SARS-COV-2 colonizes coronary thrombus and impairs heart microcirculation bed in asymptomatic SARS-CoV-2 positive subjects with acute myocardial infarction.
Aged
Analysis of Variance
Asymptomatic Infections
/ epidemiology
COVID-19
/ complications
Cohort Studies
Coronary Angiography
/ methods
Coronary Thrombosis
/ epidemiology
Echocardiography
/ methods
Female
Heart
/ physiopathology
Humans
Kaplan-Meier Estimate
Male
Microcirculation
/ physiology
Middle Aged
Myocardial Infarction
/ epidemiology
Asymptomatic SARS-COV-2 patients
Intracoronary thrombus
SARS-COV-2
STEMI
Thrombus viral load
Journal
Critical care (London, England)
ISSN: 1466-609X
Titre abrégé: Crit Care
Pays: England
ID NLM: 9801902
Informations de publication
Date de publication:
24 06 2021
24 06 2021
Historique:
received:
21
04
2021
accepted:
14
06
2021
entrez:
25
6
2021
pubmed:
26
6
2021
medline:
8
7
2021
Statut:
epublish
Résumé
The viral load of asymptomatic SAR-COV-2 positive (ASAP) persons has been equal to that of symptomatic patients. On the other hand, there are no reports of ST-elevation myocardial infarction (STEMI) outcomes in ASAP patients. Therefore, we evaluated thrombus burden and thrombus viral load and their impact on microvascular bed perfusion in the infarct area (myocardial blush grade, MBG) in ASAP compared to SARS-COV-2 negative (SANE) STEMI patients. This was an observational study of 46 ASAP, and 130 SANE patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention and thrombus aspiration. The primary endpoints were thrombus dimension + thrombus viral load effects on MBG after PPCI. The secondary endpoints during hospitalization were major adverse cardiovascular events (MACEs). MACEs are defined as a composite of cardiovascular death, nonfatal acute AMI, and heart failure during hospitalization. In the study population, ASAP vs. SANE showed a significant greater use of GP IIb/IIIa inhibitors and of heparin (p < 0.05), and a higher thrombus grade 5 and thrombus dimensions (p < 0.05). Interestingly, ASAP vs. SANE patients had lower MBG and left ventricular function (p < 0.001), and 39 (84.9%) of ASAP patients had thrombus specimens positive for SARS-COV-2. After PPCI, a MBG 2-3 was present in only 26.1% of ASAP vs. 97.7% of SANE STEMI patients (p < 0.001). Notably, death and nonfatal AMI were higher in ASAP vs. SANE patients (p < 0.05). Finally, in ASAP STEMI patients the thrombus viral load was a significant determinant of thrombus dimension independently of risk factors (p < 0.005). Thus, multiple logistic regression analyses evidenced that thrombus SARS-CoV-2 infection and dimension were significant predictors of poorer MBG in STEMI patients. Intriguingly, in ASAP patients the female vs. male had higher thrombus viral load (15.53 ± 4.5 vs. 30.25 ± 5.51 CT; p < 0.001), and thrombus dimension (4.62 ± 0.44 vs 4.00 ± 1.28 mm In ASAP patients presenting with STEMI, there is strong evidence towards higher thrombus viral load, dimension, and poorer MBG. These data support the need to reconsider ASAP status as a risk factor that may worsen STEMI outcomes.
Sections du résumé
BACKGROUND
The viral load of asymptomatic SAR-COV-2 positive (ASAP) persons has been equal to that of symptomatic patients. On the other hand, there are no reports of ST-elevation myocardial infarction (STEMI) outcomes in ASAP patients. Therefore, we evaluated thrombus burden and thrombus viral load and their impact on microvascular bed perfusion in the infarct area (myocardial blush grade, MBG) in ASAP compared to SARS-COV-2 negative (SANE) STEMI patients.
METHODS
This was an observational study of 46 ASAP, and 130 SANE patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention and thrombus aspiration. The primary endpoints were thrombus dimension + thrombus viral load effects on MBG after PPCI. The secondary endpoints during hospitalization were major adverse cardiovascular events (MACEs). MACEs are defined as a composite of cardiovascular death, nonfatal acute AMI, and heart failure during hospitalization.
