Covid-19: Is the placenta a safe space

Problem: Several large studies have demonstrated that COVID-19 pregnant individuals are at a significant risk for severe disease and adverse pregnancy outcomes. The mechanisms underlying these phenomena remain to be elucidated and are the focus of our project. Although fetal and placental infection is rare, placental abnormalities and adverse pregnancy outcomes associated with placental dysfunction in COVID-19 cases have been widely reported. In particular, placental thrombosis and lesions consistent with maternal vascular malperfusion (MVM) of the placenta are common in individuals with COVID-19. Since thrombotic complications have been associated with COVID-19, it is not surprising that pregnant individuals with COVID- 19 are at risk for placental thrombosis. Method of Study: Placentas were evaluated histologically. Extracellular vesicles were isolated by serial centrifugation. Result(s): Adverse pregnancy outcomes associated with these placental lesions, including hypertensive disorders of pregnancy (gestational hypertension and preeclampsia), small for gestational age (SGA, birthweight < 10th percentile for gestational age), and preterm birth (PTB, < 37 weeks) are significantly increased among pregnant individuals with COVID-19. Placental infection with SARSCoV- 2 is uncommon, but multiple inflammatory and metabolic factors are likely to affect the placenta, including circulating extracellular vesicles (EVs) derived from various organs that have been associated with COVID-19 pathology and disease severity.We have analyzed over 500 placentas from COVID-19 pregnancies and found marked changes in placental morphology, characterized by abnormal maternal and fetal vessels, intervillous thrombi, and fibrin deposition, even in the face of mild or asymptomatic disease. We detected increased levels of small EVs in maternal serum from COVID-19 cases compared to controls and increased levels of mitochondrial DNA in EVs from COVID-19 cases. In in vitro experiments, we found increased oxidative stress in uterine endothelial cells and primary trophoblasts. Syncytialization of trophoblast cells following exposure to EVs from pregnant COVID-19 patients was markedly reduced. RNAseq of trophoblast cells exposed to EVs from pregnant COVID-19 patients revealed disruption of multiple pathways related to mitochondria function, oxidative stress, coagulation defects, and inflammation. Timing of infection during pregnancy (first, second, and third trimester) altered EV size distribution, cargo content, and functional consequences of trophoblast EV exposure. Conclusion(s): Our studies show that COVID-19 infection during pregnancy has profound effects on placenta morphology and function. It remains to be determined what the long-term consequences are on the offspring.

ST-SEGMENT-ELEVATION MYOCARDIAL INFARCTION in COVID-19

Introduction: The Severe Acute Respiratory Syndrome Coronavirus-2 have been associated with cardiovascular adverse events including acute myocardial infarction due to a prothrombotic and hypercoagulable status, and endothelial dysfunction. Case report: We report the case of a 62-year-old women, admitted to the hospital via the emergency room for acute chest pain and dyspnea. A nasopharyngeal swab was positive for COVID19 real-time reverse transcriptase-polymerase chain reaction 11 day ago. On admission, she was hypotensive with systolic blood pressure measering 87 mmHg and tachycardic with 117 beats/min, oxygen saturation (SO2) was 94%. An 18-lead ECG revealed an infero-postero-lateral ST-elevation myocardial infarction with right ventricular involvement and a seconddegree- Mobitz Type 1 atrioventricular block. The coronary angiography from the right femoral artery showed acute thrombotic occlusion of the first diagonal branch with TIMI 0 flow and acute thrombotic occlusion of proximal right coronary artery with TIMI 0 flow. The most likely diagnosis was myocardial infarction secondary to a non-atherosclerotic coronary occlusion. The angioplasy was performed with dilatations with a semi compliant balloon, bailout implant of BMS, manual thrombus aspiration and intracoronary injection of tirofiban in the right coronary artery. The myocardial revascularization was ineffective. The patient developed significant severe hemodynamic instability and cardiac arrest for pulseless electric activity after 24 hours. Conclusion(s): The COVID-19 outbreak implies deep changes in the clinical profile and therapeutic management of STEMI patients who underwent PCI. At present, the natural history of coronary embolism is not well understood;however, the cardiac mortality rate are hight. This suggests these patients require further study to identify the natural history of the condition and to optimize management to improve outcome.

