Cardiovascular causes of perinatal loss.

High risk changes in the cardiac action, mostly manifesting with arrhythmias, may be caused by microscopic malformation of the conduction system. The finding of accessory AV communications, particularly nodo-fasciculoventricular Mahaim bundles are rather frequent in perinatal loss as well as in SIDS, but a clinicopathological assessment of their lethal arrhythmogenic potential is often impossible. These congenital abnormalities, under particular conditions and/or neurovegetative stimuli, are liable to provoke electrical inhomogeneity, instability, and desynchronization with impeding risk of malignant junctional arrhythmias. Mahaim fibers have been detected in 39% of sudden perinatal death and in 23% of SIDS victims. These lesions have been attributed to the variable outcome of a “resorptive degeneration” process that normally “reshapes” the junctional pathways in the early postnatal period. Another approach to the same problem can be made by taking into consideration the persistence of ontogenically specialized ring tissue, astride the AV annuli or, as seen in neonatal death victims, putting together a sort of “arrhythmogenic interface” with the ordinary myocardium, at the top of the ventricular septum. Also, the central cardiac structure supporting the conduction system, could possibly interfere with the causation of impulses, as in the cases of cartilaginous metaplasia of the fibrous body, detected in 6% of SIDS and in 19% of sudden perinatal victims. Regarding the long QT syndrome, as a favoring condition for ventricular tachycardia-fibrillation with a high risk of sudden cardiac death, one can say that this thesis is losing ground; the implications of the neurovegetative reflex mechanisms, does not correspond to any clear-cut pathologic changes. Early atherosclerotic lesions of the cerebral and coronary arteries, involving also the sino-atrial and atrio-ventricular arteries, significantly associated with maternal cigarette smoking, are common in the perinatal period. Lastly, cases of fibromuscolar hyperplasia of the pulmonary artery were detected.