Isabella Canavero, MD
The hypothetical “democracy” of diseases potentially affecting everyone has to be retracted when analyzing real-world data. We must acknowledge that, actually, nothing is fair about diseases. Access to medical care, nutrition, socioeconomic status, and education are relevant factors in determining course and outcome of many diseases, especially in the vascular area. Stroke follows this rule: As compared to White people, other underrepresented racial-ethnic populations are featured by a disproportionately higher prevalence of traditional vascular risk factors (hypertension, diabetes, obesity above all).
Besides socioeconomic and cultural determinants of lifestyle resulting in vascular risk factors, Kamin Mukaz et al. explored genetic and biological factors partly accounting for the racial disparity of stroke by reviewing current evidence from large cohorts.
In fact, the biological basis of racial disparities lay on circulating factors. Inflammation is a mainstay of vascular pathology. The higher levels of inflammatory biomarkers found in Black people than other racial groups suggest an explanation for their higher stroke risk, though only InterLeukin-6 values were found to be a race-specific detrimental factor by multivariate analyses. C-reactive protein levels and white blood cell count were directly associated with stroke risk, but not mediating racial disparities.
Black and White patients differ also for thrombotic biomarker profiles: Black people more frequently show increased levels of procoagulant factors and reduced levels of anticoagulants. Furthermore, the blood type AB, which is common in Black people, is associated with higher levels of factor VIII. However, the complexity of the coagulation pathway prevents a thorough characterization of pathogenesis in the different races.
In addition, lipoprotein (a) levels are largely genetically determined and correlate with increased cardio-cerebrovascular risk. Black patients have smaller Lp(a) isoforms, resulting in higher circulating Lp(a) levels, and genetic variation relating to subclinical atherosclerosis, likely accounting for the excess of stroke risk as compared to other racial groups and potentially representing a target for pharmacological treatment.
Beyond focusing on the clinical evaluation of stroke patients, selecting the risk factors that feature one race as compared to the others could help the mirroring process of pre-clinical stroke models involving rodents with genetic restrictions resulting in exaggerated expression of such risk factors (for example, the Spontaneously Hypertensive Rats and the Stroke-Prone Spontaneously Hypertensive Rats).
In the aim of tailoring medicine on patients’ features, investigating biological and genetic determinants of racial disparity in stroke is crucial for implementing preventive strategies and diagnostic work-up in acute stroke patients, and targeting intervention and treatments. Developing such a customized approach shouldn’t be misinterpreted as a discrimination strategy, but as a key to the prompt recognition and management of race-specific risks and comorbidities, thus actually fighting disparities in stroke care.
*This article is part of a Focused Updates series of articles on topics related to health equity published in the November 2020 issue of Stroke.