Multifactorial Effects of Covid-19: A Review of Published Autopsy Reports

Introduction: SARS-CoV-2 is responsible for the current global pandemic. SARS-CoV-2 infection underlies the novel viral condition coronavirus disease 2019 (COVID-19). COVID-19 causes significant pulmonary sequelae contributing to serious morbidities. The pathogenesis of COVID-19 is complex with a multitude of factors leading to varying levels of injury numerous extrapulmonary organs. This review of 124 published articles documenting COVID- 19 autopsies included 1,142 patients. Method(s): A PubMed search was conducted for COVID-19 autopsy reports published before March 2021 utilizing the query COVID-19 Autopsy. There was no restriction regarding age, sex, or ethnicity of the patients. Duplicate cases were excluded. Findings were listed by organ system from articles that met selection criteria. Result(s): Pulmonary pathology (72% of articles;866/1142 patients): diffuse alveolar damage (563/866), alveolar edema (251/866), hyaline membrane formation (234/866), type II pneumocyte hyperplasia (165/866), alveolar hemorrhage (164/866), and lymphocytic infiltrate (87/866). Vascular pathology (41% of articles;771/1142 patients): vascular thrombi (439/771)-microvascular predominance (294/439)-and inflammatory cell infiltrates (116/771). Cardiac pathology (41% of articles;502/1142 patients): cardiac inflammation (186/502), fibrosis (131/502), cardiomegaly (100/502), hypertrophy (100/502), and dilation (35/502). Hepatic pathology (33% of articles;407/1142 patients): steatosis (106/402) and congestion (102/402). Renal pathology (30% of articles;427/1142 patients): renal arteries arteriosclerosis (111/427), sepsis-associated acute kidney injury (81/427) and acute tubular necrosis (77/427). Conclusion(s): This review revealed anticipated pulmonary pathology, along with significant extrapulmonary involvement secondary to COVID-19, indicating widespread viral tropism throughout the human body. These diverse effects require additional comprehensive longitudinal studies to characterize short-term and long-term COVID-19 sequelae and inform COVID-19 treatment.

Long-term coagulation abnormalities after COVID-19.

Objective: Hypercoagulation and high incidence of thrombosis during COVID-19 is well established. However, there is a lack of data, how it changes over time. The main purpose of our study was to access different parts of hemostasis in few months after acute disease. Material and methods. Patients discharged from our hospital were invited for follow up examination in 2,3-3,8 (group 1 - 55 pts) or 4,6-5,7 months (group 2 - 45 pts) after admission. Control group (37 healthy adults) had been collected before pandemic started. Standard coagulation tests, aggregometry, thrombodynamics and fibrinolysis results were compared between groups. Result(s): D-dimer was significantly higher, and was APPT was significantly lower in group 2 compared to group 1, while fibrinogen, prothrombin levels didn't differ. Platelet aggregation induced by ASA, ADP, TRAP, spontaneous aggregation didn't differ significantly between groups. Thrombodynamics revealed hypocoagulation in both group 1 and group 2 compared to control: V, mum/min 27,3 (Interquartile range (IQR) 26,3;29,4) and 28,3 (IQR 26,5;30,1) vs. 32,6 (IQR 30,4;35,9) respectively;all p < 0,001. Clot size and density in both group 1 and group 2 were significantly lower than in control group. Fibrinolysis appeared to be enhanced in x2 compared to control and group 1. Lysis progression, %/min was higher: 3,5 (2,5;4,8) vs. 2,4 (1,6;3,5) and 2,6 (2,2;3,4) respectively, all p < 0,05. Lysis onset time in both group 1 and group 2 was significantly shorter compared to control. Conclusion(s): We revealed normalization of parameters of clot formation process in 2-6 months after COVID-19, while fibrinolysis remained still enhanced. Further study is required to investigate the clinical significance of these changes.Copyright © Creative Cardiology 2021.

COVID-19-Related Spontaneous Aortic Arch Thrombus With Delayed Embolization.

Presentation of a 62-year-old man with baseline chronic obstructive pulmonary disease admitted to the hospital with dyspnea and newly diagnosed COVID-19 infection. CT scan of the chest was obtained to rule out pulmonary embolism. This revealed a mural thrombus of the inner curvature of the aortic arch with a floating component. Therapeutic full dose anticoagulation was initiated in combination with close clinical observation and treatment for modest hypoxia. He did well for 1 month and then returned with ischemic rest pain of the right foot. Angiography revealed thrombosis of all 3 tibial arteries in the right leg. Percutaneous mechanical thrombectomy with tissue plasminogen activator injection and angioplasty was performed with success in 1 tibial artery to achieve in line flow to the foot. After continued anticoagulation, the remainder of the tibial arteries autolysed and the aortic thrombus was noted to be resolved 4 months later. A brief pathophysiology discussion is included.

