**6. Conclusions**

As shown across the sections of this chapter, the numerous hypothesis about pathogenic pathways of CCC have supporting data and pitfalls. Finally all proposals interact with each other, giving us the idea that none of these theories explains the very complex development of CCC by itself. Rather, it seems more feasible that all these hypothesis conform a network of damaging elements, and that all ingredients cause and/or enhances each other. The triggering factor is obviously the interaction between parasite and host's immune system. Cell parasitism, the inflammatory process and consequent necrosis and fibrosis cause damage to contracting myocardium, autonomic system, conduction system and microcirculation. Autonomic damage causes impaired regulation of microvasculature and further alterations in blood flow. Ischemia causes more myocardial damage. Necrosis exposes intracellular epitopes and causes autoantibodies production with more necrosis, fibrosis and so on. It seems that, if adequate down modulator immune mechanisms work properly, this vicious circle stops and patients do not develop cardiomyopathy, rather they remain in the indeterminate form lifelong.
