Tuberculous (TB) pericarditis with tamponade is a relatively rare manifestation of extrapulmonary tuberculosis and a major cause of cardiovascular death and morbidity. Even with aggressive anti-TB regimen, 30-60% of patients may require a surgical pericardiectomy for constrictive pericarditis. Several articles have reported the co-occurrence of COVID-19 and TB pericarditis with massive pericardial tamponade.
Mycobacterium tuberculosis shows a preference for oxygen-rich tissues, so, the lungs are a primary site of infection. Bacilli can reach the pericardium through hematogenous spread, lymphatic dissemination, or direct extension from a contiguous focus of infection, such as the lungs, mediastinal lymph nodes, or the spine. In the pericardium, bacilli trigger an inflammatory response leading to the formation of granulomas which are nodular inflammatory lesions that characterize TB.
Granulomas erode the pericardium and cause an influx of protein-rich fluid into the pericardial space, resulting in pericardial effusion. The bacilli may further induce necrosis and release more debris into the pericardial space, resulting in a thicker, more “constrictive” pericardial effusion and constrictive pericarditis. Importantly, the host’s immune response influences progression from pericardial effusion to constrictive pericarditis.
It is assumed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause the reactivation of latent TB. This assumption is consistent with the theory of interaction between the first and the second intracellular pathogens (viruses, bacteria, fungi, or protozoan parasites) infecting the same host cell simultaneously and T-cell exhaustion, facilitating the reactivation of latent intracellular pathogens, leading to potentially severe consequences. https://discovermednews.com/the-presence-of-concurrent-intracellular-pathogens-can-lead-to-t-cell-exhaustion-and-potentially-severe-consequences/
This is illustrated by the interaction between the human immunodeficiency virus (HIV), and Mycobacterium tuberculosis. It is estimated that one-third of global HIV mortality is due to the reactivation of Mycobacterium tuberculosis, triggered by HIV. As for TB pericarditis, TB causes more than 85 % of pericardial effusions in HIV-infected individuals. In addition, HIV alters the natural history and outcome of TB pericarditis, making HIV-associated TB a more aggressive disease with more severe myocardial involvement.
1st Case Report
A man aged 47 years presented with a productive cough, pleuritic chest pain, and fever for two days. The vital signs were 130/83mmHg blood pressure, 104 beats/min heart rate, 97% oxygen saturation, and 16/min respiratory rate. A chest radiograph revealed left-side lower zone retrocardiac opacities. He tested positive on the polymerase chain reaction (PCR) of nasopharyngeal swab for SARS-CoV-2.
His condition worsened after three days of hospitalization. There was no evidence of heart failure or tamponade. ECG showed sinus tachycardia with normal QRS complexes. There was absolute monocytosis and elevated levels of C-reactive protein. The heart size was markedly increased on a repeated chest radiograph. He initiated remdesivir as a part of an ongoing trial.
The transthoracic echocardiogram showed a hyperdynamic left ventricle with a left ventricular ejection fraction of 65%, the right atrial collapse, diastolic collapse of the right ventricle, and 3.5 cm of pericardial effusion. The effusion contained fibrin deposits adhering to the myocardium. Pericardiocentesis yielded 900mL of haemoserous fluid. Cytology was negative for malignancy. The PCR was negative for adenovirus, enterovirus, and SARS-CoV-2.
Original illustration from the article of Wong et al.
Acid-fast bacilli were detected in the pericardial fluid, PCR analysis was positive for Mycobacterium tuberculosis and the levels of adenosine deaminase in the pericardial fluid were significantly elevated. The authors stated that these findings in the pericardial fluid, in the absence of coagulopathy, malignancy, and autoimmune etiologies, are pathognomonic of TB involvement. The patient initiated an anti-TB regimen comprising rifampicin, isoniazid, ethambutol, and pyrazinamide. Subsequent echocardiography showed the resolution of effusion with marked improvement of symptoms.
He was discharged after two weeks of anti-TB treatment. Four weeks after a discharge, a chest X-ray showed a resolution of pericardial effusion and residual left retrocardiac consolidation.
This article was published in the European Heart Journal – Case Reports.
Journal Reference
Wong SW, et al. Tuberculous pericarditis with tamponade diagnosed concomitantly with COVID-19: a case report, European Heart Journal- Case Reports, Volume 5, Issue 1, January 2021, ytaa491 (Open Access) https://doi.org/10.1093/ehjcr/ytaa491
2nd Case Report
The authors presented a case of TB pericarditis and cardiac tamponade diagnosed simultaneously with COVID-19.
A man aged 52 years with chronic kidney disease who was not on hemodialysis was admitted with shortness of breath, fluid overload, and hypoxemia. He tested positive for SARS-CoV-2 and was treated with steroids, remdesevir, tocilizumab, and hemodialysis.
On day 60 of hospitalization, he deteriorated with stuporous mentation and hypotension. Echocardiography showed a new large circumferential pericardial effusion with right ventricular diastolic collapse and increased respiratory variation in peak E-wave mitral inflow velocity, consistent with tamponade physiology. An emergency pericardiocentesis was performed, and hemodynamic instability was resolved immediately after aspiration of 750 milliliters of frank pus. Empiric antibiotics were given initially.
The pericardial fluid was positive for acid-fast bacilli and adenosine deaminase, therefore, anti-TB therapy was started. His state was further aggravated by septic shock and cardiac arrest. Even though there was a reaccumulated pericardial effusion, there was no tamponade, suggesting a partial response to the TB treatment.
This article was published in Chest.
Journal Reference
Khosa JK et al. Tuberculous tamponade with a twist: a case of TB and COVID-19. Chest. 2022 Oct; 162(4): A553. (Open Access) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9548719/
Conclusion
These case reports presented individuals who were diagnosed with COVID-19 and who developed TB pericarditis and pericardial tamponade. The authors suggested that COVID-19 could trigger an inflammatory response that serves as a nidus for TB reactivation. They recommended that clinicians should incorporate TB into the differential diagnosis for patients with viral pericarditis and tamponade. Serial echocardiography and imaging techniques, including CT, may be appropriate, particularly in young patients who deteriorate at an alarming speed. Nevertheless, the gold standard for confirming TB pericarditis is the identification of the Mycobacterium tuberculosis in the pericardial fluid or tissue.
