I am studying the pathogenesis of atypia in cardiac cells where the etiology is most commonly irritation or infection and where the precancerous risk depends on the context of diagnosis. This fact motivates me to think how they can generally arise, from superficial or stromal origin, and how - multifactorial and/or polygenic. Cardiac tumours are mostly secondary (30x1) in comparison to primary tumours. I am thinking the sources of these metastases. I did not understand if benign tumours can be secondary such as myxoma. Therefore, I assume now that myxomas (superficial) and stromal origin can be secondary. I am mostly interested in superficial changes of the heart in atypia. It is interesting to notice that benign cardiac tumours originates from the left side of the heart mostly, while the malignant from the right side. I am thinking the mechanisms here and how the myxoma could be related to the pathogenesis of stromal procesesses in the right part of the heart and the pacemakers' function (AV, SA). It would be nice to understand the links between myxoma, AV and SA.

Myxoma in the left chamber

  • Benign.
  • Origin - superficial mostly in left atrium.
  • Pathogenesis - polygenetic and/or multifactorial. Mobile mass obstructs blood flow in chambers and cause an increase in pulmonary capillary wedge.
  • Myxoma (benign tumor of connective tissue containing mucus and gelatinous material) most commonly in left atrium, fossa ovalis in septum.
  • Imaging DX sound after S2 in ECHO and sometimes ECG; ECHO heterogenic mass.
  • Differential DX lipomas, rhabdomyomas, teratomas.

Stromal Processes

  • Malignant diagnostically mostly.
  • Right side of the heart mostly.
  • Most commonly haemangiosarcoma (= angiosarcoma).
  • Pathogenesis. There can be some pathways which are activating atypia such as lymphoma.

Myxoma and Stromal Processes?

I did not understand the link between these two processes. The former resides mostly in the left side of the heart, while the latter in the right side of the heart. Their link or their individual links to the pacemaking (SA, AV) would be nice to understand. I am not sure if we can exclude Purkinje cells, although they reside physically far from the atrias because their low conduction frequency and because the myxoma is about benign tumor of connective tissue which would well reside there, probably even better energetically than in SA/AV.


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How can you describe the pathogenesis of Cardiac Atypia?



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