Key result
Asymptomatic SARS-CoV-2 infection in STEMI patients was associated with significantly lower rates of normal myocardial perfusion after primary PCI compared to uninfected patients (26.1% vs 97.7%).
Why the study?
Viral load in asymptomatic SARS-CoV-2 positive patients equals that of symptomatic patients, but outcomes of STEMI in asymptomatic SARS-CoV-2 positive patients had not been reported.
Does asymptomatic SARS-CoV-2 infection worsen thrombus burden and myocardial blush grade in STEMI patients undergoing primary PCI?
Cohort (n=176)
Yes
Does asymptomatic SARS-CoV-2 infection worsen thrombus burden and myocardial blush grade in STEMI patients undergoing primary PCI?
Absolute Event Rate: 26.1% vs 97.7%
p-value: p=<0.001
Asymptomatic SARS-CoV-2 infection in STEMI patients is associated with higher thrombus viral load, larger thrombus dimensions, and poorer microvascular reperfusion after primary PCI.
ASAP STEMI patients show markedly poorer post-PPCI perfusion; hypothesis-generating for asymptomatic SARS-CoV-2 effects on thrombus and microcirculation.
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 mm2; p < 0.001). ASAP vs. SANE patients had a significantly lower in-hospital survival for MACE following PPCI (p < 0.001). 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.
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Marfella et al. (2021) conducted a cohort in ST-elevation myocardial infarction (STEMI) (n=176). Asymptomatic SARS-CoV-2 infection vs. SARS-CoV-2 negative was evaluated on Myocardial blush grade 2-3 (normal perfusion) after primary PCI (p=<0.001). Asymptomatic SARS-CoV-2 infection in STEMI patients was associated with significantly lower rates of normal myocardial perfusion after primary PCI compared to uninfected patients (26.1% vs 97.7%).
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