ABSTRACT
S cience evolves as a continuous turnover o f hypotheses that require constant review/ revision. It is time to reconsider each single caryatid which sustains the present conceptual temple dealing with the etiopathogenesis of CHD. Readers will recognize that most, if not all, current etiopathogenic assumptions are only
hypotheses and that they are mainly derived from clinical images of questionable interpreta tion. They will appreciate that, at present, clinicians deal with patients who have symptoms and usually have disease that is well advanced. Perforce, they do not often examine individuals when a pathologic process begins. On the other hand, while pathologists often study advanced disease at postmortem, they can investigate (a) evolving disease in persons dead at its different stages; (b) the meaning of common variables by studying other diseases and normal people dying from different type of accident; and (c) substantiate the structure of clinical images without which the latter remained unexplained. Also, at present, we have no experimental model reproducing the natural history of this disease.
