Coronary Thrombus Research Articles

A Hemolytic Event in a Heartmate 3 Patient in the Setting of Polycythemia

Introduction The Heartmate 3 (HM3) LVAD has significantly reduced hemocompatibility events. We present a case of a hemolytic event in a HM3 patient likely related to underling polycythemia. Case Report A 49-year-old man with multisystem sarcoidosis (pulmonary and cardiac) complicated by stage D systolic heart failure status post HeartMate 3 left ventricular assist device (LVAD) implantation and secondary polycythemia attributed to chronic hypoxic respiratory disease and pulmonary hypertension presented with symptoms of left arm numbness and tingling followed by severe substernal chest pain. Initial examination was unremarkable. EKG revealed nonspecific intraventricular conduction delay. Troponin I was elevated at 6.1. Hemoglobin was elevated to 19. LDH was elevated to LDH 568 from baseline of 300s. INR was 1.6 upon arrival. LVAD interrogation revealed speed 5600 rpm, flow 4.5 L/min, power 4.4 Watts and pulsatility index of 4.8. Heparin drip, aspirin and statin were initiated for presumed NSTEMI. LDH remained elevated to 600s. Left heart catherization revealed an acute clot in mid-circumflex associated with 50% stenosis consistent with partial resolution of thrombosis. Further workup revealed normal haptoglobin, erythropoietin and total bilirubin levels however plasma free hemoglobin was elevated to 63.1. Urine hemoglobin was not detected. A JAK2 mutation was excluded. Slow therapeutic phlebotomies with replacement of 125cc of blood with equivalent normal saline were initiated given concern for hemolytic event in the setting of worsening polycythemia. Renal imaging was negative and pretest probability for hematologic malignancies remained low. Of note, the patient reported non-compliance with home oxygen therapy used only at the time of exertion. Compliance was reinforced. Subsequently, LDH trended down to baseline following successful heparin bridge to therapeutic warfarin level. The patient was discharged in stable condition. Summary An acute hemolytic event (and possible cardioembolic NSTEMI) was seen in our patient evidenced by an elevation of LDH, plasma hemoglobin and new coronary thrombus in the setting of worsening polycythemia. Despite a remarkable low rate of pump thrombosis, HM3 recipients with acquired pro-thrombotic states such as polycythemia maybe at risk for adverse hemocompatibility events. Close surveillance is warranted for these special populations.

Pre-Hospital Antiplatelet Therapy for STEMI Patients Undergoing Primary Percutaneous Coronary Intervention: What We Know and What Lies Ahead.

Early recanalization of the infarct-related artery to achieve myocardial reperfusion is the primary therapeutic goal in patients with ST-elevation myocardial infarction (STEMI). To decrease the duration of ischaemia, continuous efforts have been made to improve pre-hospital treatment and to target the early period after symptom onset. In this period the platelet content of the fresh coronary thrombus is maximal and the thrombi are dynamic, and thus more susceptible to powerful antiplatelet agents. There have been substantial advances in antiplatelet therapy in the last three decades with several classes of oral and intravenous antiplatelet agents with different therapeutic targets, pharmacokinetics, and pharmacodynamic properties. New parenteral drugs achieve immediate inhibition of platelet aggregation, and fast and easy methods of administration may create the opportunity to bridge the initial gap in platelet inhibition observed with oral P2Y12 inhibitors. Moreover, potential future management of STEMI could directly involve patients in the process of care with self-administered antiplatelet agents designed to achieve rapid reperfusion. However, the potential anti-ischaemic benefits of potent antiplatelet agents will need to be balanced against their risk of increased bleeding. This study presents a comprehensive and updated review of pre-hospital antiplatelet therapy among STEMI patients undergoing primary percutaneous intervention and explores new therapies under development.

Gensini Score and Thrombus Burden Add Predictive Value to the SYNTAX Score in Detecting No-Reflow after Myocardial Infarction.

