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Published on: August 17, 2022
Coronary microvascular dysfunction: a key step in the development of uraemic cardiomyopathy?
Ashwin Radhakrishnan1,2, Luke C Pickup1,2, Anna M Price1,3
1Birmingham Cardio-Renal Group, Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK.
Insights
Uraemic cardiomyopathy, common in chronic kidney disease, involves heart muscle changes and increases cardiovascular risk. Coronary microvascular dysfunction may be a key factor driving its development.
Area of Science:
- Cardiology
- Nephrology
- Cardiovascular Medicine
Background:
- Uraemic cardiomyopathy (UCM) is prevalent in chronic kidney disease (CKD).
- UCM presents as left ventricular hypertrophy, fibrosis, and impaired systolic/diastolic function.
- It significantly elevates cardiovascular morbidity and mortality risk in CKD patients.
Purpose of the Study:
- To review the current understanding of UCM pathophysiology.
- To explore the potential role of coronary microvascular dysfunction (CMD) in UCM.
- To evaluate methods for assessing coronary microvascular function and evidence for CMD in CKD.
Main Methods:
- Literature review of UCM and CMD.
- Analysis of pathophysiological mechanisms linking CKD and cardiac dysfunction.
- Evaluation of diagnostic techniques for coronary microvascular function.
Main Results:
- The exact mechanisms of UCM remain incompletely understood.
- CMD is a shared feature in phenotypically similar myocardial diseases (e.g., hypertrophic cardiomyopathy, HFpEF).
- Growing evidence suggests CMD is a significant factor in CKD-related cardiac pathology.
Conclusions:
- Coronary microvascular dysfunction is proposed as a key mediator in UCM development.
- Further research is needed to elucidate the precise role of CMD in CKD.
- Understanding CMD mechanisms may offer new therapeutic targets for UCM.
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.
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