Do COVID STEMIs have a higher thrombus burden? More questions & implications

by:
Aaysha Cader

Whilst much has been written about COVID-19 and its inflammation-thrombosis-hypercoagulability cascade, this has to a large extent focused on venous thromboembolism (VTE). As more data emerges, it is evident that the intense inflammatory response associated with SARS-COV-2 infection may trigger thrombosis across multiple vascular beds, with large thrombus burden in ST-segment elevation myocardial infarction (STEMI) being one of many potential manifestations (1,2).

In a single-center, observational study published in the Journal of American College of Cardiology, Choudry et al. (1) reported a strong signal toward higher thrombus burden and poorer outcomes among COVID-19-positive STEMI patients undergoing primary percutaneous coronary intervention (PCI), in comparison with those who were COVID-negative.

Representing the largest comparative data-set of real-world consecutive STEMI patients during the COVID-19 pandemic, this study compared patient characteristics, laboratory variables, procedural characteristics and outcomes between 39 COVID-positive and 76 COVID-negative cases presenting at the Barts Heart Centre in London, United Kingdom between March 1, 2020, and May 20, 2020.

The median age of the 115 patients was 62 years, and included 48.7% from Black, Asian, or minority ethnic (BAME) groups. 78% were male. The predominant conclusion derived from the analysis was the unique burden of coronary thrombus leading to greater technical complexity during primary PCI in COVID-related STEMIs.

Angiographic data analysis showed significantly higher rates of multivessel coronary thrombosis in COVID-19 STEMI patients (17.9% vs 0%; p= 0.0003). This was consistent with a previously reported case of STEMI from Spain, published earlier-on during the pandemic, in which a critical thrombotic stenosis of the right coronary artery, and concomitant non-occlusive thrombus in the left anterior descending artery were observed, without underlying atherosclerotic plaque and confirmed by optical coherence tomography (OCT) imaging (3).

The London registry also reported significantly higher rates of stent thrombosis in the COVID-19 positive STEMI group in comparison to those testing negative (10.3% vs. 1.2%; p= 0.0445). Furthermore, large thrombus burden (post first device modified thrombus grade 4/5) was more than twice as likely in patients with COVID-19 STEMI compared with those without COVID-19 (75.0% vs. 31.4%; p= 0.0006). Laboratory findings indicated significantly higher median peak plasma hs-troponin (p=0.0028) and D-dimer levels (p= 0.0012) in COVID STEMI cases; these patients also had a lower left ventricular ejection fraction (p=0.019).

In the setting of higher thrombotic burden, there was also significantly greater use of aspiration thrombectomy (17.9% vs. 1.3%; p= 0.0021) and GP IIb/IIIa inhibitors (59.0% vs. (9.2%; p<0.0001) in patients with COVID-19. Although no significant differences were observed in the total dose of heparin administered, there was a suggestion of higher heparin doses required to achieve therapeutic activated clotting times (ACTs) in the COVID-positive cohort.

In terms of procedural success, TIMI flow grade 3 was achieved at similarly high levels in both groups, however myocardial blush grade was significantly lower in the COVID-19 group (myocardial blush grade of 2 to 3 in 54% vs. 93% for COVID-positive and COVID-negative respectively, p < 0.0001).

Despite more thrombotic STEMI, only numerically higher rates of in-hospital mortality were observed among the COVID-19 STEMI patients (17.9% vs. 6.5%, p =0.10). However, COVID-19 STEMI group had longer in-patient admission (p = 0.0004) and higher rates of intensive care admission (p = 0.003).

The findings in this UK registry are in contrast to data that emerged at the beginning of the pandemic,  where much emphasis was placed on the presence of the so-called “STEMI-mimickers”, with two early registries, one from New York and another from Lombardy, Italy both reporting a significant percentage of COVID-positive STEMI patients with no obstructive culprit lesion on angiography (≥50% from New York and 39.3% in the Lombardy registry) (4,5).

Also of note, is the 10-fold higher incidence of stent thrombosis reported among COVID STEMIs in the London registry.   Prieto-Lobato et al similarly reported an increase in stent thrombosis during the COVID-19 pandemic peak at their centre in Albacete, Spain (5). They described a series of four cases: one acute and 3 cases of very late stent thrombosis.  The case of acute ST was seen in a 49-year-old, where OCT demonstrated in-stent mixed thrombus with mild proximal stent under expansion, and was effectively managed with intracoronary tirofiban and proximal over-expansion of the stent. The 3 cases of very late stent thrombosis all occurred in patients over the age of 70 years, two of them requiring aspiration thrombectomy and tirofiban infusions. The authors also used more potent P2Y12 inhibitors (ticagrelor and prasugrel) in these patients.  These cases potentially demonstrate the SARS-CoV-2 hypercoagulable state leading to a stent thrombosis trigger in the presence of other mechanical and biological risk factors (6).

While none of these registry associations nor case series can adequately prove causality for a coronavirus-inflammation-thrombosis–mediated mechanism of STEMI, the increased thrombotic burden and resulting angiographic complexity observed in these COVID STEMI subsets have led to important questions and implications regarding optimum therapeutic strategies, particularly the use of thrombectomy, Glycoprotein IIb/IIIa inhibitors and more potent P2Y12 inhibitors in these patients.

References:

1. Choudry FA, Hamshere SM, Rathod KS, et al. High thrombus burden in patients with COVID-19 presenting with ST-segment elevation myocardial infarction. J Am Coll Cardiol 2020; 76:1168–76.

2. Dauerman HL. The Unbearable Thrombus of COVID-19: Primary PCI, Thrombus, and COVID-19. J Am Coll Cardiol. 2020;76(10):1177-1180.

3. Dominguez-Erquicia P, Dobarro D, Raposeiras-Roubín S, et al. Multivessel coronary thrombosis in a patient with COVID-19 pneumonia. Eur Heart J. 2020 Jun 7;41(22):2132.

4. Bangalore S, Sharma A, Slotwiner A, et al. ST-segment elevation in patients with COVID-19—a case series. N Engl J Med 2020; 382:2478–80.

5. Stefanini GG, Montorfano M, Trabattoni D, et al. ST-elevation myocardial infarction in patients with COVID-19: clinical and angiographic outcomes. Circulation 2020;141:2113–6.

6. Prieto-Lobato A, Ramos-Martínez R, Vallejo-Calcerrada N, et al. A Case Series of Stent Thrombosis During the COVID-19 Pandemic. JACC Case Rep. 2020;2(9):1291-1296.

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