Figure 5:

(a,b) T2 axial MRI (magnetic resonance imaging) images reveals hyperintense ill-defined conglomerated masses in the anterior and posterior portions of superior aortic recesses (white arrow). (c) Coronal post contrast T1 image shows the peripherally enhancing masses with necrotic areas within along the left ventricular pericardium (white arrow). Axial T1 post contrast images (d-f) also show peripherally enhancing masses within the (d) Superior aortic recess (white arrow) (e) Left pulmonic recess (white arrow) and (f) Left pulmonary venous recess (white arrow).

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Additional findings observed were mild thickening of the mitral valve leaflets, trivial tricuspid regurgitation, trivial aortic regurgitation, and mild mitral regurgitation.

On clinical follow-up in April 2025 (after 6 months), the patient was symptomatically better. A chest radiograph [Figure 6] revealed resolution of pericardial masses.

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Figure 6:

Chest radiograph dated April 2025 revealed clear bilateral lung fields especially right middle zone (white circle) and normal cardiac silhouette (white arrows) suggesting resolution of the radiopacities and bilateral pericardial masses noted in the previous radiograph dated April 2024.

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CONCLUSION

In this case, with a histopathology-proven case of mediastinal masses suggestive of granulomatous inflammation, evident in cases of TB.

TP represents a severe form of extrapulmonary TB, which has become more common with the rising prevalence of HIV. Diagnosing HIV-related TB pericarditis is challenging and is frequently associated with widespread TB infection, larger effusions, myocardial involvement, and an increased risk of mortality. There are still significant gaps in our understanding of this condition, which should be explored through well-structured prospective studies.

MRI is a critical diagnostic tool regarding the assessment of pericardial pathologies, especially infection, providing both morphologic and functional information important for further management of the patient. Also, MRI, being safe, can be used as a follow-up imaging for assessing the efficacy of the medical line of treatment given.