Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance
Abstract Background Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients. Methods and results One hundred and forty-eight...
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| Veröffentlicht in: | European heart journal 2021-05, Vol.42 (19), p.1866-1878 |
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| creator | Kotecha, Tushar Knight, Daniel S Razvi, Yousuf Kumar, Kartik Vimalesvaran, Kavitha Thornton, George Patel, Rishi Chacko, Liza Brown, James T Coyle, Clare Leith, Donald Shetye, Abhishek Ariff, Ben Bell, Robert Captur, Gabriella Coleman, Meg Goldring, James Gopalan, Deepa Heightman, Melissa Hillman, Toby Howard, Luke Jacobs, Michael Jeetley, Paramjit S Kanagaratnam, Prapa Kon, Onn Min Lamb, Lucy E Manisty, Charlotte H Mathurdas, Palmira Mayet, Jamil Negus, Rupert Patel, Niket Pierce, Iain Russell, Georgina Wolff, Anthony Xue, Hui Kellman, Peter Moon, James C Treibel, Thomas A Cole, Graham D Fontana, Marianna |
| description | Abstract
Background
Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients.
Methods and results
One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms).
Conclusions
During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.
Graphical Abstract |
| doi_str_mv | 10.1093/eurheartj/ehab075 |
| format | Article |
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Background
Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients.
Methods and results
One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms).
Conclusions
During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.
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Background
Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients.
Methods and results
One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms).
Conclusions
During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.
Graphical Abstract</description><subject>Contrast Media</subject><subject>COVID-19</subject><subject>Editor's Choice</subject><subject>Fast Track Clinical Research</subject><subject>Female</subject><subject>Gadolinium</subject><subject>Humans</subject><subject>Magnetic Resonance Imaging, Cine</subject><subject>Magnetic Resonance Spectroscopy</subject><subject>Male</subject><subject>Myocarditis - diagnostic imaging</subject><subject>Myocardium</subject><subject>Predictive Value of Tests</subject><subject>SARS-CoV-2</subject><subject>Troponin</subject><subject>Ventricular Function, 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Prapa</creatorcontrib><creatorcontrib>Kon, Onn Min</creatorcontrib><creatorcontrib>Lamb, Lucy E</creatorcontrib><creatorcontrib>Manisty, Charlotte H</creatorcontrib><creatorcontrib>Mathurdas, Palmira</creatorcontrib><creatorcontrib>Mayet, Jamil</creatorcontrib><creatorcontrib>Negus, Rupert</creatorcontrib><creatorcontrib>Patel, Niket</creatorcontrib><creatorcontrib>Pierce, Iain</creatorcontrib><creatorcontrib>Russell, Georgina</creatorcontrib><creatorcontrib>Wolff, Anthony</creatorcontrib><creatorcontrib>Xue, Hui</creatorcontrib><creatorcontrib>Kellman, Peter</creatorcontrib><creatorcontrib>Moon, James C</creatorcontrib><creatorcontrib>Treibel, Thomas A</creatorcontrib><creatorcontrib>Cole, Graham D</creatorcontrib><creatorcontrib>Fontana, Marianna</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kotecha, Tushar</au><au>Knight, Daniel S</au><au>Razvi, Yousuf</au><au>Kumar, Kartik</au><au>Vimalesvaran, Kavitha</au><au>Thornton, George</au><au>Patel, Rishi</au><au>Chacko, Liza</au><au>Brown, James T</au><au>Coyle, Clare</au><au>Leith, Donald</au><au>Shetye, Abhishek</au><au>Ariff, Ben</au><au>Bell, Robert</au><au>Captur, Gabriella</au><au>Coleman, Meg</au><au>Goldring, James</au><au>Gopalan, Deepa</au><au>Heightman, Melissa</au><au>Hillman, Toby</au><au>Howard, Luke</au><au>Jacobs, Michael</au><au>Jeetley, Paramjit S</au><au>Kanagaratnam, Prapa</au><au>Kon, Onn Min</au><au>Lamb, Lucy E</au><au>Manisty, Charlotte H</au><au>Mathurdas, Palmira</au><au>Mayet, Jamil</au><au>Negus, Rupert</au><au>Patel, Niket</au><au>Pierce, Iain</au><au>Russell, Georgina</au><au>Wolff, Anthony</au><au>Xue, Hui</au><au>Kellman, Peter</au><au>Moon, James C</au><au>Treibel, Thomas A</au><au>Cole, Graham D</au><au>Fontana, Marianna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2021-05-14</date><risdate>2021</risdate><volume>42</volume><issue>19</issue><spage>1866</spage><epage>1878</epage><pages>1866-1878</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Abstract
Background
Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients.
Methods and results
One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms).
Conclusions
During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.
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| fulltext | fulltext |
| identifier | ISSN: 0195-668X |
| ispartof | European heart journal, 2021-05, Vol.42 (19), p.1866-1878 |
| issn | 0195-668X 1522-9645 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7928984 |
| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Contrast Media COVID-19 Editor's Choice Fast Track Clinical Research Female Gadolinium Humans Magnetic Resonance Imaging, Cine Magnetic Resonance Spectroscopy Male Myocarditis - diagnostic imaging Myocardium Predictive Value of Tests SARS-CoV-2 Troponin Ventricular Function, Left |
| title | Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance |
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