Perspective: Conundrums in CVD: Deciphering the Role of Race/Ethnicity

Although health, life expectancy and overall cardiovascular care has improved dramatically for all Americans over the last several decades, the distribution of benefits has not occurred equably. There remains a persistent and disturbing mortality gap between black and white Americans which has been noted since the 1960s.

A major component of this disparity in cardiovascular disease morbidity and mortality in African Americans is due to higher risk of hypertension and heart failure, along with a unique, perhaps higher risk related to Lipoprotein(a) (Lp(a)). Cardiovascular morbidity and mortality needs to be addressed since atherosclerotic cardiovascular disease and stroke are the leading causes of death for all populations, but account for the largest proportion of inequality in life expectancy between blacks and whites.

Today, a joint symposium of the ACC and the Association of Black Cardiologists will be an opportunity to highlight contemporary concepts about the basis of and potential solutions for cardiovascular disease disparities. Recognizing that race, at best, is a crude proxy for genetics, the important discussion of the impact of genomics on heart failure and cardiovascular disease in blacks will be presented by Michael R. Bristow, MD, PhD, FACC. Bristow will advocate for better understanding of the association between race and response to specific pharmacotherapy in heart failure. As a counterpoint, Ivor J. Benjamin, MD, FACC, will provide contemporary evidence on the presence or absence of underlying genetic factors. He will highlight some of the late-breaking concepts in genomics and how we can better understand which patients are at risk for cardiovascular disease based on inherited characteristics that go beyond the blunt assessment of race, which is not a scientific category at all.

Unique aspects of cardiovascular risk in blacks include high prevalence and severity of hypertension. Kenneth A. Jamerson, MD, will present current concepts on best approaches to hypertension in this high-risk population. He will give information on best practices or concepts in approaching high-risk African Americans with hypertension, and perhaps critique some of our current understanding in an effort to better control blood pressure, a potent risk factor, especially in the U.S. black population.

While awaiting interim results from cardiovascular outcomes trials, proprotein convertase subtilisin/kexin 9 (PCSK9) inhibition remains a potentially prominent means to reduce cardiovascular risk. The unique aspects of Lp(a) in blacks will be discussed, and the potential benefit, or lack thereof, of PCSK9 inhibition in African Americans will be highlighted by Karol E. Watson, MD. Our understanding of the risk of Lp(a) has been recently improving, and there may be unique means of reducing Lp(a) and cardiovascular outcomes on the horizon. PCSK9 inhibitors are now approved and their ability to approach low-density lipoprotein and Lp(a) may offer positive opportunities, especially considering the high degree of premature atherosclerosis in African Americans.

The session will conclude with adequate time for group discussion, audience questions and debate as clinicians, public health officials and governmental agencies all strive to elucidate best practices to control the unnecessary and unacceptable disparities in cardiovascular disease. Overall, the session will be a unique opportunity to address cardiovascular disease disparities, which are persistent and significant, though hopefully modifiable.

Clinical Topics: Arrhythmias and Clinical EP, Clinical Topic Collection: Dyslipidemia, Heart Failure and Cardiomyopathies, Prevention, Genetic Arrhythmic Conditions, Lipid Metabolism, Novel Agents, Acute Heart Failure, Hypertension

Keywords: ACC Publications, ACC Annual Scientific Session, Atherosclerosis, Blood Pressure, Blood Pressure Determination, Cardiovascular Diseases, Cause of Death, Genomics, Heart Failure, Hypertension, Life Expectancy, Prevalence, Proprotein Convertases, Stroke


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