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Santos et al. Vessel Plus 2021;5:21 https://dx.doi.org/10.20517/2574-1209.2020.69 Page 5 of 16

their non-Indigenous counterparts [11,15,36,40-44] . Why stroke occurs at a younger age in Indigenous people is
[44]
unclear. It may be attributed to a greater burden of modifiable risk factors , linked to social determinants
of health as well as the effects of colonisation, systemic racism, institutional bias and loss of traditional
cultural practices [3-5,45] .

The Table 1 summarises the available studies identified in our narrative review that specifically address
cardiovascular risk factors in Indigenous populations with stroke.

Management of Indigenous patients with stroke
Stroke management has been revolutionised over recent years. Initial momentum started with multi-
disciplinary stroke units and development of national guidelines to enable protocol development and
[59]
[58]
standardisation of care . Intravenous thrombolysis with alteplase , more recently tenecteplase , and
[60]
endovascular clot retrieval has given patients a chance of recovery from what could previously have been
[61]
lifelong disability, or death. In particular, endovascular thrombectomy is now one of the most powerful
treatments in medicine with a number-needed-to-treat as low as 2.6 to reduce disability from stroke .
[61]
Despite the strong evidence that exists in support of treatment, analysis of Indigenous patients receipt of
this care is lacking. The limited data that exist demonstrate that Indigenous patients may be less likely to
receive evidence-based care [40,42,62-64] .
[40]
In Australia, Kilkenny et al. reported that out of the 33 hospitals included in the 2009 study, rates of
thrombolysis were low (< 10%). Of major concern, no Indigenous patient included in the audit received
intravenous thrombolysis. Additionally, Indigenous patients were less likely to receive care in a stroke unit
(adjusted odds ratio of 0.53), and when their stroke was ischaemic, Indigenous patients were less likely to
receive aspirin within 48 h or be discharged on antithrombotic medications than non-Indigenous patients.
Indigenous patients with stroke were also less likely to have an allied health assessment within 48 h of
admission. This may have contributed to the greater dependency of Indigenous patients at discharge.
Tiedeman et al. reported that Indigenous patients were less likely to have in-hospital cardiac monitoring
[42]
and upon discharge were less likely to be followed up by a specialist.

[62]
Similarly, in a population-based cohort study from Ontario , First Nations people admitted with stroke
were less likely to receive thrombolysis than other Canadians (6.3% vs. 11.0%), although no difference was
detected when comparing assessment with neuroimaging, carotid revascularisation or referral to
rehabilitation.

In research from the United States, racial disparities are evident when analysing the use of intravenous
thrombolysis for treatment of ischaemic stroke [65-67] . However, most studies fail to include identification of
Indigenous Peoples as a separate treatment group and largely characterise race as “non-Hispanic White” or
“Black”. Within the studies that specifically mention American Indigenous groups (Native American,
American Indians or Pacific Islander), Indigenous Peoples are sometimes grouped with other minority
[68]
groups. For example, Aparicio et al. analysed the difference in treatment rates of patients presenting to
primary stroke centres versus non-primary stroke centres. They performed a retrospective cohort study
using data from the Nationwide Inpatient Sample (NIS) from 2004 to 2010. The NIS classifies race/ethnicity
as White, Black, Hispanic, Asian/Pacific, Native American or Other. There were 304,152 patients included
in the analysis, 71.5% were White, 15.0% Black, 7.9% Hispanic and 5.6% were grouped as Other
(Asian/Pacific Islander, Native American or other). When they compared thrombolysis rates between
groups, all racial groups compared to Whites were significantly less likely to be treated. The adjusted odds
ratio (OR) for “others” vs. White at the primary stroke centres was 0.75 (CI: 0.64-0.89) and at the non-