Ahmet Güçlü1, Paul Knaapen2, Hendrik J Harms3, Alexander B A Vonk4, Willem Stooker5, Herman Groepenhoff6, Adriaan A Lammertsma3, Albert C van Rossum2, Tjeerd Germans7, Jolanda van der Velden8. 1. Department of Cardiology, VU University Medical Center, ZH 5D-14, De Boelelaan 1117, 1081HV Amsterdam, The Netherlands ICIN-The Netherlands Heart Institute, Utrecht, The Netherlands a.guclu@vumc.nl. 2. Department of Cardiology, VU University Medical Center, ZH 5D-14, De Boelelaan 1117, 1081HV Amsterdam, The Netherlands. 3. Department of Radiology and Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands. 4. Department of Cardiothoracic Surgery, VU University Medical Center, Amsterdam, The Netherlands. 5. Department of Cardiothoracic Surgery, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands. 6. Department of Pulmonology, Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands. 7. Department of Cardiology, VU University Medical Center, ZH 5D-14, De Boelelaan 1117, 1081HV Amsterdam, The Netherlands Medical Center Alkmaar, Alkmaar, The Netherlands. 8. ICIN-The Netherlands Heart Institute, Utrecht, The Netherlands Department of Physiology, VU University Medical Center, Amsterdam, The Netherlands.
Abstract
AIMS: The pathophysiology underlying aortic valve stenosis (AVS)-induced cardiac dysfunction and reduced exercise capacity is unclear. We hypothesize that improvement of myocardial external efficiency (MEE)--the ratio between external work and myocardial oxygen consumption (MVO2)--underlies functional improvement of AVS patients after aortic valve replacement (AVR). Therefore, the aim of this proof-of-concept study was to investigate whether myocardial efficiency is reduced in patients with cardiac hypertrophy caused by AVS and to assess the effect of AVR on myocardial efficiency in relation to exercise capacity. METHODS AND RESULTS: Echocardiography, cardiopulmonary exercise test, [(11)C]-acetate positron emission tomography and cardiovascular magnetic resonance imaging were performed in 10 AVS patients prior to (pre-AVR) and 4 months after AVR (post-AVR). Fourteen healthy individuals served as control group. MEE was significantly lower in pre-AVR patients (32 ± 7%) than in controls (49 ± 6%). AVR significantly decreased left ventricle mass and MVO2. Also, external work significantly decreased post-AVR reaching similar values as in controls. AVR significantly improved MEE from 32 ± 7 to 37 ± 5% (P = 0.02). Moreover, significant correlations were present between the AVR-induced increase in MEE and changes in both exercise work (r = 0.74, P = 0.01) and peak VO2 (r = 0.67, P = 0.03). However, four AVS patients did not show improved MEE, which was associated with no or minimal improvement in exercise parameters. CONCLUSION: MEE is significantly reduced in patients with AVS-induced hypertrophy. Improved MEE is an important predictor of AVR-induced improvement of exercise capacity in AVS patients. Future investigation is needed to confirm our observations in a large prospective, multicenter clinical trial. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: The pathophysiology underlying aortic valve stenosis (AVS)-induced cardiac dysfunction and reduced exercise capacity is unclear. We hypothesize that improvement of myocardial external efficiency (MEE)--the ratio between external work and myocardial oxygen consumption (MVO2)--underlies functional improvement of AVS patients after aortic valve replacement (AVR). Therefore, the aim of this proof-of-concept study was to investigate whether myocardial efficiency is reduced in patients with cardiac hypertrophy caused by AVS and to assess the effect of AVR on myocardial efficiency in relation to exercise capacity. METHODS AND RESULTS: Echocardiography, cardiopulmonary exercise test, [(11)C]-acetate positron emission tomography and cardiovascular magnetic resonance imaging were performed in 10 AVS patients prior to (pre-AVR) and 4 months after AVR (post-AVR). Fourteen healthy individuals served as control group. MEE was significantly lower in pre-AVRpatients (32 ± 7%) than in controls (49 ± 6%). AVR significantly decreased left ventricle mass and MVO2. Also, external work significantly decreased post-AVR reaching similar values as in controls. AVR significantly improved MEE from 32 ± 7 to 37 ± 5% (P = 0.02). Moreover, significant correlations were present between the AVR-induced increase in MEE and changes in both exercise work (r = 0.74, P = 0.01) and peak VO2 (r = 0.67, P = 0.03). However, four AVS patients did not show improved MEE, which was associated with no or minimal improvement in exercise parameters. CONCLUSION:MEE is significantly reduced in patients with AVS-induced hypertrophy. Improved MEE is an important predictor of AVR-induced improvement of exercise capacity in AVS patients. Future investigation is needed to confirm our observations in a large prospective, multicenter clinical trial. Published on behalf of the European Society of Cardiology. All rights reserved.
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