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Microvascular disease and arrhythmias: a renewed focus on the myocardial microvasculature?
  1. Celine Gallagher1,
  2. Gemma Wilson1,
  3. Dennis H Lau1,2
  1. 1Australian Dysautonomia and Arrhythmia Research Collaborative, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia
  2. 2Department of Cardiology, Royal Adelaide Hospita, Adelaide, South Australia
  1. Correspondence to Dr Dennis H Lau, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide 5000, South Australia, Australia; dennis.h.lau{at}adelaide.edu.au

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Arrhythmias, and in particular atrial fibrillation (AF), are one of the greatest healthcare challenges of our time. Hospitalisation due to this condition is exponentially growing, and now outnumbers those for both heart failure and myocardial infarction.1 While much effort has been directed at pharmacological and interventional techniques to improve outcomes for those living with these conditions, less has been directed towards identifying factors associated with increased incident risk of AF and non-AF arrhythmias, and strategies to ameliorate them. Arrhythmia prediction models have long relied on conventional risk factors such as age, diabetes, hypertension, and history of myocardial infarction and heart failure. Additional ways to strengthen such models, and contribute to risk prediction for arrhythmias more broadly, are a welcome addition to current knowledge. Mechanistically, a link between microvascular disease and arrhythmias is certainly plausible. Diabetes and cardiometabolic disease are known to result in microvascular dysfunction and such remodelling in the myocardium can result in structural changes and increased arrhythmogenicity. In adults with type 2 diabetes, the presence and burden of microvascular disease (diabetic kidney disease, retinopathy or neuropathy) have been shown to be associated with increased incident AF, although broader arrhythmia risk associated with microvascular disease is less clear.2 In this context, the work by Li and colleagues in their Heart study, provides additional insights about the impact of microvascular …

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Footnotes

  • Contributors All authors contributed to this work in manuscript preparation, critical revision, analysis of data and final approval.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests DHL reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Abbott Medical, Biotronik, Medtronic and MicroPort CRM. All other authors have no disclosures.

  • Provenance and peer review Commissioned; internally peer reviewed.

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