Association between echocardiographic features and inflammatory biomarkers with clinical outcomes in COVID-19 patients in Saudi Arabia.

Background: Respiratory infections are one of the most common comorbidities identified in hospitalized patients. The coronavirus disease 2019 (COVID-19) pandemic greatly impacted healthcare systems, including acute cardiac services. Aim: This study aimed to describe the echocardiographic findings of patients with COVID-19 infections and their correlations with inflammatory biomarkers, disease severity, and clinical outcomes. Methods: This observational study was conducted between June 2021 and July 2022. The analysis included all patients diagnosed with COVID-19 who had transthoracic echocardiographic (TTE) scans within 72 h of admission. Results: The enrolled patients had a mean age of 55.6 ± 14.7 years, and 66.1% were male. Of the 490 enrolled patients, 203 (41.4%) were admitted to the intensive care unit (ICU). Pre-ICU TTE findings showed significantly higher incidence right ventricular dysfunction (28 [13.8%] vs. 23 [8.0%]; P = 0.04) and left ventricular (LV) regional wall motion abnormalities (55 [27.1%] vs. 29 [10.1%]; p < 0.001) in ICU patients compared to non-ICU patients. In-hospital mortality was 11 (2.2%), all deaths of ICU patients. The most sensitive predictors of ICU admission (p < 0.05): cardiac troponin I level (area under the curve [AUC] = 0.733), followed by hs-CRP (AUC = 0.620), creatine kinase-MB (AUC = 0.617), D-dimer (AUC = 0.599), and lactate dehydrogenase (AUC = 0.567). Binary logistic regression showed that reduced LV ejection fraction (LVEF), elevated pulmonary artery systolic pressure, and dilated right ventricle were echocardiographic predictors of poor outcomes (p < 0.05). Conclusion: Echocardiography is a valuable tool in assessing admitted patients with COVID-19. Lower LVEF, pulmonary hypertension, higher D-dimer, C-reactive protein, and B-type natriuretic peptide levels were predictors of poor outcomes.

Catheter-Related Venous Thrombosis in Patients with Systemic Sclerosis: A Case Series

Background/Aims Systemic sclerosis (SSc) is characterised by endothelial dysfunction and vasculopathy, which may lead to venous thrombosis. Here, we report four cases of extensive venous thrombosis of the upper limbs and right atrium associated with implantable venous access devices (port-a-cath) in patients with a diagnosis of SSc, who presented to our specialist centre between 2018 and 2022. Methods We retrospectively reviewed four patients with SSc and port-a-cathassociated thrombosis who presented to the Department of Rheumatology, Royal Free Hospital NHS Trust between 2018 and 2022. All patients are diagnosed with systemic sclerosis according to the 2013 ACR/EULAR classification criteria. Results Three patients were diagnosed with a port-a-cath-associated thrombosis in 2022, and one in 2018. Two patients had limited cutaneous SSc with positive anti-centromere antibodies, and 2 had diffuse subset with anti-U3RNP antibodies. All patients had a right-sided port-a-cath that had been in-situ for at least 3 years. Two patients were diagnosed with right atrium thrombus (measuring 2.2 and 3cm respectively), one patient with an internal jugular vein and right subclavian thrombosis, and one with a left subclavian thrombosis. None had a history of previous thromboembolic event. A full thrombophilia screen was negative in 2 patients, and is pending in the others. Of note, 2 patients had COVID-19 infection within the 3 months prior the thrombotic event. 1 patient had tocilizumab administered through the line, 1 rituximab and IVIG, the other 2 had prostanoids only. Conclusion We described four recent cases of port-a-cath-associated thrombosis of the upper limbs and right atrium in SSc patients with no previous history of thrombosis. This highlights the increased risk of thrombosis related to long term indwelling catheters in SSc and demonstrates the potential interplay between covid microvasculopathy and the associated thrombotic risks reported with both ACA and antiU3RNP antibodies in SSc. We note that from previous reports the relative lower risk of adverse outcomes in SSc patient receiving parenteral nutrition. Further research into frequency of port-a-cath-related thrombosis in SSc patients is warranted, especially with use of prostanoids, and adequate screening and non-invasive follow up might be needed to avoid life-threatening thromboembolic complications. (Table Presented).

