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Published on: August 17, 2022
Association between coronary microvascular dysfunction and exercise capacity in dilated cardiomyopathy
Abhishek Dattani1, Benjamin A Marrow1, Gaurav S Gulsin1
1Department of Cardiovascular Sciences, University of Leicester and the National Institute for Health and Care Research Leicester Biomedical Research Centre, Leicester, UK.
Insights
Dilated cardiomyopathy (DCM) patients show reduced myocardial perfusion reserve (MPR) and stress blood flow. MPR, left ventricular ejection fraction, and fibrosis are key factors linked to exercise capacity in DCM patients.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Exercise Physiology
Background:
- Aerobic exercise capacity predicts mortality in dilated cardiomyopathy (DCM).
- Mechanisms of exercise intolerance in DCM remain unclear.
- Coronary microvascular function in DCM requires characterization.
Purpose of the Study:
- To assess coronary microvascular function in DCM patients.
- To determine associations between cardiovascular magnetic resonance (CMR) measures and aerobic exercise capacity in DCM.
Main Methods:
- Prospective case-control study comparing DCM patients and matched controls.
- Adenosine-stress perfusion CMR for cardiac structure, function, and myocardial blood flow quantification.
- Cardiopulmonary exercise testing to measure peak VO2; multivariable regression analysis.
Main Results:
- DCM patients had significantly lower peak VO2 compared to controls.
- DCM group exhibited reduced stress myocardial blood flow and myocardial perfusion reserve (MPR).
- Left ventricular ejection fraction, extracellular volume fraction, and MPR independently correlated with peak VO2 in DCM.
Conclusions:
- DCM patients demonstrate impaired stress myocardial blood flow and MPR.
- MPR, LV ejection fraction, and fibrosis are independent predictors of aerobic exercise capacity in DCM.
Background:
Aerobic exercise capacity is an independent predictor of mortality in dilated cardiomyopathy (DCM), but the central mechanisms contributing to exercise intolerance in DCM are unknown. The aim of this study was to characterize coronary microvascular function in DCM and determine if cardiovascular magnetic resonance (CMR) measures are associated with aerobic exercise capacity.
Methods:
Prospective case-control comparison of adults with DCM and matched controls. Adenosine-stress perfusion CMR to assess cardiac structure, function and automated inline myocardial blood flow quantification, and cardiopulmonary exercise testing to determine peak VO2 was performed. Pre-specified multivariable linear regression, including key clinical and cardiac variables, was undertaken to identify independent associations with peak VO2.
Results:
Sixty-six patients with DCM (mean age 61 years, 47 male) were propensity-matched to 66 controls (mean age 59 years, 47 male) based on age, sex, body mass index, and diabetes. DCM patients had markedly lower peak VO2 (19.8 ± 5.5 versus 25.2 ± 7.3 mL/kg/min; P < 0.001). The DCM group had greater left ventricular (LV) volumes, lower systolic function, and more fibrosis compared to controls. In the DCM group, there was similar rest but lower stress myocardial blood flow (1.53 ± 0.49 versus 2.01 ± 0.60 mL/g/min; P < 0.001) and lower myocardial perfusion reserve (MPR) (2.69 ± 0.84 versus 3.15 ± 0.84; P = 0.002). Multivariable linear regression demonstrated that LV ejection fraction, extracellular volume fraction, and MPR, were independently associated with percentage-predicted peak VO2 in DCM (R2 = 0.531, P < 0.001).
Conclusion:
In comparison to controls, DCM patients have lower stress myocardial blood flow and MPR. In DCM, MPR, LV ejection fraction, and fibrosis are independently associated with aerobic exercise capacity.
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