Key result
Cardiac amyloidosis is linked to ~11-point lower myocardial external efficiency vs. healthy controls.
Why the study?
This study evaluated myocardial oxygen consumption and myocardial external efficiency in patients with cardiac amyloidosis, and compared these parameters between subjects with light chain amyloidosis and transthyretin amyloidosis.
Do patients with cardiac amyloidosis have impaired myocardial oxygen consumption and myocardial external efficiency compared with healthy controls, and do these metabolic parameters correlate with systolic myocardial performance?
Case-Control (n=35)
No
Do patients with cardiac amyloidosis have impaired myocardial oxygen consumption and myocardial external efficiency compared with healthy controls, and do these metabolic parameters correlate with systolic myocardial performance?
Demonstrates that patients with cardiac amyloidosis have disturbed myocardial oxidative metabolism with increased total oxygen consumption and severely reduced myocardial external efficiency, which correlates closely with echocardiographic LVGLS and myocardial work efficiency.
Myocardial efficiency assessment may aid cardiac amyloidosis evaluation; extends echocardiographic correlations but leaves open therapeutic implications.
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.
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Clemmensen et al. (2018) conducted a case-control in Cardiac Amyloidosis (ATTRwt, ATTRm, and AL) (n=35). Cardiac amyloidosis vs. Healthy control subjects without cardiac amyloidosis was evaluated on Myocardial external efficiency (MEE, %) measured by 11C-acetate positron emission tomography (p=<0.0001). Cardiac amyloidosis patients exhibited severely reduced myocardial external efficiency (13±5% vs 24±5%, P<0.0001) and higher total myocardial oxygen consumption (18±6 vs 13±3 mL/min, P<0.01) than controls.
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