Clyde W. Yancy
PHILADELPHIA — While HF is more prevalent in the black population than in the white population, reasons for the disparity are more complicated than simply race, Clyde W. Yancy, MD, MSc, MACC, FAHA, MACP, FHFSA, said during a plenary session at the Heart Failure Society of America Scientific Meeting.
There are real differences in HF risk between the black and white populations, including that black individuals have onset at an earlier age, have symptoms of greater consequence, have a higher incidence of HF, are more likely to have a nonischemic cause of HF, are more likely to have had hypertension implicated as a cause of their HF and have a greater risk for ventricular remodeling, Yancy, vice dean of diversity and inclusion, Magerstadt Professor of Medicine, professor of medical social sciences and chief of the division of cardiology at Northwestern University Feinberg School of Medicine, associate director of Bluhm Cardiovascular Institute, Northwestern Memorial Hospital and past president of the American Heart Association, said.
One problem, he said, is that black Americans have low rates of meeting the seven ideal CV health behaviors labeled as Life’s Simple 7 by the AHA.
“There has been demonstrated an obvious absence of these health variables in African Americans and Hispanics,” Yancy said. “This may predispose these groups to disease.”
Also of note, he said, is that ventricular abnormalities appear to disproportionately affect black individuals. “When adjusted for the duration and burden of hypertension, there is still an excess signal of ventricular thickness and increased ventricular mass, and the response to this is exaggerated and more deleterious in African Americans,” he said.
Researchers have established that nitric oxide is important to CV health, and the absence of it leads to oxidative stress, which affects protein signaling, Yancy said, noting that there are genetic polymorphisms that impede the response to nitric oxide, and “the absence of European ancestry is a defining characteristic” of those with these predilections.
“There are differences in nitric oxide homeostasis; differences in the bioavailability of nitric oxide; differences in response to a nitric oxide donor and antioxidant therapy; and differences in single nucleotide polymorphisms that impact nitric oxide signaling which appear to be associated with heart failure in certain individuals currently defined by race alone,” he said.
He also noted that “we’re learning that the ‘exposome’ — potential triggers in the built environment, eg, diet — may have an impact on protein transcription and our burden of disease. This necessarily implicates epigenetics, where environmental stimuli, aging and diet are associated with DNA methylations that in turn drive protein expression.”
Consumption of heavily processed foods, common in socioeconomically disadvantaged areas, may be uniquely problematic because of unforeseen risks inherent in inorganic phosphate consumption, Yancy said.
He mentioned that researchers have identified that increased inorganic phosphate intake is associated with higher levels of fibroblast growth factor-23 (FGF-23), especially in persons of African ancestry. The combination of hypertension and elevated FGF-23 confer “a striking 63% increase in the association with heart failure.”
It is now remarkably plausible that individuals who reside in certain at-risk communities with diets high in preserved foods/inorganic phosphates have increased upregulation of FGF-23, which in the setting of hypertension confers cardiac hypertrophy further exacerbated by chronic renal disease, and subsequently with more HF, Yancy said, noting these concepts are not yet proven but the evidence is mounting.
“To answer the question in HF, ‘is everyone the same,’? I would answer without hesitancy that the answer is no, but is it because of race per se?” Yancy said. “Perhaps it is because of the unusual epidemiology currently described by race. The unique exposure to risk factors, especially hypertension, occurring in the context of an inherited genetic profile that is further impacted by environmental exposures and the attendant epigenetic influences may substantially impact the development of disease. We believe as well that the social determinants of health and the emerging biological influence of them further defines the expression of disease. After many years of study, it can now be argued that skin color alone as a biological construct is a non-sequitur.” – by Erik Swain
Yancy CW. Plenary Session: Independence from Heart Failure: Awareness, Empathy and Activism. Presented at: Heart Failure Society of America Scientific Meeting; Sept. 13-16, 2019; Philadelphia.
Disclosure: Yancy reports no relevant financial disclosures.