UCSF

The intersection of cardiovascular disease, heart transplantation and gene-environment interactions are laying a new landscape in how genes and environmental risk factors connect. Methods for next gene sequencing and whole genome sequencing, once thought too novel for use in common disease states like heart transplantation are becoming more common in understanding this gene-environment interaction. Cardiac ion channel disease is not assessed routinely during the procurement phase of heart transplantation yet hidden diseases like Brugada Syndrome can occur. Cardiac disease as we once thought is not necessarily inherited. Instead, we acquire a set of susceptible risk factors to certain environmental influences, and this heightened risk is what causes a certain disease. This is why certain individuals who live a healthy lifestyle can suffer from a myocardial infarction at a young age yet others who seem immune to the effects of unhealthy living and can live long lives. It is this variation to susceptibility that increases disease. Hence, all humans carry some variation genetically and understanding this variation will ultimately assist in intervention strategies aimed at high-risk individuals (i.e., the heart transplant population). Therefore, further research is required to determine how these variations can affect individuals in the pre-/post-transplant phase.