Adult heart disease could stem from fetal infections

Heart disease in adults could be a result of fetal infection and inflammation before birth, especially if a baby is born prematurely, researchers from the University of Washington School of Medicine reported this week.

There’s an established link between premature birth and a higher likelihood of developing heart disease as an adult, lead author Kristina M. Adams Waldorf, MD, and colleagues wrote in the American Journal of Obstetrics and Gynecology—but current research tells us little about why that might be.

“This study connects the dots between preterm birth and heart disease in adult life by defining the gene networks disrupted by infection and inflammation that program normal heart development,” Adams Waldorf said in a release from UW.  “When I was in training, we talked to women in preterm labor about the risk to their infants of lung and brain injury. We now know that long-term health risks of a preterm birth extend beyond the developing lungs and brain to involve vision, hearing, kidney and even heart function.”

The researchers studied fetal reactions to infection in pigtail macaque monkeys—animals that share close similarities with human pregnancies—and found that gene programming in the fetal primates was compromised when the mother was exposed to an infectious disease. An inability to program genes correctly can lead to incomplete cardiac development, which can branch into heart failure or arrhythmia as the baby ages.

Monkeys were mostly infected with Group B Streptococcus and Escherichia coli, Adams Waldorf and co-authors wrote, because both strains are common infectors in human pregnancies. Expectant moms infected by these bacteria are often triggered into preterm labor.

Infection quickly triggered an inflammatory response in affected fetuses, the team found. Inflammation spanned from heart tissue to inflammatory proteins like interleukin-6 and interleukin-8, as well as altering the expression of a handful of genes responsible for heart development.

In addition to those genes, which included NPPA, MYH6 and ACE2, gene networks involved in heart and blood vessel formation, cardiomyocyte growth and the migration of endothelial cells were compromised.

“Future research should investigate whether combining antibiotics to treat the infection and anti-inflammatory drugs can lessen inflammation and damage to the fetal heart,” Adams Waldorf said. “If we can better understand how to prevent infections that cause preterm birth, we can protect fetuses and enhance their long-term health into adulthood.”