Contemporary Outcomes of Acute Coronary Syndromes in Indigenous Compared With Non-Indigenous Patients: A Northern Saskatchewan Perspective.

Background: In patients presenting with an acute coronary syndrome (ACS), the impact of efforts to bridge historical care gaps between Indigenous and non-Indigenous patients remains limited.

Methods: For consecutive ACS presentations (ST-segment elevation myocardial infarction [STEMI] and non-ST-segment elevation myocardial infarction [NSTEMI]/unstable angina [UA], respectively) at the Royal University Hospital, Saskatoon, we compared self-identified Indigenous and non-Indigenous patients' demographics, treatments, and all-cause mortality (in-hospital and within 3 years). We used propensity score inverse probability weighting to mitigate confounding and Cox regression models to estimate the adjusted hazard ratio (aHR) for all-cause mortality.

Mitochondrial dysfunction in neurodegenerative disorders.

Recent advances in understanding the role of mitochondrial dysfunction in neurodegenerative diseases have expanded the opportunities for neurotherapeutics targeting mitochondria to alleviate symptoms and slow disease progression. In this review, we offer a historical account of advances in mitochondrial biology and neurodegenerative disease. Additionally, we summarize current knowledge of the normal physiology of mitochondria and the pathogenesis of mitochondrial dysfunction, the role of mitochondrial dysfunction in neurodegenerative disease, current therapeutics and recent therapeutic advances, as well as future directions for neurotherapeutics targeting mitochondrial function.

The Canadian WATCHMAN Registry for Percutaneous Left Atrial Appendage Closure.

Background: Access to left atrial appendage closure (LAAC) in Canada is limited, due to funding restrictions. This work aimed to assess Canadian clinical practice on patient selection, postprocedural antithrombotic therapy, and safety and/or efficacy with WATCHMAN device implantation.

Methods: Seven Canadian centres implanting the WATCHMAN device participated in this prospective multicentre, observational registry.

Canadian Spontaneous Coronary Artery Dissection Cohort Study: 3-Year Outcomes.

Background: Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction (MI) in young to middle-aged women.

Objectives: We aim to define the long-term natural history of SCAD.

Methods: We performed a multicenter, prospective, observational study of patients with nonatherosclerotic SCAD presenting acutely from 22 North American centers.

Erratum to: Advanced Glycation End Products: Receptors for Advanced Glycation End Products Axis in Coronary Stent Restenosis: A Prospective Study.

[This corrects the article DOI: 10.1055/s-0038-1673660.].

Canadian spontaneous coronary artery dissection cohort study: in-hospital and 30-day outcomes.

Aims: Spontaneous coronary artery dissection (SCAD) was underdiagnosed and poorly understood for decades. It is increasingly recognized as an important cause of myocardial infarction (MI) in women. We aimed to assess the natural history of SCAD, which has not been adequately explored.

Advanced Glycation End Products:Receptors for Advanced Glycation End Products Axis in Coronary Stent Restenosis: A Prospective Study.

This study was aimed to correlate the pre- and 6-month postpercutaneous coronary intervention (PCI) serum concentrations of advanced glycation end products (AGE), soluble receptors for advanced glycation end products (sRAGE), AGE/sRAGE ratio, and serum malondialdehyde (MDA) levels with in-stent restenosis (ISR) among patients receiving either a drug-eluting stent (DES) or a bare-metal stent (BMS).In-stent restenosis remains as an adverse outcome following PCI. Sixty consecutive nondiabetic, Caucasian male patients, diagnosed with a non-ST-elevation myocardial infarction who received either a DES or BMS via PCI, were enrolled.

Atherosclerosis and the Hypercholesterolemic AGE-RAGE Axis.

Background Interaction of advanced glycation end products (AGE) with the receptor for advanced glycation end products (RAGE) has been implicated in the pathogenesis of atherosclerosis. Soluble receptors for advanced glycation end products (sRAGE) act as a decoy for AGE by competing with RAGE and suppressing developing atherosclerosis. Hypercholesterolemia and the oxidative stress are known factors involved in atherosclerosis.

Inverse Association between Cardiac Troponin-I and Soluble Receptor for Advanced Glycation End Products in Patients with Non-ST-Segment Elevation Myocardial Infarction.

Interaction of advanced glycation end products (AGEs) with the receptor for advanced AGEs (RAGE) results in activation of nuclear factor kappa-B, release of cytokines, expression of adhesion molecules, and induction of oxidative stress. Oxygen radicals are involved in plaque rupture contributing to thromboembolism, resulting in acute coronary syndrome (ACS). Thromboembolism and the direct effect of oxygen radicals on myocardial cells cause cardiac damage that results in the release of cardiac troponin-I (cTnI) and other biochemical markers.

Soluble receptors for advanced glycation end products (sRAGE) as a predictor of restenosis following percutaneous coronary intervention.

Background: Interaction of advanced glycation end products (AGEs) with their receptor (RAGE) increases expression of inflammatory mediators (tumor necrosis factor alpha [TNF-α] and soluble vascular cell adhesion molecule-1 [sVCAM-1]) and induces oxygen radicals that are implicated in atherosclerosis. Balloon-injury-induced atherosclerosis is associated with increased expression of AGEs and RAGE. The soluble receptor for AGE (sRAGE), which acts as a decoy for RAGE ligands (AGEs), prevents atherosclerosis in this model.

Modulation of high sensitivity C-reactive protein by soluble receptor for advanced glycation end products.

High sensitivity C-reactive protein (hs-CRP) is synthesized mainly by hepatocytes in response to tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interleukin-6 (IL-6). The interaction of advanced glycation end products (AGEs) with the receptor for advanced glycation end products (RAGE) increases the expression of the cytokines TNF-alpha, IL-1, and IL-6. Soluble receptor for advanced glycation end products (sRAGE) competes with RAGE for binding with AGEs.

Low levels of soluble receptor for advanced glycation end products in non-ST elevation myocardial infarction patients.

Background: Interaction of the receptors for advanced glycation end products (RAGEs) with advanced glycation end products (AGEs) results in expression of inflammatory mediators (tumor necrosis factor-alpha [TNF-α] and soluble vascular cell adhesion molecule-1 [sVCAM-1]), activation of nuclear factor-kappa B and induction of oxidative stress - all of which have been implicated in atherosclerosis. Soluble RAGE (sRAGE) acts as a decoy for the RAGE ligand and is protective against atherosclerosis.

Objectives: To determine whether levels of serum sRAGE are lower, and whether levels of serum AGEs, TNF-α and sVCAM-1 are higher in non-ST elevation myocardial infarction (NSTEMI) patients than in healthy control subjects; and whether sRAGE or the ratio of AGEs to sRAGE (AGEs/sRAGE) is a predictor/biomarker of NSTEMI.