Access to Cardiovascular Care for Indigenous Peoples in Canada: A Rapid Review.

Indigenous peoples in Canada are at an increased risk of cardiovascular disease compared to non-Indigenous people. Contributing factors include historical oppression, racism, healthcare biases, and disparities in terms of the social determinants of health. Access to and inequity in cardiovascular care for Indigenous peoples in Canada remain poorly studied and understood. A rapid review of the literature was performed using the PubMed/MEDLINE, Web of Science, and Indigenous Studies Portal (iPortal) databases to identify articles describing access to cardiovascular care for Indigenous peoples in Canada between 2002 and 2021. Included articles were presented narratively in the context of delays in seeking, reaching, or receiving care, or as disparities in cardiovascular outcomes, and were assessed for their successful engagement in indigenous health research using a preexisting framework. Current research suggests that gaps most prominently present as delays in receiving care and as poorer long-term outcomes. The literature is concentrated in Alberta, Manitoba, and Ontario, as well as among First Nations people, and is largely rooted in a biomedical worldview. Additional community-driven research is required to better elucidate the gaps in access to holistic cardiovascular care for Indigenous peoples in Canada. Healthcare professionals, researchers, and policymakers should reflect further upon their actions and privilege, educate themselves about historical facts and the Truth and Reconciliation Commission, tackle prevailing disparities and systemic barriers in the healthcare systems, and develop culturally safe and ethically appropriate healthcare interventions to improve the health of all Indigenous peoples in Canada.

Le risque de maladies cardiovasculaires est plus élevé chez les populations autochtones du Canada que chez les populations non autochtones. L'oppression historique, le racisme, les préjugés dans les soins de santé et les disparités quant aux déterminants sociaux de la santé sont des facteurs qui contribuent à ce phénomène. L'accès aux soins cardiovasculaires et l'équité des soins pour les personnes autochtones du Canada sont des questions peu étudiées et mal comprises. Une revue rapide de la littérature a été réalisée dans les bases de données PubMed/MEDLINE, Web of Science et Indigenous Studies Portal (iPortal) pour recenser les articles publiés entre 2002 et 2021 qui décrivent l'accès aux soins cardiovasculaires pour les peuples autochtones du Canada. Les articles retenus sont présentés de manière narrative et font état de retards dans la recherche de soins, dans l'atteinte d'un établissement de soins et dans l'obtention des soins, ou de certaines disparités quant aux résultats de santé cardiovasculaire. Ces articles ont également été évalués d'après leur intégration réussie des principes de recherche en santé autochtone à partir d'un cadre déjà établi. Selon les recherches actuelles, les écarts se manifestent principalement par des retards dans l'obtention des soins et par des résultats de santé plus défavorables à long terme. Les études publiées se concentrent surtout sur l'Alberta, le Manitoba et l'Ontario, portent principalement sur les Premières Nations et sont en grande partie abordées selon une perspective biomédicale. Des recherches plus approfondies, menées avec les communautés autochtones, sont nécessaires pour mieux comprendre les écarts dans l'accès à des soins cardiovasculaires holistiques pour les peuples autochtones du Canada. Les professionnels de la santé, les chercheurs et les décideurs politiques devraient entreprendre un processus de réflexion approfondie sur leurs actions et leurs privilèges, s'informer sur les réalités historiques ainsi que sur la Commission de vérité et réconciliation, s'attaquer aux disparités qui perdurent et aux barrières systémiques dans l'accès aux soins de santé, et mettre en place des interventions de soins culturellement sécuritaires et éthiquement adaptées, pour améliorer la santé de l'ensemble de la population autochtone du Canada.

Increased ventricular repolarization heterogeneity in patients with ventricular arrhythmia vulnerability and cardiomyopathy: a human in vivo study.

Increased repolarization heterogeneity can provide the substrate for reentrant ventricular arrhythmias in animal models of cardiomyopathy. We hypothesized that ventricular repolarization heterogeneity is also greater in patients with cardiomyopathy and ventricular arrhythmia vulnerability (inducible ventricular tachycardia or positive microvolt T wave alternans, VT/TWA) compared with a similar patient population without ventricular arrhythmia vulnerability (no VT/TWA). Endocardial and epicardial repolarization heterogeneity was measured in patients with (n = 12) and without (n = 10) VT/TWA by using transvenous 26-electrode catheters placed along the anteroseptal right ventricular endocardium and left ventricular epicardium. Local activation times (AT), activation-recovery intervals (ARI), and repolarization times (RT) were measured from unipolar electrograms. Endocardial RT dispersion along the apicobasal ventricle was greater (P < 0.005) in patients with VT/TWA than in those without VT/TWA because of greater ARI dispersion (P < 0.005). AT dispersion was similar between the two groups. Epicardial RT dispersion along the apicobasal ventricle was greater (P < 0.05) in patients with VT/TWA than in those without VT/TWA because of greater ARI dispersion (P < 0.05). AT dispersion was similar between the two groups. A plot of AT as a function of ARI revealed an inverse linear relationship for no VT/TWA such that progressively later activation was associated with progressively shorter ARI. The AT-ARI relationship was nonlinear in VT/TWA. In conclusion, patients with cardiomyopathy and VT/TWA have greater endocardial and epicardial repolarization heterogeneity than those without VT/TWA without associated conduction slowing. The steep repolarization gradients in VT/TWA may provide the substrate for functional conduction block and reentrant ventricular arrhythmias.

Effects of folic acid fortification and multivitamin therapy on homocysteine and vitamin B(12) status in cardiac transplant recipients.

BACKGROUND: Hyperhomocysteinemia is a frequent finding after cardiac transplantation, but increased folate intake induces a decrease in total homocysteine concentrations. In 1998, food in Canada was fortified nationwide with folic acid. We assessed the impact of routine folate fortification on homocysteine concentrations in our cardiac transplant population. METHODS: In 18 subjects, we measured total homocysteine (tHcy), serum folate, and cobalamin concentrations in 1997 (before folate fortification) and in 1998 (after fortification). We repeated the analysis after specific multivitamin supplementation for 10 weeks. RESULTS: We found a significant decrease in baseline tHcy concentrations and in folate concentrations between 1997 and 1998. However, we also found a decrease in serum cobalamin concentrations. We found a correlation between decreased cobalamin concentrations and the methionine synthase A2756G genotype, but not with other common polymorphisms associated with homocysteine metabolism. After multivitamin supplementation, we observed a trend toward further decrease in tHcy concentrations and a significant increase in serum folate and cobalamin concentrations. Finally, we measured serum methylmalonic acid concentrations, an index of tissue cobalamin status. We did not find a correlation between increased methylmalonic acid concentrations and decreased serum cobalamin, perhaps related to the confounding effect of altered renal status on methylmalonic acid excretion. CONCLUSIONS: National folate fortification was associated with decreased tHcy and increased folate concentrations in our cardiac transplant population. Additional administration of vitamin supplements induced a further decrease in tHcy and an increase in folate. Finally, folate fortification unveiled cobalamin deficiency in some patients, associated with the methionine synthase A2756G mutation.