COVID-19-Associated Coagulopathy: Ascending Aortic Thrombus.

The mechanism of arterial thrombosis in coronavirus disease 2019 (COVID-19) is not completely understood and is attributed to the complex interactions of endothelial injury, platelet hyperactivation, and activated pro-inflammatory cytokines. Management strategies may include a combination of surgery and anticoagulation, or anticoagulation alone. A 56-year-old woman with recent COVID-19 infection presented with chest pain and dyspnea. Chest CT angiography (CTA) and aortic magnetic resonance imaging revealed an intraluminal thrombus in the mid ascending aorta. A multidisciplinary team decided on heparin infusion. She was transitioned to apixaban and a three-month interval outpatient CTA revealed complete resolution of the aortic thrombus.

Placental Thrombosis Resulting in Hypoxic Ischemic Encephalopathy in an Infant of a Mother with Covid-19

Case Report: Since the beginning of the Coronavirus Disease 2019 (COVID-19) pandemic, there has been much work to understand the negative effects of SARS-CoV-2 on tissues expressing the Angiotensin Converting Enzyme-2 (ACE2) receptor, including the placenta. However, there is limited information regarding placental pathology findings in mothers with COVID-19 and the effects of SARS-CoV-2 on the placenta. The available research reports effects on the fetus ranging from minimal to intrauterine fetal demise. Case Description: A 4680g baby boy was born at 38+1 weeks of gestation to 36y old G4P1021 female via repeat cesarian section. The pregnancy was complicated by advanced maternal age, chronic hypertension with superimposed pre-eclampsia with severe features, BMI of 80, and SARS-CoV-2 infection. The mother had mild COVID-19 symptoms and did not require hospitalization or oxygen support. Prenatal ultrasounds were limited due to body habitus. At the time of delivery, there was clear amniotic fluid. Upon delivery the infant was cyanotic and limp and was brought to the warmer immediately. Non-invasive positive pressure ventilation was initiated at 5 minutes of life with improvement in infant color and oxygen saturation. He was then admitted to the Neonatal Intensive Care Unit (NICU). APGARs were 2, 3, 5, and 7 at 1, 5, 10, and 15 minutes respectively. Cord gases showed severe metabolic acidosis. The patient was diagnosed with hypoxic-ischemic encephalopathy (HIE) and therapeutic hypothermia was initiated. Both the NICU and obstetric teams were unable to identify a clear perinatal cause of HIE in this patient. Later, the placenta pathology report revealed a large placenta for estimated gestational age corresponding to the 75th percentile, villous parenchyma with focal chorangiosis and thrombi, with unremarkable fetal membrane and three vessel umbilical cord. The cause of HIE was then thought to be due to the placental thrombi likely caused by SARS-CoV-2 infection. Discussion(s): Fetal vascular malperfusion and fetal vascular thrombus have been noted as a common finding in the placentas of pregnant women who test positive for SARS-CoV-2. There are various causes of HIE, from maternal, placental and fetal factors. This patient had no clinically evident hypoxic event, but information was limited due to the lack of monitoring of the fetus in utero. Given the mother's SARS-CoV-2 infection and the placental pathology findings, it is likely that the cause of this patient's HIE was related to the effects on the placenta from SARS-CoV-2. Conclusion(s): As more information comes to light about the effects of SARS-CoV-2 on the placenta, it is important to consider a maternal SARS-CoV-2 infection during pregnancy as a cause of HIE in a newborn.

Covid 19 presenting as stroke and MI

Its now a well known fact that covid 19 causes coagulopathy that has been associated with the inflammatory phase of coronavirus disease (COVID-19) and might be involved in this concurrency. Here we present a case of a 55y old female with no underlying comorbidity presented with the chief complaints of mild slurry speech and weakness over the right side of the body from last 8 h. Noncontrast brain computed tomography (CT) scan showed early signs of ischemia in left middle cerebral artery (MCA) territory, and a CT angiogram demonstrated a carotid atheromatous plaque with a superficial thrombus causing 40% stenosis in the left proximal internal carotid artery (ICA), however no intracranial artery occlusion was found. On ecg patient had ST segment depression in and depression in v5 and v6 leads with transthoracic echocardiogram showed lateral wall hypokinesia of the left ventricle, with qualitative troponin-T positive. There were no respiratory or other symptoms compatible with COVID-19 infection or chest pain. Chest CT ruled out inflammatory/infectious signs in the lung parenchyma, and Rapid antigen testing for covid 19 was negative on admission however RTPCR for SARS-CoV-2 was positive. Patient was initially loaded with dual anti platelets and lmw heparin and was subsequently managed with aspirin 150 mg, clopidogrel 75 mg and atorvastatin 40 mg with resolution of the chest pain and slurry speech.