ResumoFundamento O fenômeno de no-reflow após a intervenção coronária percutânea está associado a um pior prognóstico em pacientes com infarto do miocárdio com supradesnivelamento do segmento ST (IAMCSST). O escore SYNTAX é um bom preditor de no-reflow.Objetivo Nosso objetivo foi avaliar se a carga aterosclerótica (escore Gensini) e a carga trombótica na artéria coronária culpada melhorariam a capacidade do escore SYNTAX para detectar o no-reflow.Métodos Neste estudo coorte prospectivo, foram estudados pacientes com IAMCSST consecutivos que se apresentaram dentro de 12 horas a partir do início dos sintomas. O no-reflow foi definido como fluxo TIMI < 3 ou fluxo TIMI =3 mas grau de blush miocárdico (myocardial blush grade) < 2. A carga trombótica foi quantificada de acordo com o grau TIMI de trombo (0 a 5).Resultados Foram incluídos 481 pacientes no estudo, com idade média de 61±11 anos. O fenômeno de no-reflow ocorreu em 32,8% dos pacientes. O escore SYNTAX (OR=1,05, IC95% 1,01–1,08, p<0,01), a carga trombótica (OR=1,17, IC95% 1,06–1,31, p<0,01), e o escore Gensini (OR=1,37, IC95% 1,13–1,65, p<0,01) foram preditores independentes do no-reflow. Os escores combinados apresentaram uma maior área sob a curva quando comparados ao escore SYNTAX isolado (0,78 [0,73–0,82] vs 0,73 [0,68–0,78], p=0,03). A análise da melhora da reclassificação líquida (NRI) categórica (0,11 [0,01–0,22], p=0,02) e contínua (NRI>0) (0,54 [0,035–0,73], p<0.001) mostrou melhora na capacidade preditiva do no-reflow no modelo combinado, com melhora da discriminação integrada (IDI) de 0,07 (0,04–0,09, p<0,001).Conclusões Nossos achados sugerem que, em pacientes com IAMCSST submetidos à intervenção coronária percutânea, a carga aterosclerótica e a carga trombótica na artéria culpada adicionam valor preditivo ao escore SYNTAX na detecção do fenômeno no-reflow. (Arq Bras Cardiol. 2021; [online].ahead print, PP.0-0)

Serum Ceramides as Prognostic Biomarkers of Large Thrombus Burden in Patients with STEMI: A Micro-Computed Tomography Study.

ST-elevation myocardial infarction (STEMI) remains one of the leading causes of mortality worldwide. The identification of novel metabolic and imaging biomarkers could unveil key pathophysiological mechanisms at the molecular level and promote personalized care in patients with acute coronary syndromes. We studied 38 patients with STEMI who underwent primary percutaneous coronary intervention and thrombus aspiration. We sought to correlate serum ceramide levels with micro-CT quantified aspirated thrombus volume and relevant angiographic outcomes, including modified TIMI thrombus grade and pre- or post-procedural TIMI flow. Higher ceramide C16:0 levels were significantly but weakly correlated with larger aspirated thrombus volume (Spearman r = 0.326, p = 0.046), larger intracoronary thrombus burden (TB; p = 0.030) and worse pre- and post-procedural TIMI flow (p = 0.049 and p = 0.039, respectively). Ceramides C24:0 and C24:1 were also significantly associated with larger intracoronary TB (p = 0.008 and p = 0.001, respectively). Receiver operating characteristic analysis demonstrated that ceramides C24:0 and C24:1 could significantly predict higher intracoronary TB (area under the curve: 0.788, 95% CI: 0.629–0.946 and 0.846, 95% CI: 0.706–0.985, respectively). In conclusion, serum ceramide levels were higher among patients with larger intracoronary and aspirated TB. This suggests that quantification of serum ceramides might improve risk-stratification of patients with STEMI and facilitate an individualized approach in clinical practice.

Antithrombotic Therapy in Acute Coronary Syndromes: Current Evidence and Ongoing Issues Regarding Early and Late Management.

A few decades ago, the understanding of the pathophysiological processes involved in the coronary artery thrombus formation has placed anticoagulant and antiplatelet agents at the core of the management of acute coronary syndrome (ACS). Increasingly potent antithrombotic agents have since been evaluated, in various association, timing, or dosage, in numerous randomized controlled trials to interrupt the initial thrombus formation, prevent ischemic complications, and ultimately improve survival. Primary percutaneous coronary intervention, initial parenteral anticoagulation, and dual antiplatelet therapy with potent P2Y12 inhibitors have become the hallmark of ACS management revolutionizing its prognosis. Despite these many improvements, much more remains to be done to optimize the onset of action of the various antithrombotic therapies, for further treating and preventing thrombotic events without exposing the patients to an unbearable hemorrhagic risk. The availability of various potent P2Y12 inhibitors has opened the door for individualized therapeutic strategies based on the clinical setting as well as the ischemic and bleeding risk of the patients, while the added value of aspirin has been recently challenged. The strategy of dual-pathway inhibition with P2Y12 inhibitors and low-dose non-vitamin K antagonist oral anticoagulant has brought promising results for the early and late management of patients presenting with ACS with and without indication for oral anticoagulation. In this updated review, we aimed at describing the evidence supporting the current gold standard of antithrombotic management of ACS. More importantly, we provide an overview of some of the ongoing issues and promising therapeutic strategies of this ever-evolving topic.

