Right atrial thrombus and pulmonary embolism in a young adult with COVID‑19 and tuberculosis coinfection: a case report

Abstract

Background

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Coronavirus Disease 2019 (COVID-19) has been linked to thromboembolic complications, especially in severely ill patients. Intracardiac thrombi are uncommon and pose a very high risk. Coinfection with tuberculosis (TB) may worsen the prothrombotic state and complicate treatment.

Case summary

A 21-year-old male patient from Afghanistan developed active pulmonary tuberculosis (TB) and COVID-19. He had a large, mobile thrombus in the right atrium and an acute pulmonary embolism (PE), but no deep vein thrombosis (DVT). He received remdesivir, anti-TB medication, anticoagulation, and underwent a successful surgical embolectomy. At a nine-month follow-up, he remained symptom-free.

Conclusion

This case highlights the rare occurrence of a right atrial thrombus in COVID-19, possibly exacerbated by TB co-infection. Early detection and tailored treatment, including surgery, are crucial to lowering mortality in these high-risk patients, but further research is needed to establish optimal management strategies and confirm the role of TB in thrombotic complications.

Introduction

Coronavirus Disease 2019 (COVID-19) is a multisystemic disease with known associations with coagulopathy and thromboembolic phenomena [1, 2]. Complications from coagulopathy can include Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE), arterial clots, and intracardiac clots, although the latter are less common [3,4,5]. Clots in the right atrium are rare and can lead to serious problems with blood flow [6].

There have been reports of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and Mycobacterium tuberculosis (M. tuberculosis) co-infections, which may worsen inflammation and increase clotting [7, 8]. This report describes a rare case of a young adult who had both COVID-19 and pulmonary TB, presenting with a thrombus in the right atrium and PE, which was effectively treated by surgical embolectomy.

Case report

In August 2022, a 21-year-old male Afghan immigrant to Iran for the past six months presented with progressive dyspnea, hemoptysis, cough, sore throat, and nocturnal sweats. He had no known prior medical history and had taken only one dose of COVID‑19 vaccine.

Upon presentation, he was afebrile (36.8 °C), tachycardic (HR 120 bpm), tachypneic (RR 26), normotensive (125/75 mmHg), and his oxygen saturation was 90% on room air. Coarse crackles were present in bilateral pulmonary auscultation.

A reverse-transcriptase polymerase chain reaction (RT-PCR) test confirmed COVID-19 infection from a nasopharyngeal swab. An electrocardiogram (ECG), routine blood tests, a pulmonary computed tomography (CT) scan, and transthoracic echocardiography (TTE) were done. The ECG showed sinus tachycardia. Laboratory tests showed elevated white blood cells (12,600 cells/mL), mild anemia (Hb 13 g/dL), and normal platelet levels. The C-reactive protein (CRP) level was measured at 80.4 mg/mL, while the erythrocyte sedimentation rate (ESR) was recorded at 80 mm/h. The laboratory could not measure brain natriuretic peptide (BNP) due to limitations.

The patient’s troponin level was 42.8 nanograms per liter (ng/L), which falls into the uncertain range according to the VIDAS troponin assay cutoff values. Levels up to 19 ng/L are treated as negative, values between 19 and 100 ng/L are uncertain, and levels above 100 ng/L suggest heart injury. Thus, this result requires careful interpretation and clinical context. The sputum smear and culture were positive for Koch’s bacillus (Mycobacterium tuberculosis), confirming the definitive diagnosis of active pulmonary tuberculosis. In our setting, positive AFB smear and culture are sufficient for a definitive diagnosis of pulmonary TB, and no further microbiological tests, such as cartridge-based nucleic acid amplification test (CB-NAAT), were required. Differential diagnoses such as non-tuberculous mycobacterial infections, fungal pneumonia, or other bacterial pneumonias were considered but deemed less likely given the endemic setting, classic symptoms (e.g., nocturnal sweats, hemoptysis), and positive smear and culture.

Spiral chest CT revealed centrilobular opacities and consolidations in both lungs, especially in the upper lobes, consistent with viral and/or bacterial pneumonia, and cystic bronchiectasis in the left upper lobe (LUL), probably due to chronic infection (Fig. 1).

A transesophageal echocardiogram (TTE) showed a significant, mobile clot located in the right atrium that extends into the right ventricle. A CT pulmonary angiogram confirmed an acute PE in the right pulmonary artery. The severity of the PE was assessed using the Pulmonary Embolism Severity Index (PESI), placing the patient in an intermediate-risk category.

Antiviral therapy with remdesivir was commenced, along with a tuberculosis treatment regimen consisting of rifampin, isoniazid, pyrazinamide, and ethambutol for an initial two months, followed by rifampin and isoniazid for an additional four months.

Due to the size and movement of the right atrial thrombus and resources available at the institution, the medical team chose open surgical embolectomy instead of percutaneous embolectomy or systemic thrombolysis.

