Alcohol is a recognized teratogen that affects various aspects of fetal development. Tissue that is particularly susceptible to its teratogenicity is neuronal tissue. The effect of prenatal alcohol exposure (PAE) on the central nervous system has been extensively studied, yet the knowledge on the influence of PAE on the autonomic nervous system is scarce. The purpose of this article is to review the current state of knowledge about the impact of PAE on the autonomic nervous system. Studies conducted on the PAE animal model have shown that prenatal alcohol exposure is associated with significant alterations in the autonomic nervous system, but the mechanisms and consequences are not yet clearly defined. It was established that PAE causes decreased heart rate variability (HRV) in fetal cardiotocography. Several studies have revealed that later, in infancy and childhood, reduced parasympathetic activity with or without compensating sympathetic activity is observed. This may result in behavioral and attention disorders, as well as an increased predisposition to sudden infant death syndrome. Both animal and human studies indicate that the relationship between PAE and autonomic dysfunction exists, however large, well-designed, prospective studies are needed to confirm the causal relationship and characterize the nature of the observed changes.
Increasing numbers of implanted cardiovascular electronic devices, results in a need for lead extractions, which has increased to an annual volume of over 10,000 worldwide. We present a cadaveric dissection body with a single chamber pacemaker implanted 5y before death.