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
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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.
Patient consent for publication Not required.
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