Funding Acknowledgements Type of funding sources: None. Aim Elevated troponin levels have been shown to predict in-hospital outcomes in patients with COVID-19. However, whether this relates to or predicts longer-term outcomes is unknown. We aimed to investigate the effect of troponin elevation in patients with COVID-19, looking at resource utilisation post discharge, re-hospitalisation and outcomes. Methods This was a prospective study of 7650 patients admitted from December 2019 to July 2020 across a large university hospital trust. Patients were stratified according to COVID-19 status and troponin values (elevated = troponin T ≥15 ng/mL). The primary outcome assessed was all-cause mortality. Results 1005 patients were COVID-19 positive and had elevated troponin levels, with the remaining patients troponin positive but COVID-19 negative. COVID+ patients were more likely to be older, and less likely to be Caucasian (35.7% vs 46.6%, p<0.0001), however, peak troponin did not differ significantly between the groups {54 (28-125) vs 47 (25-130) ng/mL, p=0.121}. Mortality before first discharge was four times more likely in COVID+ than COVID- patients with elevated troponins {389 (39%) vs 359 (9.9%); p<0.001}. This mortality rate was also significantly higher than in COVID-19 positive patients who were troponin negative (p=6%, P<0.0001). Post-discharge over a follow-up period of 365 days, in the discharged COVID-19 positive troponin positive group, a minority of patients (13.2%) were investigated with outpatient cardiac investigations (echocardiography, CTCA, coronary angiography and cardiac MRI) compared to the COVID-19 negative group (34.5%). Post-discharge mortality was significantly higher among the COVID+ cohort {63 (10.2%) vs COVID-19 negative troponin positive 103 (3.1%); p<0.001}. COVID+ patients who died post discharge were more likely to be Caucasian (55.4% vs 35.2%, p<0.05) and more likely to be older (81 (72-87.5) vs 67 (57-79), p<0.05) than COVID+ patients who survived post discharge. Conclusion Elevated troponin levels in patients with COVID-19 is associated with long-term mortality. Patients were unlikely to undergo cardiac investigations and the troponin rise likely reflects illness severity. Further data is needed in this area.

Background It has been previously reported during the first COVID outbreak that patients presenting with ST-Segment Elevation Myocardial Infarction (STEMI) and concurrent COVID-19 infection have increased thrombus burden and poorer outcomes [1]. Subsequently, there have been multiple further waves of the pandemic with the emergence of at least two new COVID-19 variants and the emergence of vaccinations. To-date, there have been no reports comparing the outcomes of COVID-19-positive STEMI patients across all waves of the pandemic. Purpose The purpose of this study was to compare the baseline demographic, procedural and angiographic characteristics alongside the clinical outcomes of patients presenting with STEMI and concurrent COVID-19 infection across the COVID-19 pandemic in the UK. Methods This was a single-centre, observational study of 1250 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention (PCI) at Barts Heart Centre between 01/03/2020 and 10/03/2022. COVID +ve patients were split into 3 groups based upon the time course of the pandemic (Wave 1: March 2020-June 2020, Wave 2: Sept 2020-March 2021, Wave 3: October 2021-March 2022). Comparison was made between waves and with a control group of COVID-ve patients treated during the same timeframe. Results A total of 135 COVID +ive patients with STEMI (1st Wave: 39 patients, 2nd Wave: 60 patients, 3rd wave 35 pts) were included in the present analysis; and compared with 1115 COVID negative patients. Significant changes in the baseline characteristics, angiographic features and clinical outcomes of COVID +ive patients occurred over time. Early during the pandemic (Wave 1 2020), STEMI patients presenting with concurrent COVID-19 infection had high rates of cardiac arrest, evidence of increased thrombus burden (higher rates of multi-vessel thrombosis, stent thrombosis, higher modified thrombus grade higher use of GP IIb/IIIa inhibitors and thrombus aspiration, coagulability (more heparin for therapeutic ACT), bigger infarcts (lower myocardial blush grade and left ventricular function) and worse outcomes (mortality). However, by wave 3 (late 2021/2022), no differences existed in clinical characteristics, thrombus burden, infarct size or outcomes between COVID +ive patients and those without concurrent COVID-19 infection with significant differences compared to earlier COVID +ve patients. Poor outcomes later in the study period were predominantly in unvaccinated individuals. Conclusions Significant changes have occurred in the clinical characteristics, angiographic features and outcomes of STEMI patients with COVID-19 infection treated by primary PCI during the course of the pandemic. Importantly it appears that angiographic features and outcomes of recent waves are no different to a non-COVID-19 population. Funding Acknowledgement Type of funding sources: None.

