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Background There is no universally accepted age cut‐off for defining young strokes. Aims We aimed to determine, based on the profile of young stroke patients in our regional centre, an appropriate age cut‐off for young strokes. Methods A retrospective analysis of all ischaemic stroke patients admitted to our centre from 2015 to 2017. We identified 391 ischaemic stroke patients; 30 patients between the ages of ≤50, 40 between 51–60 inclusive and 321 ≥ 61 years of age. We collected data on demographic profiles, risk factors and stroke classification using the Trial of Org 10 172 in Acute Stroke Treatment criteria. Results We found significant differences between the ≤50 and ≥61 age groups for most of the risk factors and similarities between the 51–60 inclusive and ≥ 61 age groups. At least one of the six risk factors assessed in the study was present in 86.7% of the youngest group, 97.5% of the intermediate age group and 97.2% in the oldest group. In terms of the mechanisms of stroke, the youngest and oldest age groups in our study differed in the prevalence of cryptogenic, cardioembolic and other causes of stroke. The middle and older age groups had similar mechanisms of stroke. Conclusions The prevalence of vascular risk factors and mechanisms of stroke likewise differed significantly across age groups. This study suggests that 50 years is an appropriate age cut‐off for defining young strokes and reinforces the importance of primary prevention in all age groups.

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Background Ticagrelor is an oral anti-platelet agent that is a reversible and direct inhibitor of the adenosine diphosphate P2Y12 receptor. Ticagrelor’s brady-arrhythmic potential was investigated in a sub-study of the PLATO trial, which concluded that the effects were transient and not clinically significant beyond the acute initiation phase. Since then, there have been emerging reports of ticagrelor-associated high-degree heart block, requiring drug discontinuation and pacemaker insertion. We present a case of symptomatic ventricular pauses in a patient loaded with ticagrelor post-percutaneous coronary intervention (PCI) for non-ST elevation acute coronary syndrome (NSTEACS) and review the literature relating to ticagrelor and its brady-arrhythmic potential. Case summary A 59-year-old female presented to our hospital with NSTEACS and received an oral load of ticagrelor 180 mg following PCI to her mid-left circumflex coronary artery. Three hours after, four pauses were observed on telemetry over a 20 min period, the longest being 18.5 s in duration. Ticagrelor was ceased and clopidogrel commenced in place. No arrhythmic events were recorded on loop recorder interrogation following ticagrelor discontinuation. Discussion The exact mechanism of ticagrelor-induced brady-arrhythmia is unclear, although inhibition of adenosine reuptake is proposed as likely due to structural similarities between ticagrelor and adenosine. In the setting of acute coronary syndrome treated with ticagrelor, extracellular adenosine concentrations are amplified by the ischaemic milieu with myocardial adenosine release and blunted cellular reuptake. This leads to enhanced agonism of adenosine A1 receptors, causing negative chronotropy and dromotropy. This case report highlights ticagrelor’s brady-arrhythmic potential even in the absence of baseline conduction disease or concurrent confounding medications.