Microbiota thrombus colonization may influence athero-thrombosis in hyperglycemic patients with ST segment elevation myocardialinfarction (STEMI). Marianella study

ObjectivesWe examined the association of the coronary thrombus microbiota and relative metabolites with major adverse cardiovascular events (MACE) in hyperglycemic patients with ST segment elevation myocardial infarction (STEMI). BackgroundHyperglycemia during STEMI may affect both development and progression of coronary thrombus via gut and thrombus microbiota modifications. MethodsWe undertook an observational cohort study of 146 first STEMI patients treated with primary percutaneous coronary intervention (PPCI) and thrombus-aspiration (TA). Patients were clustered, based on admission blood glucose levels, in hyperglycemic (≥140 mg/dl) and normoglycemic (<140 mg/dl). We analyzed gut and thrombus microbiota in all patients. Moreover, we assessed TMAO, CD40L and von Willebrand Factor (vWF) in coronary thrombi. Cox regressions were used for the association between Prevotellaspp. and TMAO terziles and MACE. MACE endpoint at 1 year included death, re-infarction, unstable angina. ResultsIn fecal and thrombus samples, we observed a significantly different prevalence of both Prevotellaspp. and Alistipesspp. between patients with hyperglycemia (n = 56) and those with normal glucose levels (n = 90). The abundance of Prevotella increased in hyperglycemic vs normoglycemic patients whereas the contrary was observed for Alistipes. Interestingly, in coronary thrombus, the content of Prevotella was associated with admission blood glucose levels (p < 0.01), thrombus dimensions (p < 0.01), TMAO, CDL40 (p < 0.01) and vWF (p < 0.01) coronary thrombus contents. Multivariate Cox-analysis disclosed a reduced survival in patients with high levels of Prevotella and TMAO in coronary thrombus as compared to patients with low levels of Prevotella and TMAO, after 1-year follow up. ConclusionsHyperglycemia during STEMI may increase coronary thrombus burden via gut and thrombus microbiota dysbiosis characterized by an increase of Prevotella and TMAO content in thrombi.Clinical Trial Registration: NCT03439592. September 30, 2016.Ethic Committee Vanvitelli University: 268/2016.

Functional and anatomical assessment of a spontaneously recanalized organized coronary thrombus.

Functional and anatomical assessment of a spontaneously recanalized organized coronary thrombus.

The relationship between hemoglobin A1c levels and thrombus load in patients with type 2 diabetes mellitus and non-ST-segment elevation myocardial infarction.

Background:We aimed to investigate the relationship between hemoglobin A1c (HbA1c) and coronary thrombus load in type-2 diabetes mellitus (T2DM) patients with non-ST segment elevation myocardial infarction (NSTEMI).Materials and Methods:Ninety diabetic patients with NSTEMI were recruited for the study. They were separated into two groups according to HbA1c levels. Forty-seven patients having HbA1c ≤6.5% formed Group-I (35 male, mean age 58 ± 10.5 years) and the remaining 43 patients with HbA1c >6.5% formed Group-II (23 male, mean age 58 ± 11.1 years). Both the groups were evaluated in terms of thrombolysis in myocardial infarction (TIMI) thrombus score and Syntax score.Results:Baseline patient characteristics were comparable in both the groups. TIMI thrombus score and Syntax score were higher in Group II than in Group I (3.2 ± 1.4 vs. 4.7 ± 0.5 and 20.2 ± 3.4 vs. 26.3 ± 3.0 respectively, P < 0.05). No significant difference was found in other parameters. In stepwise linear regression analysis, prepercutaneous coronary intervention (PCI) and post-PCI TIMI frame number and HbA1c were significantly related to the coronary thrombus scale. However, no significant relationship has been found between thrombus formation and hypertension, previous PCI history, pre-PCI heart rate, pre-PCI cholesterol status, and high-sensitive troponin T.Conclusion:In NSTEMI with T2DM, increased HbA1c (HbA1c >6.5%) is related with coronary thrombus in the target vessel. In those patient population, strict anticoagulation should be considered to prevent potential adverse events.

A 32-Year-Old Coronary Thrombus Case Found during the COVID-19 Pandemic: Could It Be Caused By Sinovac Inactivated Vaccine Or COVID-19 Late-Term Complication?

