COVID-19 patients with STEMI prone to higher thrombus burden, worse outcomes
There appears to be a higher thrombus burden and poorer outcomes in patients with the novel coronavirus disease (COVID-19) with ST-segment elevation myocardial infarction (STEMI), according to a recent study.
“The strong signal toward significantly higher thrombus burden is a novel finding that raises the question of more aggressive antithrombotic therapy in selected COVID-19 STEMI [patients] and provides a rationale for establishing COVID-19 status in all STEMI [patients],” the researchers said.
A total of 115 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre in the UK between 1 March 2020 and 20 May 2020 were included in this single-centre, observational study.
Patients with STEMI and concurrent COVID-19 infection showed higher levels of troponin T and lower lymphocyte count, but increased D-dimer and C-reactive protein. Rates of multivessel thrombosis and stent thrombosis were also significantly elevated. In addition, these patients had higher modified thrombus grade post first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration. [J Am Coll Cardiol 2020;76:1168-1176]
STEMI patients with COVID-19 also had significantly lower myocardial blush grade and left ventricular function. Higher doses of heparin were administered to achieve therapeutic activated clotting times. Notably, these patients had a longer in-patient admission and higher rates of intensive care admission.
“COVID-19 infection is associated with a pro-thrombotic state,” the researchers said. “The occurrence of venous thromboembolic complications, both clinically apparent and subclinical, appears to be an important manifestation of the disease and one that is related to disease severity and outcome.” [Lancet Haematol 2020;7:e438-e440; Am J Hematol 2020;95:e131-e134; Thromb Res 2020;191:145-147; J Thromb Haemost 2020;18:844-847]
Currently, no mechanisms have been identified yet to explain the presentation of STEMI and its associated higher arterial thrombus burden in COVID-19 patients. Platelet activation and endothelial dysfunction appeared to cause arterial thrombus formation in relation to venous thromboembolism, according to the researchers.
Previous data on the influenza virus suggested the association of acute respiratory infections with a significantly higher risk for developing atherosclerotic plaque rupture, which leads to myocardial infarction due to the profound inflammatory response and haemodynamic changes. [N Engl J Med 2018;378:345-353]
A recent study found that infection with SARS-CoV-2, the causative agent of COVID-19, results in a systemic inflammatory response leading to endothelial and haemostatic activation, including activation of platelets and the coagulation cascade. [Circulation 2020;142:611-614]
In addition, another study reported an increased incidence of COVID-19 and subsequent case fatality among patients in the coronary risk groups of diabetes and hypertension. [Lancet 2020;395:1054-1062]
“In keeping with this, the data presented here show significantly higher rates of diabetes, hyperlipidaemia, and hypertension in the COVID-19 group, suggesting that these conditions may also confer an increased risk of STEMI in COVID-19-infected patients,” the researchers said.
“Further work is required to unravel the underlying mechanism of coronary thrombosis in patients with COVID-19 infection,” they added.