Read more

December 14, 2020
2 min read
Save

Race alone may not explain ASCVD risk disparities in FH

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Race alone may not explain disparities in risk for atherosclerotic CVD among patients with familial hypercholesterolemia, according to data presented at the virtual National Lipid Association Scientific Sessions.

According to the researchers, differences in prevalence of risk factors such as hypertension and smoking status may explain the increased risk for ASCVD.

Atherosclerosis 3D_Adobe Stock
Source: Adobe Stock

Researchers analyzed 821 adults with familial hypercholesterolemia (179 Black; 642 of European ancestry) to evaluate for potential racial disparities in risk for ASCVD. Also examined were the strongest predictors for ASCVD among Black patients with familial hypercholesterolemia.

According to the poster, ASCVD was defined as coronary, peripheral and cerebrovascular events, including angina, MI, coronary angioplasty, peripheral artery surgery, claudication, peripheral angioplasty, transient ischemic attack, stroke and carotid endarterectomy.

After adjustment for study site, researchers observed that Black race was a significant predictor for ASCVD (OR = 1.68; 95% CI, 1.13-2.5; P = .01).

After additional adjustment for hypertension, smoking and diabetes, however, race was no longer a significant predictor for ASCVD among patients with familial hypercholesterolemia (OR = 1.08; 95% CI, 0.67-1.76; P = 0.7516).

Among the overall cohort, independent predictors of ASCVD included age (OR = 1.03; 95% CI, 1.01-1.04; P = .001), male sex (OR = 0.45; 95% CI, 0.31-0.65; P < .0001), hypertension (OR = 4.23; 95% CI, 2.8-6.49; P < .0001) and current smoking (OR = 2.92; 95% CI, 1.67-5.14; P = .0002), Nathan Bekele, MD, internal medicine resident at Barnes-Jewish Hospital and Washington University in St. Louis, and colleagues found.

“One limitation of this study is the relatively small sample size. Thus, it may be underpowered to detect an independent effect of race on CVD risk in Black patients that could be mediated through other factors such as psychosocial stress or lack of early treatment in addition to the apparent racial disparities,” Bekele and colleagues wrote in the poster. “It is not race alone, but racial disparities that lead to the discrepancy in ASCVD.”

Black patients presented with higher on-treatment LDL levels compared with patients of European ancestry, but this finding did not meet statistical significance (129.08 mg/dL vs. 119.85 mg/dL; P = .069).

The strongest predictors of ASCVD among Black patients with familial hypercholesterolemia were current smoking (OR = 3.83; 95% CI, 1.49-10.83; P = .0072) and hypertension (OR = 3.39; 95% CI, 1.33-9.69; P = .0146).

“Aggressive primary prevention strategies focused on the management of hypertension and smoking cessation may have a substantial impact on the cardiovascular risk profile of Black patients with [familial hypercholesterolemia],” Bekele and colleagues wrote.