Coronavirus disease 2019 (COVID-19) infection is a public health problem, which globally is considered a pandemic, causing a significant level of morbidity and mortality. It has been defined as a viral infection, the etiology of which is unknown, causing mostly respiratory tract infections. It is surely beyond doubt that vaccine development also plays an important role in ending such pandemics as well as hygiene rules and personal protective equipment. It is becoming gradually more apparent that cardiovascular complications associated with COVID-19, such as myocardial damage, arrhythmia, acute heart failure, and venous thromboembolism, occur more frequently than what was thought before. The precise pathophysiological mechanisms of myocardial damage remain unclear but are thought to be the main pathway, with microthrombi, cytokine storm, and plaque rupture due to hypoxic damage, coronary spasm, direct endothelial, or vascular injury. In this study, we wanted to present a 32-year-old coronary thrombus case with no medical history and no risk factors, which we think may develop due to the Sinovac inactivated COVID-19 vaccine or as a late complication of COVID-19 disease. While cardiac side effects associated with inactive COVID-19 vaccines are still limited in the literature, this issue can be clarified if there are more case reports.

Role of Intravascular Imaging for the Diagnosis of Recanalized Coronary Thrombus

IntroductionRecanalized thrombus (RCT) of coronary arteries is frequently unrecognized in interventional cardiology practice. Intravascular imaging conclusively establishes its diagnosis, which otherwise is often misdiagnosed as fresh thrombus, spontaneous coronary artery dissection, or severe calcification based on angiography, alone. We hereby report our experience of 10 RCT patients, who had the intravascular imaging-guided diagnosis, followed by the successful percutaneous coronary intervention (PCI). MethodsIt was a retrospective analysis of 10 patients, who had angiographic haziness of the target lesion during PCI, which were found to be RCT on intravascular imaging. Either optical coherence tomography (OCT) or intravascular ultrasound (IVUS) was performed to characterize RCT in 9 and 1 patient, respectively. ResultsThe mean age was 53 ± 13.1 years, comprising 9 men and 1 woman. Six patients had acute coronary syndrome, while four had chronic stable angina. Coronary angiography revealed ≥ 70% angiographic stenosis, with intracoronary haziness/filling defects which were linear, spiral or braided in appearance. OCT findings in 9 patients include signal-rich, high backscattered septa dividing the lumen into multiple small cavities communicating with each other, giving a “Swiss cheese” or “honeycomb” appearance. Intravascular ultrasound (IVUS) findings in one patient showed multiple cavities filled with blood speckling consistent with recanalized thrombus. All patients underwent successful PCI with image-guided optimization. ConclusionWith the increasing use of intravascular imaging during PCI, RCT is frequently identified. OCT remains the investigation of choice to differentiate it from other similar entities on angiography.

Acute myocardial infarction,arterial thrombosis and thrombophilia in young patients

Acute coronary syndrome (ACS) represent emergency state in an intensive cardiovascular care unit, which implies immediate and specific treatment. Of peculiar interest for cardiologists are young patients with acute myocardial infarction (AMI). The family history taking for premature coronary artery disease (CAD) and establishment of genetic factors, responsible for coagulation, both are on target for this group of patients. Gold standard for AMI diagnosis is coronary angiography (CA), which usually implies endovascular treatment (EVT). When coronary thrombus formation is found in young patients, different diagnostic opportunities are possible. Thrombophilia (TF) represents blood coagulation abnormality resulting in an increased risk of thrombosis. It could affect different sections of the cardiovascular system, most commonly venous, but also arterial. This clinical condition could be confirmed by performing laboratory genetic tests. We studied a group of forty-one young patients with first appearance of ACS ≤ 55 years old included for a five-year period. All of them were evaluated with CA and received EVT. According to the thrombotic risk, we defined a high-risk group, treated with anticoagulant (AC) on top of dual antiplatelet therapy (DAPT). The patients were followed-up for recurrent ischemic and bleeding events. We performed laboratory tests for the most frequent TF gene mutations in Bulgarian population. There is a conflicting data about this issue in different ethnic origins. The aim of our study is to estimate the possible relationship between the TF and the arterial thrombosis in young ACS patients, to defi ne specific treatment strategies, improving the prognosis of the patients.

Therapeutic Implications of COVID-19 for the Interventional Cardiologist.

Although COVID-19 is viewed primarily as a respiratory disease, cardiovascular risk factors and disease are prevalent among infected patients and are associated with worse outcomes. In addition, among multiple extra-pulmonary manifestations, there has been an increasing recognition of specific cardiovascular complications of COVID-19. Despite this, in the initial stages of the pandemic there was evidence of a reduction in patients presenting to acute cardiovascular services. In this masterclass review, with the aid of 2 exemplar cases, we will focus on the important therapeutic implications of COVID-19 for interventional cardiologists. We summarize the existing evidence base regarding the varied cardiovascular presentations seen in COVID-19 positive patients and the prognostic importance and potential mechanisms of acute myocardial injury in this setting. Importantly, through the use of a systematic review of the literature, we focus our discussion on the observed higher rates of coronary thrombus burden in patients with COVID-19 and acute coronary syndromes.

