Right Ventricular Strain Secondary to Tumour-Induced Pulmonary Artery Obstruction: An Incidental ¹⁸F-FDG PET/CT Finding in Small Cell Pancoast Tumour

A 65-year-old male chronic smoker presented with right-sided ptosis, miosis, and anhidrosis, indicative of Horner syndrome. A magnetic resonance imaging revealed a mass in the apical region of the right lung, and a biopsy confirmed the diagnosis of small cell carcinoma. For initial staging, an ¹⁸F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) scan was performed. The scan revealed a large FDG-avid mass in the right upper lobe measuring 10.8 cm × 8.4 cm × 12.0 cm (anterior–posterior × transverse × craniocaudal) with a maximum standardised uptake value (SUVmax) of 12.8 [Fig 1a-f]. The mass is infiltrating the pleura and chest wall and encasing the right subclavian artery [Fig 1e]. Furthermore, the scan showed a few metabolically active mediastinal lymph nodes, particularly in the right lower paratracheal region, with an SUVmax of 2.4. In addition, there was a left parietotemporal brain lesion measuring 4.0 cm × 2.7 cm × 3.0 cm, with peripheral FDG uptake and an SUVmax of 3.7 and significant perilesional oedema [Fig 1a, g-i]. Notably, the tumour obstructed the right upper segmental pulmonary artery [Fig 1e], which led to pulmonary hypertension (PH) and subsequent right heart strain. Cardiac findings included diffuse increased FDG uptake in the right ventricular (RV) myocardium (SUVmax 4.9), marked right ventricular dilation, right atrial enlargement, and pulmonary trunk enlargement [Fig 1f, j–l].

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Fig 1: The ¹⁸F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) scan revealed several significant findings. The maximum intensity projection image (a) shows a large FDG-avid mass located in the right apical lung, along with diffuse FDG uptake in the right ventricular (RV) myocardium. In addition, there is relatively reduced uptake in the left cerebral hemisphere. (b–e) Axial PET, fused PET/CT, and CT images illustrate a peripherally FDG-avid mass in the right upper lobe (arrows), which has central necrosis and invades the pleura and adjacent pulmonary artery (arrow) with mild ipsilateral pneumothorax. (f) The fused coronal image demonstrates diffuse increased FDG uptake in the dilated RV myocardium (arrows), along with the hypermetabolic lung mass and hypometabolism in the left cerebral hemisphere. (g) Axial PET, (h) fused PET/CT, and (i) CT image reveal a ring-enhancing FDG-avid lesion (arrows in g, h and i) with central necrosis and perilesional vasogenic oedema in the left temporoparietal region, indicative of cerebral metastasis. (j–l) Images show intense diffuse FDG uptake in the markedly dilated right atrium and ventricle (arrows), consistent with RV myocardial strain.

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Echocardiography confirmed these findings, displaying a significantly increased RV to left ventricular basal diameter ratio of 2.5, a dilated right atrium, and moderate tricuspid and pulmonary regurgitation. There was also evidence of septal flattening, and the estimated pulmonary artery systolic pressure exceeded 50 mmHg. No evidence of RV hypertrophy noted on echocardiography. These findings are consistent with PH secondary to tumour-induced vascular obstruction, leading to acute RV pressure overload and myocardial strain, supported by both metabolic evidence from the ¹⁸F-FDG PET/CT and functional evidence from the echocardiography.

RV myocardial strain represents a specific type of myocardial metabolic stress that occurs in response to acute pressure overload, most commonly associated with conditions like pulmonary embolism or chronic PH.^[1] This case highlights a rare but clinically significant variant associated with malignancy, where tumour-induced pulmonary artery obstruction led to acute RV strain. In this case, the diffuse FDG uptake in RV reflects a well-documented metabolic shift from fatty acid oxidation to glucose utilisation under pressure overload conditions.^[2,3] In addition, echocardiographic findings, such as RV dilation and septal flattening, confirm the mechanical consequences of this metabolic adaptation.^[4] Small cell lung cancer has a particular tendency for vascular involvement, with Pancoast tumours showing direct vascular invasion in up to 25% of cases.^[5] The resulting PH due to tumour-related vascular compression carries important prognostic implications, as the RV has a limited capacity to adapt to acute increases in afterload.^[6,7] The metabolic changes observed on ¹⁸F-FDG-PET scans occur before any structural remodeling, suggesting that these changes could be an early biomarker for RV dysfunction in these patients.^[8]

This case emphasises the dual diagnostic role of ¹⁸F-FDG PET/CT in oncology practice: while primarily used for tumour staging, it can also detect metabolic evidence of cardiac strain. Early identification of this pattern may help guide interventions such as targeted pulmonary vasodilators or tumour debulking;^[9] however, optimal management strategies require further investigation.