eComment: Cardiac papillary endothelial hyperplasia: a current assessment

Your report is of great interest [1] as it refers to a well recognised but infrequently reported histological diagnosis – papillary endothelial hyperplasia (PEH). The fact that PEH discovered by intra-operative palpation during mitral valve repair constitutes a tutorial example highlights the importance of accurate examination of the structures within the operating field. Papillary endothelial hyperplasia, as you have already mentioned, is thought to be the result of reactive endothelial proliferation rather than neoplasia and was first described by Pierre Masson in 1923. Especially, the lesion is characterised by papillary lobules of proliferating endothelial cells with an underlying fibrous stroma and often resembles angiosarcoma. PEH may occur either in a pure primary form, as a focal change in a pre-existing vascular lesion (haemangioma, pyogenic granuloma, or vascular malformation), and rarely in an extravascular location following organisation of a haematoma [2]. It is generally accepted that stasis and thrombosis are prerequisites for the development of PEH; a fact that is in accordance with your case, as this lesion probably represents reactive changes within an organising thrombus formed during paroxysmal atrial fibrillation [1]. Re-assessing the relation of thrombosis and papillary endothelial hyperplasia, it is notable to underline that initially it was believed that the vessel endothelium underwent hyperplasia with secondary thrombus formation. However, Salyer et al. [3], demonstrated foci of papillary endothelial hyperplasia in venous thrombi and arterial thrombo-emboli and suggested that the thrombus may be the primary event with secondary organisation leading to the formation of vascular channels lined by endothelium. The vascular channels, however, are disorderly and interspersed by endothelialised papillae rather than discrete as is found in recanalised thrombus [2,3]. On the other hand, the strong relation of intravascular or primary PEH with the co-existent atherosclerotic disease should be also noted. Specifically, as early as 1876, it had been observed that vascularisation of the arterial intima was associated with overlying atheroma [2]. Similarly, O'Brien et al. found that there was a significant association of endothelial cell replication with the presence of microvessels in atheromatous lesions removed by atherectomy [4]. As angiogenesis is growth factor-dependent, these growth factors might also be responsible for the development of papillary endothelial hyperplasia in overlying thrombus. This theory is also supported by Levere et al. [5] who examined frozen section samples of intravascular papillary endothelial hyperplasia. After staining the samples, by using immunoreactive techniques for basic fibroblast growth factor and basic fibroblast growth factor protein, they demonstrated a significant increase in these factors in thrombi containing papillary endothelial hyperplasia compared to those without. In conclusion, the data mentioned above suggest interventional techniques – such as transluminal extraction catheter (TEC) and directional coronary atherectomy – and the further ability of these devices to remove intracoronary tissue, as an alternative approach of early PEH recognition in arterial vessels.