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Review
Coronary microvascular dysfunction: a key step in the development of uraemic cardiomyopathy?
  1. Ashwin Radhakrishnan1,2,
  2. Luke C Pickup1,2,
  3. Anna M Price1,3,
  4. Jonathan P Law1,3,
  5. Nicola C Edwards1,4,
  6. Richard P Steeds1,2,
  7. Charles J Ferro1,3,
  8. Jonathan N Townend1,2
  1. 1 Birmingham Cardio-Renal Group, Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK
  2. 2 Department of Cardiology, Queen Elizabeth Hospital Birmingham, Birmingham, UK
  3. 3 Department of Nephrology, Queen Elizabeth Hospital Birmingham, Birmingham, UK
  4. 4 Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand
  1. Correspondence to Professor Jonathan N Townend; john.townend{at}uhb.nhs.uk

Abstract

The syndrome of uraemic cardiomyopathy, characterised by left ventricular hypertrophy, diffuse fibrosis and systolic and diastolic dysfunction, is common in chronic kidney disease and is associated with an increased risk of cardiovascular morbidity and mortality. The pathophysiological mechanisms leading to uraemic cardiomyopathy are not fully understood. We suggest that coronary microvascular dysfunction may be a key mediator in the development of uraemic cardiomyopathy, a phenomenon that is prevalent in other myocardial diseases that share phenotypical similarities with uraemic cardiomyopathy such as hypertrophic cardiomyopathy and heart failure with preserved ejection fraction. Here, we review the current understanding of uraemic cardiomyopathy, highlight different methods of assessing coronary microvascular function and evaluate the current evidence for coronary microvascular dysfunction in chronic kidney disease.

  • myocardial disease

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

https://doi.org/10.1136/heartjnl-2019-315138

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    Footnotes

    • Contributors All authors contributed to the writing of this manuscript: conception of the review (AR, CJF and JNT), drafting of the manuscript (AR, RPS, CJF and JNT) and critical revision of the manuscript (all authors).

    • Funding AR is funded by a Birmingham Health Partners Starter Fellowship. LCP, AMP and JPL are holders of British Heart Foundation Clinical Research Training Fellowships.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Author note References with a w can be found in the supplementary material which is loaded online with this article.

    • Correction notice Since this article was first published online, the paper has been published as open access with a CC-BY licence.

    • Patient consent for publication Not required.