Valvular Heart Disease
Nicholas Jex, MD
PhD Fellow
Leeds Institute of Cardiovascular and Metabolic Medicine, England, United Kingdom
Nicholas Jex, MD
PhD Fellow
Leeds Institute of Cardiovascular and Metabolic Medicine, England, United Kingdom
Amrit Chowdhary, MD
Cardiology
University of Leeds
WAKEFIELD, England, United Kingdom
Sharmaine Thirunavukarasu, MbCHB
Cardiology
University of Leeds
WILMSLOW, England, United Kingdom
Henry Procter, MD
Research Fellow
University of Leeds, United Kingdom
Sindhoora Kotha, MD
Research Fellow
University of Leeds, United Kingdom
Marilena Giannoudi, MD
Research Fellow
University of Leeds, United Kingdom
Hui Xue, PhD
Director, Imaging AI Program
National Institutes of Health
Bethesda, Maryland, United States
Peter Kellman, PhD
Senior Scientist
National Institutes of Health, Maryland, United States
Sven Plein, MD, PhD
Professor
University of Leeds
Leeds, England, United Kingdom
John P. Greenwood, PhD
Professor
University of Leeds
Leeds, England, United Kingdom
Marc Dweck, PhD
Professor
The University of Edinburgh
Edinburgh, Scotland, United Kingdom
Eylem Levelt, PhD
Associate Professor and Honorary Consultant
University of Leeds
Leeds, England, United Kingdom
Aortic stenosis (AS) and type 2 diabetes mellitus (T2DM) are frequent co-morbidities. It is not known if T2DM comorbidity is associated with altered myocardial recovery after aortic valve replacement (AVR) in severe AS. We sought to compare myocardial alterations pre-AVR and their recovery post-AVR in severe AS patients with and without T2DM.
Methods:
Ninety-five severe AS patients with (n=30) and without T2DM (n=65) and 15 healthy volunteers were recruited. Significant obstructive coronary artery disease was excluded in all AS patients. The main outcome measures of change in myocardial energetics, perfusion, function and physical performance after AVR were assessed by phosphorous magnetic resonance spectroscopy and cardiovascular magnetic resonance scans, 6-minute walk test, within 1-month prior to and 6-months after AVR.
Results:
At baseline all groups were comparable in aortic valve parameters, left ventricular volumes and ejection fraction. AS patients with T2DM displayed more significant reductions in cardiac energetics (1.44(1.32,1.56) versus 1.74(1.62,1.86), p=0.002) and global stress myocardial blood flow (1.25(1.22,1.38) versus 1.67(1.5,1.84) ml/min/g, p=0.001) than AS patients without T2DM pre-AVR respectively. Post-AVR, AS patients without T2DM showed restoration of global stress myocardial blood flow (1.67(1.5,1.84) to 1.80(1.59,2.0) ml/min/g, p=0.0017) and energetics (1.74(1.62,1.86) to 2.11(1.79,2.43), p=0.0014), with improvements in exercise tolerance (396(365,436) to 434(398,472) m, p=0.02). Despite improvements post-AVR (1.25(1.22,1.38) to 1.48(1.29,1.66) ml/min/g, p=0.006), AS patients with T2DM continued to display significantly lower stress myocardial blood flow (1.48(1.29,1.66) versus 1.80(1.59,2.0) ml/min/g, p=0.03) than AS patients without T2DM. Post-AVR, AS patients with T2DM showed no improvements in myocardial energetics (1.44(1.32,1.56) to 1.30(1.07,1.53), p=0.47) or exercise tolerance (360(306,415) to 331(267,393) m, p=0.45). Diastolic function was lower in AS patients with T2DM than AS patients without T2DM pre-AVR (0.66(0.57,0.75) versus 0.83(0.74,0.92) s-1, p=0.01), and showed no improvements post-AVR in this group (0.66(0.57,0.75) to 0.68(0.59,0.76), p=0.98).
Conclusion:
While AVR is effective in reversing myocardial alterations in AS patients without T2DM, AS patients with T2DM comorbidity show residual myocardial abnormalities and continued limitations in exercise capacity after AVR.