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Editorial
Invasive coronary microvascular function assessment: pharmacological versus exercise testing
  1. Robert Sykes1,2,
  2. Daniel Tze Yee Ang1,2,
  3. Colin Berry1,2,3
  1. 1 School of Cardiovascular and Metabolic Health, University of Glasgow College of Medical Veterinary and Life Sciences, Glasgow, UK
  2. 2 Department of Cardiology, West of Scotland Regional Heart and Lung Centre, Golden Jubilee National Hospital, Clydebank, UK
  3. 3 Department of Cardiology, Queen Elizabeth University Hospital, Glasgow, UK
  1. Correspondence to Professor Colin Berry, School of Cardiovascular and Metabolic Health, BHF Glasgow Cardiovascular Research Centre, University of Glasgow College of Medical Veterinary and Life Sciences, Glasgow, G12 8TA, UK; colin.berry{at}glasgow.ac.uk

https://doi.org/10.1136/heartjnl-2023-322512

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    Coronary microvascular dysfunction is characterised by functional and/or structural abnormalities.1 It is associated with acute and chronic coronary syndromes, heart failure, non-ischaemic cardiomyopathies and impaired prognosis.2–6 Since the heart is a deep organ, safe and accurate assessment of coronary microvascular function is challenging. Myocardial ischaemia is a blood supply:demand problem (figure 1). Most research into coronary microvascular dysfunction is focused on perturbations in blood supply. Few studies of myocardial metabolism, particularly during exercise, have been undertaken.

    Figure 1

    Differential aetiology of myocardial ischaemia. CAD, coronary artery disease; CMD, coronary microvascular dysfunction.

    The mechanistic study by Noaman et al 7 provides new insights. Twenty-four patients presenting with myocardial injury, infarction or ischaemia with no obstructive coronary artery disease (MINOCA or INOCA) underwent microcirculatory resistance and myocardial metabolic assessment at the time of invasive coronary angiography. Microvascular resistance was measured in the left anterior descending coronary artery using coronary thermodilution. Measurements were taken at rest (basal resistance) and during hyperaemia …

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    Footnotes

    • Twitter @_RobSykes

    • Contributors All authors contributed to the drafting and revision of the editorial.

    • Funding CB is supported by a British Heart Foundation Centre of Research Excellence award (RE/18/6/34217), EPSRC (EP/N014642/1; EP/S030875/1) and UKRI (MR/S018905/1).

    • Competing interests CB is employed by The University of Glasgow, which employs CB, holds research and consultancy agreements with Abbot Vascular, AstraZeneca, Coroventis, GSK, HeartFlow, Menarini, Neovasc, Novartis, Siemens Healthcare and ValoHealth. These companies had no involvement in this manuscript. The other authors do not have any potential conflicts of interest.

    • Provenance and peer review Commissioned; internally peer reviewed.

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