TY - JOUR
T1 - Ischemic heart failure mortality is not predicted by cardiac insulin resistance but by diabetes per se and coronary flow reserve
T2 - A retrospective dynamic cardiac 18F-FDG PET study
AU - Luong, Thien Vinh
AU - Pedersen, Mette Glavind Bülow
AU - Kjærulff, Mette Louise Blouner Gram
AU - Madsen, Simon
AU - Lauritsen, Katrine Meyer
AU - Tolbod, Lars Poulsen
AU - Søndergaard, Esben
AU - Gormsen, Lars Christian
N1 - Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
PY - 2021/10
Y1 - 2021/10
N2 - Background & aims: The connection between peripheral insulin resistance (IR) and coronary artery disease is well-established. Both are major risk factors for the development of ischemic cardiomyopathy potentially leading to heart failure (HF). Whether cardiac IR also impacts overall survival and morbidity is still debated. We therefore aimed to test if cardiac IR predicts mortality and major cardiovascular events (MACE) in patients with HF scheduled for cardiac viability testing before revascularization. Methods: This retrospective study included 131 patients with a clinical diagnosis of ischemic HF (114 (87%) male, 33 (25%) with diabetes) referred to a viability Rubidium-82 (perfusion) and dynamic 18F-Fluorodeoxyglucose (metabolism) positron emission tomography combined with computed tomography prior to a potential revascularization procedure. Cardiac IR was assessed by myocardial glucose uptake (MGU) in a remote (non-scarred) area of the left ventricle during a hyperinsulinemic-euglycemic clamp (1mIE/kg/min). Results: MGU correlated with skeletal muscle glucose uptake (p < 0.001) and whole-body glucose uptake (M-value) (p < 0.001), whereas no association was observed for individuals with diabetes. MGU did not predict the risk of death or MACE. However, both overt diabetes and reduced coronary flow reserve predicted overall survival. Conclusion: Even though diabetes and related small-vessel disease is associated with increased mortality, cardiac IR per se does not predict cardiovascular morbidity and mortality.
AB - Background & aims: The connection between peripheral insulin resistance (IR) and coronary artery disease is well-established. Both are major risk factors for the development of ischemic cardiomyopathy potentially leading to heart failure (HF). Whether cardiac IR also impacts overall survival and morbidity is still debated. We therefore aimed to test if cardiac IR predicts mortality and major cardiovascular events (MACE) in patients with HF scheduled for cardiac viability testing before revascularization. Methods: This retrospective study included 131 patients with a clinical diagnosis of ischemic HF (114 (87%) male, 33 (25%) with diabetes) referred to a viability Rubidium-82 (perfusion) and dynamic 18F-Fluorodeoxyglucose (metabolism) positron emission tomography combined with computed tomography prior to a potential revascularization procedure. Cardiac IR was assessed by myocardial glucose uptake (MGU) in a remote (non-scarred) area of the left ventricle during a hyperinsulinemic-euglycemic clamp (1mIE/kg/min). Results: MGU correlated with skeletal muscle glucose uptake (p < 0.001) and whole-body glucose uptake (M-value) (p < 0.001), whereas no association was observed for individuals with diabetes. MGU did not predict the risk of death or MACE. However, both overt diabetes and reduced coronary flow reserve predicted overall survival. Conclusion: Even though diabetes and related small-vessel disease is associated with increased mortality, cardiac IR per se does not predict cardiovascular morbidity and mortality.
KW - Heart failure
KW - Insulin resistance
KW - Myocardial glucose uptake
KW - Positron emission tomography
KW - Prognosis
KW - MYOCARDIAL GLUCOSE-UTILIZATION
KW - MELLITUS
KW - LUMPED CONSTANT
KW - SKELETAL-MUSCLE
KW - IMPACT
KW - RISK-FACTOR
KW - METABOLISM
KW - DISEASE
UR - http://www.scopus.com/inward/record.url?scp=85112329158&partnerID=8YFLogxK
U2 - 10.1016/j.metabol.2021.154862
DO - 10.1016/j.metabol.2021.154862
M3 - Journal article
C2 - 34375646
AN - SCOPUS:85112329158
SN - 0026-0495
VL - 123
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
M1 - 154862
ER -