Further contribution to the understanding of the post-infarctual anedematous syndrome.

The authors describe an anomalous post-infarctual evolution, already revealed by Sotgiu in 1959 and defined the’ postinfarctual anedematous syndrome’ (SAPI). The syndrome, present in about 12% of MI, demonstrates a clinical picture characterized by a global hypometabolism, absence of edema and state of continuous sub-collapse; an endocrine picture characterized by a corticomedullary adrenal, thyroid and hypophisis hypoactivity. The results confirm that, in contrast to other myocardial infarction cases, in patients with SAPI low values of cortisol, aldosterone and catecholamines exist, with alteration of the glycocorticoid and adrenergic amine circadian-biorhythm. The pharmacodynamic tests, demonstrating the integrity of the adrenal gland, have revealed an alteration of the hypothalamic-pituitary function. According to the authors, the occurrence of SAPI might be interpreted on the basis of a particular vulnerability of the hypothalamic-pituitary system (often depending upon the senile age of the subjects) which is probably amplified by the stress created by the myocardial necrosis.