TY - JOUR
T1 - Arginine metabolites as biomarkers of myocardial ischaemia, assessed with cardiac magnetic resonance imaging in chronic kidney disease
AU - Shah, Ranjit J.
AU - Tommasi, Sara
AU - Faull, Randall
AU - Gleadle, Jonathan M.
AU - Mangoni, Arduino A.
AU - Selvanayagam, Joseph B.
PY - 2021/3
Y1 - 2021/3
N2 - (1) Background: Cardiovascular disease (CVD) is the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). Myocardial oxygenation and perfusion response to stress, using oxygen‐sensitive cardiovascular magnetic resonance (OS‐CMR) and stress T1 mapping respectively, are impaired in CKD patients with and without known coronary artery disease (CAD). Endothelial dysfunction, assessed by circulating levels of asymmetric dimethylarginine (ADMA) and homoarginine (HMA), promotes atherosclerosis. We hypothesized that in CKD patients, worsening endothelial dysfunction is associated with worsening myocardial oxygenation and perfusion as assessed by change in OS‐CMR signal intensity (D OS‐CMR SI) and stress T1 (DT1) values. (2) Methods: 38 patients with advanced CKD underwent cardiovascular magnetic resonance (CMR) scanning at 3 Tesla. OS‐CMR and T1 mapping images were acquired both at rest and after adenosine stress and analyzed semi‐quantitatively. Serum ADMA and HMA concentrations were assessed using mass spectrometry. (3) Results: There was no significant correlation between D OS‐ CMR SI and ADMA or HMA. Interestingly, there was a significant negative correlation seen between D T1 and ADMA (r = −0.419, p = 0.037, n = 30) but not between D T1 and HMA. (4) Conclusion: Stress T1 response is impaired in CKD patients and is independently associated with higher circulating ADMA concentrations.
AB - (1) Background: Cardiovascular disease (CVD) is the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). Myocardial oxygenation and perfusion response to stress, using oxygen‐sensitive cardiovascular magnetic resonance (OS‐CMR) and stress T1 mapping respectively, are impaired in CKD patients with and without known coronary artery disease (CAD). Endothelial dysfunction, assessed by circulating levels of asymmetric dimethylarginine (ADMA) and homoarginine (HMA), promotes atherosclerosis. We hypothesized that in CKD patients, worsening endothelial dysfunction is associated with worsening myocardial oxygenation and perfusion as assessed by change in OS‐CMR signal intensity (D OS‐CMR SI) and stress T1 (DT1) values. (2) Methods: 38 patients with advanced CKD underwent cardiovascular magnetic resonance (CMR) scanning at 3 Tesla. OS‐CMR and T1 mapping images were acquired both at rest and after adenosine stress and analyzed semi‐quantitatively. Serum ADMA and HMA concentrations were assessed using mass spectrometry. (3) Results: There was no significant correlation between D OS‐ CMR SI and ADMA or HMA. Interestingly, there was a significant negative correlation seen between D T1 and ADMA (r = −0.419, p = 0.037, n = 30) but not between D T1 and HMA. (4) Conclusion: Stress T1 response is impaired in CKD patients and is independently associated with higher circulating ADMA concentrations.
KW - Chronic kidney disease
KW - CKD
KW - Endothelial dysfunction
KW - OS‐CMR
KW - Oxygen‐sensitive cardiovascular magnetic resonance imaging
KW - Stress T1 mapping
UR - http://www.scopus.com/inward/record.url?scp=85102209910&partnerID=8YFLogxK
U2 - 10.3390/biom11030416
DO - 10.3390/biom11030416
M3 - Article
AN - SCOPUS:85102209910
SN - 2218-273X
VL - 11
JO - Biomolecules
JF - Biomolecules
IS - 3
M1 - 416
ER -