Background Left ventricular thrombus (LVT) complicates around one in six cases of acute and chronic left ventricular systolic dysfunction and is associated with an increased risk of stroke, major systemic embolism and death, believed to be ameliorated by anticoagulation. Off-label use of direct oral anticoagulants (DOACs) for LVT has steadily increased, largely based on favourable outcomes in atrial fibrillation and venous thromboembolism, but the safety and efficacy of DOACs versus vitamin K antagonists (VKA) for LVT remains uncertain. Purpose The main aim of our study was to compare treatment of LVT with VKA to DOAC, focusing on all-cause mortality, stroke, major systemic emboli and major bleeding. Methods We conducted a retrospective observational longitudinal study of patients presenting to two large quaternary centres between 2011 and 2021 with a diagnosis of LVT. Patients were eligible if they had a documented LVT and received anticoagulation with either VKA or DOAC. Baseline data, thrombus characteristics, treatment type and duration, follow up imaging and clinical events were recorded using electronic health care records. Outcome measures included thrombus resolution, stroke and systemic embolism (SSE), major bleeding and mortality. Results A total of 955 patients were identified, of whom 901 received treatment with either a VKA (567 pts, 62.9%) or a DOAC (334 pts, 37.1%) and were included in the analysis. Underlying aetiologies included acute myocardial infarction (AMI) (38.3%), chronic ischaemic cardiomyopathy (38.0%) and non-ischaemic cardiomyopathy (23.7%). Rivaroxaban (43.4%) was the most frequently prescribed DOAC followed by apixaban (35.9%), and the remaining on edoxaban (20.7%). AMI related LVT was more commonly treated with DOAC (53.0%) and chronic ischaemic cardiomyopathy with VKA (72.9%). There was a lower baseline LVEF in the VKA cohort (29.5±13.2 vs 33.1±14.2, p<0.0001). Other demographic features were comparable. Median follow up was 2.5 years (IQR: 1–3.5). There were no differences in follow up duration between the two treatments (p=0.17). Greater rates of thrombus resolution were seen in the DOAC group compared to VKA (1 year: 78.4% vs 51.4%, p<0.0001), with higher rates of persistent thrombus over the follow-up period seen in the VKA group (25.1% vs 12.9%, p<0.0001). Rates of stroke and systemic embolization were similar between the groups (VKA 9.3% vs 9.6% DOAC, p=0.93). Higher rates of bleeding (BARC >3, 8.1% VKA, 3.6% DOAC, p=0.031) (Figure 1A) and mortality (VKA 18.5%, DOAC 10.2%, p=0.001) (Figure 1B) were seen in the VKA group over the follow-up period. Conclusions In a large multi-centre registry of LVT of mixed aetiology, anticoagulation with DOAC was associated with earlier and greater rates of thrombus resolution and consequential reduced adverse events (major bleeding and mortality) during follow up. A funding application to support a multi-centre randomised control trial is underway. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): This work was supported by the British Heart Foundation (Fellowship FS/CRTF/21/24190 to HM) and the National Institute for Health Research (Biomedical Research Centre Award to Guy's and St Thomas' NHS FT and King's College London).