This case is notable due to the extreme rarity and aggressive behaviour of primary cardiac LMS [14,15]. Sadly, LMS is frequently unresectable at the time of diagnosis [16] and has a mean survival time of 17.5 months with treatment [17] and 6 months without treatment [18].

In contrast, atrial myxomas - the most common primary cardiac tumour - typically originate in the left atrium [19], are slow-growing, often curable with surgery, and associated with better outcomes [20,21,22]. While LMS most commonly involve the left atrium, our patient’s tumour involved the right atrium and extended into the IVC, a particularly rare presentation, previously reported only in isolated case studies such as this [23].

Consistent with existing literature, this tumour remained clinically silent until it led to symptoms related to mechanical obstruction and decompensated heart failure [16,23], prompting the initial diagnosis and later contributing to both admission and death. In this case, heart failure symptoms proved refractory even to high-dose IV diuretics and underscores the diagnostic challenges and rapid clinical deterioration typically associated with cardiac sarcomas - though RP was ultimately the driving process.

Data specifically addressing RP following RT for cardiac tumours are extremely limited. The majority of existing literature reports RP pertaining to patients treated with RT for thoracic malignancies such as lung, breast, and oesophageal cancers as well as lymphoma and in paediatric tumours [24-27].

Adjuvant RT has occasionally been employed for local control in cardiac sarcoma, but outcome data remain scarce. In a large modern series [28], postoperative therapy outcomes for primary cardiac sarcomas demonstrated the feasibility of adjuvant RT and improved local control, yet without reporting pulmonary toxicity. This absence of toxicity data highlights both the rarity of such cases and the likelihood of under-recognised RILI in this context. Our patient’s course therefore represents one of few documented instances of clinically significant RP following cardiac-directed RT.

In conventional RT, a significant volume of surrounding healthy lung tissue may be inadvertently irradiated, thereby increasing the risk of RP [12]. Although newer RT modalities-such as intensity-modulated radiotherapy (IMRT), volumetric-modulated arc therapy (VMAT), and stereotactic body radiotherapy (SBRT)-have minimized lung injury and are generally better tolerated, major pulmonary toxicity can still occur, with rates reported as high as 20% in some series [29,30].

The severity and distribution of RP may be influenced by several factors, including the total lung dose, volume of irradiated lung, fractionation scheme, chemotherapy, and patient-specific risk factors such as age, smoking history, and underlying comorbidities [12]. RILI can extend beyond the irradiated volume, manifesting histologically as organising pneumonia [6], or widespread interstitial pneumonitis, including contralateral lung involvement, and may be refractory to corticosteroid therapy [31].

Our patient initially presented with Grade 2 RP which unfortunately progressed to Grade 5 during his admission. He had received 30-40 Gy of RT, a dose range that is less commonly associated with overt radiographic changes of RP - these are typically observed at doses exceeding 40 Gy [32]. However, it is well-documented that doses above 20 Gy can increase the risk of developing radiation-induced lung injury [33-35].

Although he was a non-smoker - thereby lacking the paradoxical "protective" effect of tobacco exposure or smoking-induced pulmonary damage, which may confer relative radio-resistance by creating non-functional airspaces and fibrotic tissue [12] - he had a background of bronchiectasis. This underlying lung disease, evident on pre-RT CTCAP imaging, may have contributed to increased symptomatic burden [36,37].

At 66 years old, he was below the commonly cited age threshold of 70 years associated with increased risk of severe RP [38]. However, his low serum albumin at presentation (33 g/L) and the development of out-of-field RP were consistent with factors linked to poorer survival outcomes [39].

RP represents an acute inflammatory response of the lung parenchyma to radiation exposure, as illustrated in Figure 9. When the contra-lateral or non-irradiated lung is involved - as in this case - an immune-mediated lymphocytic alveolitis has been proposed as the underlying mechanism [40]. Although CXR frequently demonstrate airspace opacities, these findings are non-specific as CT is more sensitive at identifying parenchymal abnormalities with ground-glass opacities (GGO) and airspace consolidation being the most commonly reported features [6,7,41,42], as evident in this case from the post-radiotherapy CT (Figure 4).

The diagnosis of RP is more straightforward when there is a known history of thoracic RT and a clear demarcation of radiographic changes correlating with the irradiation field. In atypical distributions, however, GGOs - defined as areas of increased pulmonary attenuation without obscuration of bronchial and vascular margins - are non-specific and can represent a broad differential, including infectious pneumonia, opportunistic infections such as PJP, chronic interstitial lung disease, and acute alveolar processes such as pulmonary oedema [7].

In this case, diagnostic interpretation was confounded by multiple overlapping factors: a history of heart failure with missed doses of diuretics upon presentation, recent RT targeted at an atrial mass (rather than lung tissue), and potential infectious aetiologies in an immunocompromised patient. Consequently, our patient was treated empirically for all three leading differential diagnoses - receiving IV diuretics, broad-spectrum antibiotics, and high-dose corticosteroids, the latter being the mainstay of therapy for RILI and acute RP [6,7,10].

This therapeutic approach was initiated with an awareness of the risks associated with systemic corticosteroids, including sodium and fluid retention [43], and worsening oedema - an adverse prognostic marker in patients with cardiogenic shock [44]. While some isolated reports suggest corticosteroids may improve congestion, neurohormonal status, and renal function in selected heart failure patients [45], our patient received a combination of corticosteroids with both glucocorticoid (e.g. dexamethasone) and significant mineralocorticoid activity (e.g. methylprednisolone, prednisolone) [46] in an effort to mitigate the severity of acute RP. Unfortunately, this strategy did not prevent progression to ARDS, a condition associated with high mortality [40,41].

Moreover, moderate to high doses of systemic corticosteroids increase susceptibility to infections, including life-threatening opportunistic pathogens [8,43,47]. This risk was compounded in our patient by active cardiac malignancy, recent RT, and advanced age - all factors associated with impaired host immunity and increased infection risk [48]. In light of this, he was empirically treated with broad-spectrum IV antibiotics throughout his admission, initially piperacillin-tazobactam followed by co-trimoxazole, and subsequently meropenem. While initial microbiological cultures were negative, a later sputum culture identified Acinetobacter baumannii complex, sensitive to both meropenem and co-trimoxazole. This finding supported the antimicrobial regimen, though the likelihood of A. baumannii being pathogenic or causative in this clinical context was considered low.