Association between serum SCUBE1 levels and thrombus burden in patients with ST-segment elevation myocardial infarction

Introduction The signal peptide-CUB-EGF domain-containing protein-1 (SCUBE1) is a recently available biomarker which is expressed by activated and adhered platelets. In present study, we aimed to investigate the association between SCUBE1 levels and thrombus burden in patients with ST elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PPCI). Methods A total of 88 patients who were diagnosed with STEMI and underwent PPCI were prospectively included between July 2019 and August 2019. Blood samples were collected for routine biochemistry and serum SCUBE1 levels before PPCI and antiplatelet therapy. Angiographic coronary thrombus burden was classified based on thrombolysis in myocardial infarction (TIMI) thrombus grades. We formed two groups based on the thrombus grade: 37 (42%) patients had high thrombus burden whereas 51 (58%) patients had low thrombus burden. Results The mean age of study population was 58.2 ± 11.8 years (34% female). The mean peak troponin I level, SCUBE1 level, SYNTAX score, and pain-to-balloon time were significantly higher in the high thrombus burden group compared to the low thrombus burden group (p < .05, for all). In ROC analysis, SCUBE1 level >65.63 ng/dL had a sensitivity of 91.9% and a specificity of 76.6% to predict high thrombus burden (AUC: 0.9256; p < .001). In multivariate analysis, SCUBE1 level (HR: 1.133, p = .004) and troponin (HR: 1.002; 95% CI 1.001–1.004, p = .003) were independent predictors of high thrombus burden. Conclusion In the present study, we showed that SCUBE1, a novel platelet-endothelial adhesion molecule and a marker of platelet activation, is an independent predictor of high thrombus burden in patients with STEMI.

Comparison of thrombus, gut, and oral microbiomes in Korean patients with ST-elevation myocardial infarction: a case\u2013control study

ST-segment elevation myocardial infarction (STEMI) is characterized by thrombotic coronary artery occlusions caused by atherosclerotic plaque rupture. The gut microbiome potentially contributes to the pathogenesis of coronary artery diseases. This study investigated the microbial diversity and composition of coronary thrombi in STEMI patients and the composition of the thrombus microbiome relative to that of the oral and gut microbiomes. A case–control study was performed with 22 STEMI patients and 20 age- and sex-matched healthy controls. Coronary thrombi were acquired from STEMI patients via manual thrombus aspiration during primary coronary intervention. Oral swab and stool samples were collected from both groups, and 16S rRNA sequencing and metagenomic microbiome analyses were performed. Microbial DNA was detected in 4 of 22 coronary thrombi. Proteobacteria (p) and Bacteroidetes (p) were the most abundant phyla. The oral and gut microbiomes significantly differed between patients and healthy controls. The patient group presented microbial dysbiosis, as follows: a higher relative abundance of Proteobacteria (p) and Enterobacteriaceae (f) in the gut microbiome and a lower abundance of Firmicutes (p) and Haemophilus (g) in the oral microbiome. Furthermore, 4 significantly abundant genera were observed in the coronary thrombus in the patients: Escherichia, 1.25%; Parabacteroides, 0.25%; Christensenella, 0.0%; and Bacteroides, 7.48%. The present results indicate that the relative abundance of the gut and oral microbiomes was correlated with that of the thrombus microbiome.

Recanalized Coronary Thrombus: Role of OCT in Identifying a Slow-Evolving and Underestimated Coronary Lesion

Pathological studies have revealed spontaneous recanalized coronary thrombi as a frequent evolution of coronary occlusions; however, they are poorly recognized on coronary angiography, and the optimal therapeutic strategy for clinical evolution is unknown. We report the role of optical coherence tomography in identifying a recanalized coronary thrombus causing myocardial ischemia after 11 years of follow-up. (Level of Difficulty: Intermediate.)

