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Eur J Clin Invest ; 51(4): e13471, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1146517

ABSTRACT

The development of an obstructive luminal thrombus is pathological and considered a failure of endogenous fibrinolysis. The consequences may be fatal, or result in lasting downstream organ damage. Therefore, assessment of endogenous fibrinolytic status in an individual may identify those at risk of occlusive thrombus formation and provide prognostic information. Arterial thrombi are more platelet rich and more resistant to fibrinolysis than venous thrombi. Several recent studies using global tests of fibrinolysis in patients with acute coronary syndromes (ACS) have shown that despite dual antiplatelet therapy, patients with impaired fibrinolytic status have an increased risk of adverse cardiovascular events, compared with those with effective fibrinolytic function. Such data add significantly to the predictive value of established cardiovascular risk factors and conventional biomarkers. Most data reported have been obtained with the Global Thrombosis Test and the turbidimetric plasma clot lysis assay. A few small studies in patients with ischaemic stroke suggest a similar predictive role of fibrinolytic status assessment in these patients. Studies reporting an association between impaired fibrinolysis and future venous thrombotic events are limited, and in the form of case-control studies. Viscoelastic assays may have a role in the prediction of venous thromboembolic risk. Assays of fibrinolytic function should be used to obtain a more accurate risk of future thrombotic events, particularly in the setting of ACS. The availability of point-of-care tests helps facilitate this and should encourage future studies to assess personalised antithrombotic treatment combinations to optimise fibrinolytic status and reduce thrombosis risk.


Subject(s)
Acute Coronary Syndrome/blood , Coronary Thrombosis/blood , Fibrin Clot Lysis Time , Fibrinolysis/physiology , Ischemic Stroke/blood , Thrombelastography , Thrombosis/blood , Venous Thrombosis/blood , Acute Coronary Syndrome/epidemiology , Arteries , COVID-19/blood , Coronary Thrombosis/epidemiology , Hematologic Tests , Humans , Ischemic Stroke/epidemiology , Myocardial Infarction/blood , Myocardial Infarction/epidemiology , Risk Assessment , SARS-CoV-2 , Thrombosis/epidemiology , Venous Thromboembolism/blood , Venous Thromboembolism/epidemiology , Venous Thrombosis/epidemiology
2.
J Am Coll Cardiol ; 76(10): 1168-1176, 2020 09 08.
Article in English | MEDLINE | ID: covidwho-747590

ABSTRACT

BACKGROUND: Coronavirus disease-2019 (COVID-19) is thought to predispose patients to thrombotic disease. To date there are few reports of ST-segment elevation myocardial infarction (STEMI) caused by type 1 myocardial infarction in patients with COVID-19. OBJECTIVES: The aim of this study was to describe the demographic, angiographic, and procedural characteristics alongside clinical outcomes of consecutive cases of COVID-19-positive patients with STEMI compared with COVID-19-negative patients. METHODS: This was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020. RESULTS: Patients with STEMI presenting with concurrent COVID-19 infection had higher levels of troponin T and lower lymphocyte count, but elevated D-dimer and C-reactive protein. There were significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly lower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated clotting times were also noted. Importantly, patients with STEMI presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission. CONCLUSIONS: In patients presenting with STEMI and concurrent COVID-19 infection, there is a strong signal toward higher thrombus burden and poorer outcomes. This supports the need for establishing COVID-19 status in all STEMI cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases.


Subject(s)
Coronary Thrombosis , Coronavirus Infections , Fibrinolytic Agents/therapeutic use , Pandemics , Percutaneous Coronary Intervention/methods , Pneumonia, Viral , ST Elevation Myocardial Infarction , Aged , Betacoronavirus/isolation & purification , C-Reactive Protein/analysis , COVID-19 , Comorbidity , Coronary Angiography/methods , Coronary Thrombosis/blood , Coronary Thrombosis/diagnosis , Coronary Thrombosis/etiology , Coronavirus Infections/blood , Coronavirus Infections/complications , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Lymphocyte Count/methods , Male , Middle Aged , Outcome and Process Assessment, Health Care , Patient Selection , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , Pneumonia, Viral/epidemiology , SARS-CoV-2 , ST Elevation Myocardial Infarction/epidemiology , ST Elevation Myocardial Infarction/therapy , Severity of Illness Index , Troponin T/blood
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