The Coronavirus Double Threat: A Rare Presentation of Chest Pain in a Young Female.

Severe acute respiratory syndrome coronavirus 2 (SARS-COV 2) led to global coronavirus disease 2019 (COVID-19) pandemic. The virus affects the respiratory system predominantly and has resulted in multiorgan complications. Myocarditis, acute coronary syndrome (ACS), cardiogenic shock, and sudden cardiac death were common cardiac manifestations of COVID-19. Spontaneous coronary artery dissection (SCAD) is a rare form of coronary artery disease that is previously reported in patients with COVID-19. SCAD usually occurs in a middle-aged woman with few or without any cardiovascular risk factors. The gold standard for its diagnosis is coronary angiography. The SCAD treatment recommendations depend on the hemodynamic status: conservative therapy in hemodynamically stable SCAD patients and urgent revascularization in hemodynamically unstable SCAD patients. The exact pathophysiology of COVID-19 associated with SCAD is unknown. It is considered a combination of systemic inflammatory response and localized vascular inflammation. The case reported is of COVID-19-associated SCAD in a patient with no history of cardiovascular disease later complicated by the transient ischemic attack (TIA) and left ventricular (LV) thrombus.

Mortality And Morbidity Burden Of Covid-19 Infection In Left Ventricular Assist Device Patients

Introduction: COVID-19 pandemic has resulted in more than 6.1 million deaths and more than 480 million infections worldwide (1). Left ventricular assist device patients (LVAD) with their multiple co-morbidities are at high risk for morbidity and mortality from the COVID-19 infection. Few studies and case reports demonstrating the outcomes of COVID-19 infection in LVAD patients have been published, with the most recent study in 2021 (2-4). However, none of these studies spanned the entire stretch of the pandemic. Hypothesis: : COVID-19 infection would result in significant mortality and multi-system complications among patients with an LVAD. Method(s): IRB approval was obtained for our retrospective cohort study. 225 LVAD patients across two large centers in Texas, USA were screened for COVID-19 infection from December 1, 2019 to February 28, 2022. 68 events of COVID-19 infection were identified among 64 patients. One patient was excluded due to false positive test and 3 patients were infected twice and counted as separate events. Outcomes including mortality, respiratory failure, bleeding, and thromboembolic complications were assessed. Result(s): Baseline characteristics and results are summarized in Table 1. 51% of the patients needed hospitalization or emergency department visit for COVID infection. Five patients were intubated (7.4%). 6 patients developed chronic hypoxic respiratory failure requiring outpatient supplemental oxygen. 4 patients suffered from ventricular tachycardias while three other patients had Implantable cardioverter Defibrillator (ICD) shocks during COVID infection. 9 patients had epistaxis or gastrointestinal bleeding within 1 month of testing COVID positive. One HM2 patient had confirmed LVAD outflow cannula thrombus on CT heart and another patient with HeartWare had confirmed inflow cannula thrombus requiring emergent exchange to HM3 due to pump stoppage. Three patients suffered a stroke (5%). No events of pulmonary emboli or DVTs were noted. The mortality rate among this cohort was 14% (9 out of 64 patients). Four patients died during the same hospitalization. 33% had HM2 and 67% had HM3 LVADs, making a mortality rate of 37% (3 out of 8) for HM2 patients and 9% for HM3 (6 out of 55). 88% were males, 56% were African Americans, 67% had NICM, and 78% had at least moderate RV dysfunction at baseline. Conclusion(s): COVID-19 infection resulted in significant mortality and complications including stroke, pump thrombus, arrhythmias, respiratory failure, and bleeding events among LVAD patients.Copyright © 2022