Relationship of serum vitamin D levels with coronary thrombus grade, TIMI flow, and myocardial blush grade in patients with acute ST-segment elevation myocardial infarction

BackgroundVitamin D deficiency is a prevalent condition that is found in about 30–50% of the general population, and it is increasing as a new risk factor for coronary artery disease. Our study aimed to evaluate the relationship of serum vitamin D levels with coronary thrombus burden, Thrombolysis In Myocardial Infarction flow grade, and myocardial blush grade in patients managed by primary percutaneous coronary intervention for their first acute ST-segment elevation myocardial infarction.ResultsEighty patients were included in the study with their first acute ST-segment elevation myocardial infarction and were managed by primary percutaneous coronary intervention. According to the serum concentrations of vitamin D, the study population was divided into 2 groups: group A with abnormal vitamin D levels less than 30 ng/ml (50 patients) and group B with normal vitamin D levels equal to or more than 30 ng/ml (30 patients). Angiographic data was recorded before and after coronary intervention. On comparing thrombus grade and initial and post-procedural Thrombolysis In Myocardial Infarction flow between both groups of patients, there was no significant difference (p = 0.327, p = 0.692, p = 0.397). However, myocardial blush grade was better in patients with normal vitamin D levels (p = 0.029) without a significant correlation between vitamin D concentration values and myocardial blush grade (r = 0.164, p = 0.146).ConclusionsPatients with first acute ST-segment elevation myocardial infarction and normal vitamin D levels undergoing primary percutaneous coronary intervention had better myocardial blush grade and more successful microvascular reperfusion in comparison with patients with abnormal vitamin D levels. There was no significant difference between the normal and abnormal vitamin D groups regarding the coronary thrombus grade and Thrombolysis In Myocardial Infarction flow.

Abstract 16857: Acute Pericarditis With Concomitant Stemi Associated With Delayed Presentation in the Setting of SARS-COV-2 Pandemic

Background: The classic ST-segment elevations seen in a STEMI can similarly be found during an episode of acute pericarditis, making the two entities difficult to distinguish. The incidence of post-myocardial infarction injury syndromes presenting with findings such as acute pericarditis is estimated to be around 3%. Prompt seek of medical care is pivotal in successful outcomes, which has been affected during the pandemic. Case: A 30-year-old female with a past medical history of uncontrolled type 1 diabetes, chronic kidney disease, obesity presented with a 24-hour long history of non-radiating chest pain. Upon interrogation she endorsed that initially she delayed her coming presentation to the hospital because of fears of contracting coronavirus. Physical examination showed tachycardia and tachypnea. EKG demonstrated diffuse ST elevations in the anterolateral leads concerning for a STEMI, PR-segment depressions on most leads and troponin elevation to 0.09 ng/ml. Point of care ultrasound (POCUS) echocardiogram showed significant anterolateral wall hypokinesis. Decision making: Given her high cardiovascular risk factors the patient was urgently taken to the catheterization laboratory which found a 100% ostial left anterior descending artery and a large left main coronary artery thrombus. The thrombus was initially treated with mechanical thrombectomy and the plaque with a percutaneous coronary intervention (PCI) with a drug-eluding stent to the proximal LAD. In the days following her PCI, the patient continued to endorse sporadic sharp chest pain with the same characteristics as on presentation. Post-PCI transthoracic echocardiogram demonstrated ejection fraction of 20-25% and a small pericardial effusion. She was started on colchicine for pericarditis. She was discharged home on dual antiplatelet therapy with close follow up. Conclusion: Given that our patient had clinical pericarditis before her presentation to the hospital with a STEMI, it is unlikely that her pericarditis was due to a post myocardial infarction syndrome. Delayed presentation to the hospital associated with fear of contracting or spreading COVID-19 is a silent collateral culprit that adds up to increased cardiovascular morbidity and mortality during this pandemic.

The inflammasome signaling axis in thrombi from STEMI patients is related to degree of myocardial injury