Heparin (25,000 units) was administered, and surgery was conducted through a midline sternotomy. During, open heart surgery, both the large right atrial thrombus and pulmonary emboli were removed. The thrombus appeared elongated and branched, with a multicolored look, which suggests it was subacute.

Cardiopulmonary bypass with abicaval total inflow technique and pulmonary embolectomy were performed (Fig. 2).

A follow-up TTE two weeks after the operation showed normal heart function.

The patient was discharged on oral anticoagulation with warfarin (target INR 2.0–3.0) for six months, alongside the anti-TB regimen. Follow-up at nine months included clinical assessment, chest X-ray, and TTE, which showed no evidence of thrombus recurrence, PE, or treatment failure.

Fig. 1

Computed Tomography scan of the chest

Fig. 2

Surgical specimen of removed embolism

Discussion

COVID-19 leads to a higher risk of blood clots due to damage to blood vessel linings, increased inflammation (with higher levels of IL-6 and TNF-α), platelet activation, and disruption of normal blood clotting [2, 3, 9]. While venous thrombosis and PE are common, intracardiac thrombus—especially in the right atrium—remains rare [4, 6, 10]. The patient did not have typical risk factors (like immobility or heart disease), suggesting that COVID-19 and possibly TB co-infection may have both contributed to the higher risk of clotting. TB might worsen the body’s response to SARS-CoV-2, aggravating the damage to blood vessel linings and clotting issues [7, 11]. Recent research shows that TB can lead to worse outcomes in COVID-19 patients, increasing inflammation and altering immune response [8, 12, 13]. However, it is important to note that COVID-19 alone can cause significant thrombotic events, including massive thrombosis and embolism, without the need for co-infections [14, 15]. The exact contribution of TB in this case remains speculative, as causality cannot be definitively established without further mechanistic studies.

There are only a few reported cases worldwide of patients having both COVID-19 and active tuberculosis that led to intracardiac clots or massive PE—see Wang et al. 2024, Yang et al. 2025, and others [8, 12]. Some studies have also noted right heart clots occurring with other infections, but cases involving TB are particularly uncommon [16]. Additional recent reports include a 2023 case series by Hazra et al. describing similar co-infections with thrombotic complications in endemic regions [17], and a 2023 review by Daneshvar et al. highlighting the synergistic prothrombotic effects [18]. These underscore the need for heightened vigilance in such patients.

The thrombus extracted had an elongated, branching, and multicolored appearance, which suggests a subacute, possibly mixed origin (starting in the right atrium or extending from the pulmonary blood vessels). The absence of DVT on imaging suggested in situ thrombus formation in the right atrium rather than embolization from peripheral veins [10].

Existing guidelines do not clearly define the best treatment for combined right atrial thrombus and acute PE in patients with COVID-19 and TB. Treatment options can include systemic thrombolysis, catheter-based embolectomy with modern devices (used off-label), or surgical embolectomy. Our team chose open heart surgery due to the size and movement of the thrombus, the patient’s hemodynamic status, and the resources available. While catheter-based embolectomy is less invasive and can be effective, it wasn’t viable here due to the complexity of the thrombus and limitations in resources [10, 16]. Evidence for managing right atrial thrombi is limited, primarily from case reports and small series. For instance, the European Society of Cardiology guidelines on PE recommend considering surgical embolectomy for high-risk cases with right heart thrombi when thrombolysis is contraindicated or fails [19]. A 2024 meta-analysis by Rahouma et al. suggests comparable outcomes between surgical and catheter-based approaches, but emphasizes patient-specific factors and institutional expertise [20]. In this case, surgical embolectomy was effective, but the rarity of such cases limits generalizable conclusions.

Limitations

This is a single case report, limiting generalizability. Diagnosis of TB was confirmed with positive AFB smear and culture for Koch’s bacillus, which is sufficient for definitive diagnosis in our setting; however, resource constraints prevented additional testing (e.g., BNP). The exact role of TB in thrombosis remains unclear, as COVID-19 alone is a potent prothrombotic factor. The case’s novelty lies in the rare combination of right atrial thrombus and TB/COVID-19 co-infection, but larger studies are needed to clarify optimal management and the synergistic effects of co-infection [8, 12, 17, 18].

Early diagnosis, assessing risk (using PESI), and a collaborative approach to tailored treatment are crucial for survival in these high-risk patients, though this recommendation is based on limited evidence from this single case [21].

Conclusion

This case demonstrates the risk of significant thrombotic events in young patients with COVID‑19, potentially exacerbated by TB co-infection. Clinicians should consider intracardiac thrombi in hypoxic patients with unexplained PE, particularly in endemic TB settings. Early diagnosis and therefore intervention, including surgery, can be life saving. However, further research is needed to establish optimal management strategies and confirm the role of TB in thrombotic complications.