TY - JOUR
AU - Arnold, J. Ranjit
AU - Yeo, Jian L.
AU - Budgeon, Charley A.
AU - Shergill, Simran
AU - England, Rachel
AU - Shiwani, Hunain
AU - Artico, Jessica
AU - Moon, James C.
AU - Gorecka, Miroslawa
AU - Roditi, Giles
AU - Morrow, Andrew J.
AU - Mangion, Kenneth
AU - Shanmuganathan, Mayooran
AU - Miller, Christopher
AU - Chiribiri, Amedeo
AU - Alzahir, Mohammed
AU - Ramirez, Sara
AU - Lin, Andrew
AU - Swoboda, Peter P.
AU - McDiarmid, Adam K.
AU - Sykes, Robert
AU - Singh, Trisha
AU - Bucciarelli-Ducci, Chiara
AU - Dawson, Dana
AU - Fontana, Marianna
AU - Manisty, Charlotte
AU - Treibel, Thomas A.
AU - Levelt, Eylem
AU - Young, Robin
AU - McConnachie, Alex
AU - Neubauer, Stefan
AU - Piechnik, Stefan K.
AU - Davies, Rhodri H.
AU - Ferreira, Vanessa M.
AU - Dweck, Marc R.
AU - Berry, Colin
AU - McCann, Gerry P.
AU - Greenwood, John P.
AU - Oxford Acute Myocardial Infarction OxAMI Study Investigators
AU - COVID-HEART Investigators
PY - 2024
DA - December
TI - Myocardial ischaemia following COVID-19: a cardiovascular magnetic resonance study
JO - International Journal of Cardiovascular Imaging
EP - 256
VL - 41
DO - https://doi.org/10.1007/s10554-024-03304-7
AB - The pathophysiology of myocardial injury following COVID-19 remains uncertain. COVID-HEART was a prospective, multicentre study utilising cardiovascular magnetic resonance (CMR) to characterise COVID-related myocardial injury. In this pre-specified analysis, the objectives were to examine (1) the frequency of myocardial ischaemia following COVID-19, and (2) the association between ischaemia and myocardial injury. We studied 59 patients hospitalised with COVID-19 and elevated serum troponin (COVID + /troponin + , age 61 ± 11 years) and 37 control subjects without COVID-19 or elevated troponin and similar by age and cardiovascular comorbidities (COVID −/comorbidity + , 64 ± 10 years). Subjects underwent multi-parametric CMR (comprising assessment of ventricular volumes, stress perfusion, T1/T2 mapping and scar). The primary endpoint was the frequency of inducible myocardial ischaemia. Inducible ischaemia was evident in 11 (19%) COVID + /troponin + patients and in 8 (22%) control subjects (p= 0.72). In COVID + /troponin + patients with ischaemia, epicardial coronary disease pattern ischaemia was present in eight patients and microvascular disease pattern, in three patients. There was no significant difference in the frequency of inducible ischaemia in COVID + /troponin + patients with previous myocardial infarction and/or revascularisation compared to those without (2/12 [17%] vs. 9/47 [19%] respectively,p= 0.84), or in those with and without scar (7/27 [26%] vs. 4/32 [13%] respectively,p= 0.19). Myocardial ischaemia was present in ~ 20% of patients recently hospitalised with COVID-19 and with elevated cardiac troponin, but this was not different to matched comorbid controls. This finding coupled with the lack of an association between ischaemia and myocardial scar suggests that coronary artery abnormalities are unlikely to be the predominant mechanism underlying COVID-19 induced myocardial injury.
PB - Springer Nature
UR - https://hdl.handle.net/2164/25585
KW - Coronavirus (COVID-19)
ER