An update on this topic recently appeared in JACC.
First a little background. This was the topic of one of my very first blog posts almost 12 years ago.
Decades ago this entity was described in patients with incessant forms of SVT (eg long RP or “fast-slow reentry” tachycardias. Some of these were also ectopic atrial tachycardias). These patients had heart failure with low ejection fractions and some were cured after ablation. (See here). It wasn’t until much later when it was recognized that this entity could result from longstanding uncontrolled atrial fibrillation. Prior to that time many patients were labeled as “idiopathic” DCM with atrial fibrillation as a result. It is now recognized that the reverse is often true. That is, a DCM might evolve in a patient who started with “lone” AF. It is a chronic process. Many affected patients seem to lack cardiac awareness, thus allowing them to go for long periods with high rate atrial fibrillation.
Over time it was recognized that this was more common and occurred with varying severity. There has been some evidence, for example, that the most aggressive rate control strategy, AVN ablation and pacing, may modestly improve EF (counterbalanced, of course, by the adverse effects of RV pacing unless biV pacing is part of the management strategy).
Now on the the paper, which reported distinct inflammatory and ultrastructural patterns. From the abstract:
Results Patients with TCM, on the basis of clinical criteria, had stronger myocardial expression of major histocompatibility complex class II molecule and enhanced infiltration of CD68+ macrophages compared with patients with DCM. Furthermore, when compared with patients with ICM, the presence of T cells and macrophages was significantly reduced in TCM. Myocardial fibrosis was detected to a significantly lower degree in patients with TCM compared with patients with DCM and ICM. Electron microscopic examination revealed severe structural changes in patients with TCM. A disturbed distribution pattern of mitochondria was predominantly present in TCM. Quantitative assessment of myocyte morphology revealed significantly enhanced myocyte size compared with patients with ICM. Ribonucleic acid expression analysis identified changes in metabolic pathways among the patient groups.
Conclusions TCM is characterized by changes in cardiomyocyte and mitochondrial morphology accompanied by a macrophage-dominated cardiac inflammation. Thus, further prospective studies are warranted to characterize patients with TCM by endomyocardial biopsy more clearly.
The accompanying audio file, available as open access on the abstract page, discusses a related editorial in the same issue.