
Myocardial Oxygen Consumption and Efficiency in Patients With Cardiac Amyloidosis
Author(s) -
Clemmensen Tor Skibsted,
Soerensen Jens,
Hansson Nils Henrik,
Tolbod Lars Poulsen,
Harms Hendrik J.,
Eiskjær Hans,
Mikkelsen Fabian,
Wiggers Henrik,
Andersen Niels Frost,
Poulsen Steen Hvitfeldt
Publication year - 2018
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.118.009974
Subject(s) - medicine , ejection fraction , supine position , cardiology , cardiac amyloidosis , amyloidosis , heart failure , transthyretin , population , nuclear medicine , environmental health
Background This study evaluated myocardial oxygen consumption (MVO 2 ) and myocardial external efficiency (MEE) in patients with cardiac amyloidosis (CA). Furthermore, we compared MEE and MVO 2 in subjects with light chain amyloidosis versus transthyretin (ATTR) amyloidosis. Methods and Results The study population comprised 40 subjects: 25 patients with confirmed CA and 15 control subjects. All subjects underwent an 11 C‐acetate positron emission tomography. Furthermore, the CA patients underwent comprehensive echocardiography and right heart catheterization during a symptom‐limited, semi‐supine exercise test. MEE was calculated from 11 C‐acetate positron emission tomography as the ratio of left ventricular (LV) stroke work and the energy equivalent of MVO 2 . Myocardial work efficiency was calculated as echocardiography‐derived work pressure product divided by three‐dimensional LV mass. CA patients had significantly lower LV‐ejection fraction (54±13% versus 63±4%, P <0.05) and LV‐global longitudinal strain (LVGLS) (12±4% versus 19±2%, P <0.0001) and a more restrictive filling pattern (E/e′‐ratio 18 [12–25] versus 8 [7–9], P <0.0001) than controls. MEE was severely reduced (13±5% versus 22±5%, P <0.0001) whereas total MVO 2 was higher (18±6 mL/min versus 13±3 mL/min, P <0.01) in CA patients than controls. MEE decreased with increasing New York Heart Association symptom burden ( P <0.0001). We found a good relationship between MEE and peak exercise systolic performance (LVGLS: R 2 =0.60, P <0.0001; myocardial work efficiency: R 2 =0.48, P <0.0001; cardiac index: R 2 =0.52, P <0.0001) and between MEE and myocardial blood flow ( R 2 =0.44, P <0.0001). Conclusion Myocardial oxidative metabolism is disturbed in CA patients with increased total MVO 2 and reduced MEE. MEE correlated significantly with echocardiographic derived systolic parameters such as myocardial work efficiency and LVGLS that might be used as surrogate MEE markers.