Abstract Background The NLRP3-inflammasome and the IL-6-pathways, i.e. the inflammasome signaling axis, seems to be central mechanisms in the inflammatory response related to myocardial reperfusion injury after revascularization. The beneficial results shown by treating MI-patients with canakunimab, an antibody blocking IL1-β, in the CANTOS trial*, and by treatment of NSTEMI patients with the IL6-receptor antagonist tocilizumab**, are looked upon as proof of concept for inflammasome inhibition. Purpose To study whether genes encoding inflammasome-related proteins are present in coronary thrombi and in circulating cells from STEMI patients, and whether these are related to the degree of myocardial injury as measured by troponin T, and time from symptoms to PCI. Methods Intracoronary thrombi were aspirated from 33 patients with STEMI treated with primary PCI. The thrombi were snap-frozen in RNA-later solution for gene expression analyses. Peripheral blood samples with Pax-gene tubes were drawn at end of the PCI-procedure. mRNA of NLRP3, caspase1, IL1-β, IL18, IL6, IL6-receptor (IL6-R) and gp130 were isolated from the thrombi and leukocytes in peripheral blood, and relatively quantified by RT PCR. Peak troponin was collected from clinical records. Results Genes coding for the 7 different markers were present in 76–100% of the thrombi. The expression of NLRP3 in thrombi significantly correlated to peak troponin T (r=0.468, p=0.024). Dividing peak troponin T values into quartiles, the median value of NLRP3 mRNA in Q4 was 2.0-fold higher compared to Q1–3 (p=0.012). Peak troponin T also correlated with the expression in circulating leukocytes of NLRP3 (r=0.420, p=0.0149) and IL1-β (r=0.394, p=0.023), and borderline to caspase1 (r=0.321, p=0.069) and IL18 (r=0.310, p=0.079). IL6-R expression in thrombi correlated significantly to peak troponin T (r=0.434, p=0.019), with a 2.5-fold higher median level in Q4 vs Q1–3 of troponin T (p=0.017). gp130 expression in thrombi correlated inversely with peak troponin T (r=−0.398, p=0.050), as did IL6-R expression in circulating leukocytes (r=−0.421, p=0.015). There were no significant correlations between genes expressed in the thrombi and time from symptom to PCI (median 152 minutes), whereas genes for IL6 in circulating leukocytes correlated inversely (r=−0.385, p=0.027). Conclusion The inflammasome signaling pathway was actively regulated in coronary thrombi and in circulating leukocytes from patients with STEMI. Genes encoding NLRP3 and IL6-R were increasingly expressed in thrombi from patients with increased myocardial damage, measured by troponin T, supporting the beneficial effects of medically targeting this pathway. Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): Stein Erik Hagens Foundation for Clinical Heart Research

MANAGEMENT OF ACUTE CORONARY SYNDROME AND SUBACUTE IN-STENT THROMBOSIS IN SETTING OF FACTOR V LEIDEN MUTATION

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Factor V Leiden (FVL) results from mutation in the F5 gene resulting in hypercoagulable state. Although, venous thromboembolism (VTE) is frequently reported with FVL, cases of arterial thrombosis, especially MI in setting of FVL are rare. CASE PRESENTATION: 55-year-old Caucasian woman, diagnosed with FVL (heterozygous) 3 weeks ago in setting of unprovoked right lower extremity DVT, presented with substernal chest pain radiating to left arm. Past medical history was insignificant. She was up to date on cancer screening. Home medication was recently initiated rivaroxaban. No family history of premature CAD or thrombophilia and no smoking, alcohol, or drug use reported. Of note, the patient presented 1 week prior to this visit with chest pain, peak troponin I of 1.99 ng/ml, without ST changes on EKG. CT arteriogram at that time showed no occlusions, calcified or non-calcified coronary plaques. Echocardiogram at that time was normal. EKG on this visit showed ST-elevations in leads II, III, aVF, V3-V6. Emergent coronary angiography revealed 80% focal mid LAD stenosis due to thrombus, and distal showering of thrombus in the apical region. Left ventriculography showed apical dyskinesis with normal EF. Remaining coronary vessels were 100% patent. She was treated with DES to mid LAD, aspirin, ticagrelor, beta-blocker and statin. Hematology was consulted for possible anticoagulation failure given acute LAD thrombus and recommended heparin to warfarin bridge with INR goal of 2-3. 5 days later, patient had chest pain again and left heart catheterization this time showed subacute in-stent thrombosis, treated with manual aspiration and balloon angioplasty. She was switched to therapeutic enoxaparin and remains asymptomatic to date. DISCUSSION: Hereditary thrombophilias are associated with increased risk of thromboembolic events. Association of FVL with VTE is well established, but its role in arterial thrombotic events is controversial. While the patient received dual anti-platelet therapy following stent implantation, the subacute in-stent thrombosis likely resulted from her underlying hypercoagulable state. We can possibly infer that the dual anti-platelet therapy alone may not be effective for the carriers of FVL. Also, the role of NOACs to prevent coronary artery thrombosis is questionable. Higher INR goal on warfarin or therapeutic doses of LMWH may be necessary to prevent coronary thrombus in setting of FVL. CONCLUSIONS: More studies are needed to establish the role of thrombophilic disorders and coronary artery and stent thrombosis. Higher INR goal on warfarin or therapeutic LMWH may be required to prevent future coronary thrombotic events. In patients with acute or subacute stent thrombosis, hypercoagulable workup should be pursued, and such patients can potentially benefit from anticoagulation therapy on top of dual antiplatelet therapy. Reference #1: J Cardiovasc Med (Hagerstown). 2008;9(4):410–413. DISCLOSURES: No relevant relationships by Mohammad Hamza, source=Web Response No relevant relationships by Usman Naseer, source=Web Response No relevant relationships by Sheikh Raza Shahzad, source=Web Response Speaker/Speaker's Bureau relationship with Amgen Please note: $5001 - $20000 Added 06/01/2020 by Ira Zackon, source=Web Response, value=Honoraria Speaker/Speaker's Bureau relationship with Takeda Please note: $1001 - $5000 Added 06/01/2020 by Ira Zackon, source=Web Response, value=Honoraria Consultant relationship with G1 Therapeutics Please note: $1-$1000 Added 06/01/2020 by Ira Zackon, source=Web Response, value=Consulting fee

