Race, Socioeconomic Factors Contribute to Heart Failure Outcomes
– In a study of end-stage heart failure patients, researchers at the University of Alabama at Birmingham (UAB) found that race and socioeconomic factors may contribute to differences heart failure outcomes in black and white men.
Published in the American Journal of Physiology: Heart and Circulatory Physiology, the findings showed differences in methylation of the DNA in the heart among patients – and that race was the sole variable in patient records that explained the difference.
Researchers subsequently looked at the census tracts where the patients lived and saw that black subjects lived in neighborhoods with more racial diversity and poverty, indicating that the underlying variable may be a socioeconomic difference.
Despite the high prevalence of heart failure, researchers noted that only half of heart failure patients respond to guideline-directed medical management. This disparity has led investigators to examine the underlying molecular differences that contribute to the heterogeneity of heart failure.
Methylation of DNA is a form of epigenetics, an indirect method of gene regulation that can differ with gene-environment interaction.
The UAB study included a pilot cohort of eleven heart failure patients, followed by a testing cohort of 31 heart failure patients – all of them male. Researchers obtained the heart muscle tissue for the study when patients underwent surgery to install a left ventricular assist device, or LVAD. This device is a small mechanical pump carried outside the body to help a weakened heart pump blood.
Until now, epigenetics has been an unexamined source of heterogeneity among patients with end-stage heart failure. UAB researchers found differential promoter hyper-methylation of genes involved in fatty acid metabolism among black patients’ heart muscle samples compared to white patients’ samples. The team also saw higher expression of lipogenesis genes.
These molecular alterations are pathological signs of end-stage heart failure, because the heart gets more of its energy from glucose sugar as it fails.
This finding led to two hypotheses among the researchers. The first was that epigenetic remodeling of cardiac gene regulation determines the treatment potential of LVADs.
The group also theorized that epigenetic reprogramming of cardiac gene regulation includes a process that may impact a patient’s responsiveness to LVADs, when the heart possibly improves because the pump takes over part of the work.
In contrast to the hyper-methylated promoters, genes that had differentially hypo-methylated promoters – or lower levels of methylation – in black patients’ hearts disproportionately represented inflammatory signaling cascades.
UAB researchers also conducted a retrospective analysis of deaths from any cause in the…