Myocardial Oxygen Consumption and Efficiency in Aortic Valve Stenosis Patients With and Without Heart Failure.
Myocardial oxygen consumption (MVO2) and its coupling to contractile work are fundamentals of cardiac function and may be involved causally in the transition from compensated left ventricular hypertrophy to failure. Nevertheless, these processes have not been studied previously in patients with aortic valve stenosis (AS).



Participants underwent11C-acetate positron emission tomography, cardiovascular magnetic resonance, and echocardiography to measure MVO2and myocardial external efficiency (MEE) defined as the ratio of left ventricular stroke work and the energy equivalent of MVO2. We studied 10 healthy controls (group A), 37 asymptomatic AS patients with left ventricular ejection fraction ≥50% (group B), 12 symptomatic AS patients with left ventricular ejection fraction ≥50% (group C), and 9 symptomatic AS patients with left ventricular ejection fraction <50% (group D). MVO2did not differ among groups A, B, C, and D (0.105±0.02, 0.117±0.024, 0.129±0.032, and 0.104±0.026 mL/min per gram, respectively; P=0.07), whereas MEE was reduced in group D (21.0±1.6%, 22.3±3.3%, 22.1±4.2%, and 17.3±4.7%, respectively; P<0.05). Similarly, patients with global longitudinal strain greater than -12% and paradoxical low-flow, low-gradient AS had impaired MEE (P<0.05 versus controls). The ability to discriminate between symptomatic and asymptomatic patients was superior for global longitudinal strain compared with MVO2and MEE (area under the curve 0.98, 0.48, and 0.61, respectively; P<0.05).



AS patients display a persistent ability to maintain normal MVO2and MEE (ie, the ability to convert energy into stroke work); however, patients with left ventricular ejection fraction <50%; global longitudinal strain greater than -12%; or paradoxical low-flow, low-gradient AS demonstrate reduced MEE. These findings suggest that mitochondrial uncoupling contributes to the dismal prognosis in patients with reduced contractile function or paradoxical low-flow, low-gradient AS.
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark nilhan@rm.dk.
Nils Henrik Stubkjær
NH
Hansson
Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Aarhus, Denmark.
Jens
J
Sörensen
Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Aarhus, Denmark.
Hendrik Johannes
HJ
Harms
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Won Yong
WY
Kim
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Roni
R
Nielsen
Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Aarhus, Denmark.
Lars P
LP
Tolbod
Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Aarhus, Denmark.
Jørgen
J
Frøkiær
Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Aarhus, Denmark.
Kirsten
K
Bouchelouche
Department of Cardiology, Horsens Regional Hospital, Horsens, Denmark.
Karen Kaae
KK
Dodt
Aarhus Hjerteklinik, Aarhus, Denmark.
Inger
I
Sihm
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Steen Hvitfeldt
SH
Poulsen
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Henrik
H
Wiggers
D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications / Q000175:diagnosis / Q000378:metabolism*; D018450:Disease Progression; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D049268:Positron-Emission Tomography; D011379:Prognosis; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology*; D016277:Ventricular Function, Left
aortic valve stenosis; myocardial external efficiency; myocardial metabolism; myocardial oxygen consumption; positron emission tomography