PANCREATITIS-INDUCED ACUTE ST SEGMENT ELEVATION AND REGIONAL WALL MOTION ABNORMALITY

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Acute myocardial infarction (AMI) mimics causing ST segment elevation present a diagnostic conundrum for physicians. Recognition of uncommon causes of AMI mimics is essential in reducing patient exposure to unnecessary intervention. CASE PRESENTATION: A 49-year-old male with a past medical history of hypertension presented to the emergency with a chief complaint of severe epigastric pain radiating to his back. He had undergone ERCP earlier in the day for removal of a common bile duct (CBD) stone. Severe epigastric tenderness was observed on physical exam. Laboratory evaluation revealed WBC count of 25700/mcL, Hb 19.8 g/L, BUN 25 mg/dL, creatinine 1.3 mg/dL, alkaline phosphatase 188 IU/L, AST 42 IU/L, ALT 89 IU/L, total bilirubin 1.4 mg/dL, amylase 1059 IU/ L, lipase 21,417 units/L and troponin < 0.015 ng/mL. CT scan of the abdomen revealed an enlarged pancreas with surrounding fat stranding and the presence of a distal CBD stone. EKG was unremarkable (figure 1). The following day, the patient developed tachycardia and reported recurrent epigastric pain. He denied chest pain. EKG evidenced sinus tachycardia, 2-3mm convex ST segment elevation in inferior leads, 1-2mm ST depression in the anterolateral leads was also observed (figure 2). Serial troponin I levels were within the undetectable range. Repeat EKG after 3 hours showed tachycardia with no ST segment elevation (figure 3). Echocardiography revealed a small area of dyskinesia in the inferoseptal wall of the left ventricle. Patient was managed without percutaneous coronary intervention (PCI), thrombolysis or anticoagulation. Patient’s hospital stay was complicated by pancreatic necrosis, abscess, pseudocyst formation, and sepsis. He was discharged on day 19 after recovery. DISCUSSION: The most common EKG changes in pancreatitis are secondary to metabolic derangements such as hypocalcemia, hyponatremia, hypokalemia, hypomagnesemia, and insulin-induced hypoglycemia. QT prolongation, ST depression, U waves, and low amplitude T wave changes are frequently seen. On the other hand, ST elevation is rarely seen. Proposed mechanisms for ST elevation and wall motion abnormality include the cytotoxic effect of proteolytic enzymes on cardiac myocytes, a cardiobiliary reflex resulting in increased vagal tone, coronary vasospasm, exacerbation of underlying coronary artery disease, or coronary thrombus formation from increased platelet adhesiveness and/or pancreatic enzyme induced coagulopathy [1,2,3]. Takotsubo stress cardiomyopathy has been linked to pancreatitis in several reports. Hypothesized pathomechanisms for this transient myocardial dysfunction include catecholamine excess and sympathetic stimulation [2]. CONCLUSIONS: Acute pancreatitis may mimic EKG and echocardiography findings of AMI. In selected cases, knowing this can help avoid unnecessary PCI, thrombolysis or anticoagulation which may lead to serious hemorrhagic complications. Reference #1: Coppola G, Carità P, Corrado E, Borrelli A, Rotolo A, Guglielmo M, et al. ST segment elevations: Always a marker of acute myocardial infarction? Indian Heart Journal. 2013 Jul;65(4):412–23. Reference #2: Yu ES, Lange JJ, Broor A, Kutty K. Acute Pancreatitis Masquerading as Inferior Wall Myocardial Infarction: A Review. Case Rep Gastroenterol. 2019 Aug;13(2):321–35. Reference #3: Ro TK, Lang RM, Ward RP. Acute pancreatitis mimicking myocardial infarction: evaluation with myocardial contrast echocardiography. Journal of the American Society of Echocardiography. 2004 Apr;17(4):387–90. DISCLOSURES: No relevant relationships by Maryam Moghareh, source=Web Response No relevant relationships by Prashank Neupane, source=Web Response No relevant relationships by Zed Seedat, source=Web Response No relevant relationships by Touqir Zahra, source=Web Response