RESULTS
In the study population, ASAP vs. SANE showed a significant greater use of GP IIb/IIIa inhibitors and of heparin (p < 0.05), and a higher thrombus grade 5 and thrombus dimensions (p < 0.05). Interestingly, ASAP vs. SANE patients had lower MBG and left ventricular function (p < 0.001), and 39 (84.9%) of ASAP patients had thrombus specimens positive for SARS-COV-2. After PPCI, a MBG 2-3 was present in only 26.1% of ASAP vs. 97.7% of SANE STEMI patients (p < 0.001). Notably, death and nonfatal AMI were higher in ASAP vs. SANE patients (p < 0.05). Finally, in ASAP STEMI patients the thrombus viral load was a significant determinant of thrombus dimension independently of risk factors (p < 0.005). Thus, multiple logistic regression analyses evidenced that thrombus SARS-CoV-2 infection and dimension were significant predictors of poorer MBG in STEMI patients. Intriguingly, in ASAP patients the female vs. male had higher thrombus viral load (15.53 ± 4.5 vs. 30.25 ± 5.51 CT; p < 0.001), and thrombus dimension (4.62 ± 0.44 vs 4.00 ± 1.28 mm
CONCLUSIONS
In ASAP patients presenting with STEMI, there is strong evidence towards higher thrombus viral load, dimension, and poorer MBG. These data support the need to reconsider ASAP status as a risk factor that may worsen STEMI outcomes.
Identifiants
pubmed: 34167575
doi: 10.1186/s13054-021-03643-0
pii: 10.1186/s13054-021-03643-0
pmc: PMC8222703
doi:
Types de publication
Journal Article
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
217Subventions
Organisme : PRIN 2017
ID : 2017FM74HK_002
Références
Scott Med J. 2021 Feb;66(1):34-39
pubmed: 32631149
Int J Infect Dis. 2020 May;94:154-155
pubmed: 32179137
Eur Heart J. 2018 Jan 7;39(2):119-177
pubmed: 28886621
J Am Coll Cardiol. 2020 Jul 7;76(1):122-124
pubmed: 32387623
J Am Heart Assoc. 2018 Jan 9;7(1):
pubmed: 29317403
Front Physiol. 2020 Oct 09;11:575600
pubmed: 33162899
BMC Cardiovasc Disord. 2020 Aug 14;20(1):373
pubmed: 32799852
Eur Heart J. 2012 Oct;33(20):2569-619
pubmed: 22922416
Eur Heart J. 2019 Jan 7;40(2):87-165
pubmed: 30165437
Blood. 2020 Jun 4;135(23):2033-2040
pubmed: 32339221
J Thromb Thrombolysis. 2018 Feb;45(2):240-249
pubmed: 29274046
MMWR Morb Mortal Wkly Rep. 2020 Apr 03;69(13):377-381
pubmed: 32240128
Thromb Res. 2020 Jul;191:145-147
pubmed: 32291094
JAMA Cardiol. 2020 Dec 29;:
pubmed: 33372956
JCI Insight. 2020 Jun 4;5(11):
pubmed: 32329756
Front Pharmacol. 2020 Aug 06;11:1124
pubmed: 32848743
Cancer Cell. 2020 Nov 9;38(5):661-671.e2
pubmed: 32997958
Circulation. 2020 Nov 24;142(21):2080-2082
pubmed: 33054349
N Engl J Med. 2018 Jan 25;378(4):345-353
pubmed: 29365305
JAMA. 2020 Mar 17;323(11):1061-1069
pubmed: 32031570
Ann Intern Med. 2020 Sep 1;173(5):362-367
pubmed: 32491919
J Neurol Neurosurg Psychiatry. 2020 Aug;91(8):889-891
pubmed: 32354768
JAMA. 2020 Apr 14;323(14):1406-1407
pubmed: 32083643
J Invasive Cardiol. 2010 Oct;22(10 Suppl B):6B-14B
pubmed: 20947930
Intensive Care Med. 2020 May;46(5):846-848
pubmed: 32125452
Circulation. 1998 Jun 16;97(23):2302-6
pubmed: 9639373
J Clin Med. 2020 May 11;9(5):
pubmed: 32403217
J Am Coll Cardiol. 2020 Sep 8;76(10):1168-1176
pubmed: 32679155
Circ Cardiovasc Interv. 2017 Oct;10(10):
pubmed: 29042400
N Engl J Med. 2020 Mar 19;382(12):1177-1179
pubmed: 32074444
Blood. 2020 Sep 10;136(11):1317-1329
pubmed: 32573711
J Am Coll Cardiol. 2014 Nov 4;64(18):1926-8
pubmed: 25444148
Cells. 2020 Oct 31;9(11):
pubmed: 33142844
Lancet Respir Med. 2020 May;8(5):475-481
pubmed: 32105632
J Am Soc Echocardiogr. 2019 Jan;32(1):1-64
pubmed: 30282592
Diabetes Metab. 2020 Oct;46(5):403-405
pubmed: 32447102
Radiol Cardiothorac Imaging. 2020 Mar 17;2(2):e200110
pubmed: 33778566
J Am Coll Cardiol. 2000 Sep;36(3):959-69
pubmed: 10987628
Circ Cardiovasc Interv. 2010 Jun 1;3(3):216-23
pubmed: 20442359