Right atrial thrombus in a patient after COVID-19 pneumonia

Background: Significant coagulopathy and hyperinflamation are found in patients with coronavirus disease 2019 (COVID-19). Case report: 44-year-old male patient was admitted to the Infective Clinic with a severe form of pneumonia COVID-19.The disease is complicated, with sub-segmental embolization of the lungs and pneumothorax, which are confirmed with laboratory and computed tomography (CT) lung with angiography. On the third day of hospitalization, an echocardiogram is performed, which shows global hypocontractility of the left ventricular walls with a reduced ejection fraction EF 45%. The right ventricle was borderline. After the applied therapy, the patient's condition improves and he is discharged home with anticoagulant therapy. An echocardiography (Figure 1) performed as part of a cardiology examination one months after discharge from the hospital diagnosed a mass in the right atrium (35x27mm), which could correspond to a thrombus. Calcifications were visualized in the mass. The patient is readmitted to the Cardiology Clinic and intravenous heparin is indicated. Perform transesophageal echocardiography (Figure 2) and confirm the presence of a mass consistent with thrombus. Cardiac CT (Figure 3) shows mass in right atrium extending into the inferior vena cava, and CT of the abdomen shows thrombosis of the inferior vena cava. Cardiac magnetic resonance (Figure 4) showed a mass in the right atrium, which, corresponds to a thrombus adherent to the interatrial septum. After application of contrast, focal zones of higher intensity are visualized, zones of fibrosis on interventricular septum, anterior l and inferior and lateral wall of subepicardial and intramyocardial localization, which correspond to the sequelae of the inflammatory process, with ejection fraction 45%. The right ventricle has normal dimensions. After unsuccessful therapy with unfractionated heparin, the thrombus was successfully surgically extracted. Conclusions: Cardiac imaging modalities, including transthoracic or transesophageal echocardiography, cardiac magnetic resonance, cardiac computed tomography, and 18Ffluorodeoxyglucose positron emission tomography have a complementary and reinforcing role for the evaluation of cardiac masses. [ FROM AUTHOR] Copyright of Cardiologia Croatica is the property of Croatian Cardiac Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

Comparison of thrombus burden in patients with COVID-19 presenting with ST-segment elevation myocardial infarction across the three waves of outbreak in the United Kingdom

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(s): 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. Method(s): 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. Result(s): 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. Conclusion(s): 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.

Successful Treatment of Subclavian Artery Thrombosis by Catheter-Based Thrombus Aspiration and Thrombolytic Therapy: A Case Report

Clinical Information Patient Initials or Identifier Number: BP4****/22 Relevant Clinical History and Physical Exam: A 55 Y / Female C/C : Pain, numbness, cold sensation & weakness of left upper limb for 2 hours. Risk Factor : Hypertension, diabetes mellitus O/E : Pale, cold and absent of radial, ulnar, brachial pulse of left upper limb. Muscle power 3/5 left side. So2 86%, BP undetectable. Right upper limb were normal. BP 160/90 mm of hg, pules : 112 b/min, RR : 26/min. Body Temperature 37.5 C [Formula presented] [Formula presented] Relevant Test Results Prior to Catheterization: CBC : WBC 7450, HB % 10.8 g/dl, ESR 20mm in 1st hour, Platelets : 262000, SARS Cov2 Antigen : Negative PT 14.3 sec, INR : 1.07 APTT : 32.4 sec. blood group: O positive Serum Creatinine : 1.1 mg/dl Plasma glucose 9.7 mmmol/l HIV Ab : Negative HBs Ag : Negative Anti-HCV : Negative Urine R/E : Normal lipid profile : Cholesterol 280mg/dl Vascular duplex ultrasound of left upper limb : A dilated echogenic thrombus had blocked the left subclaviav artery lumen. Relevant Catheterization Findings: Conventional angiography with the lowest amount of contrast agent through the right femoral artery, revealed that left subclavian artery thrombosis with total occlusion distal to Left internal mammary artery. [Formula presented] [Formula presented] [Formula presented] Interventional Management Procedural Step: A5Fr MPA catheter with side holes was negotiated through a right femoral sheath and was placed in the left subclavian artery. Initially thrombus aspiration was done with Eliminate aspiration catheter (TERUMO) with no success. Then suction was done with the MPA catheter itself with partial removal of thrombus. Then a 5Fr Pigtail catheter was placed inside the thrombus and kept in situ. For residual thrombus 250,000u of Inj. Streptokinase as a thrombolytic drug was given through the Pigtail catheter as bolus over 30 min. The maintenance dose 100,000 u per hour was given over 24 hours through the Pigtail catheter via infusion pump. After 24 hours of thrombolytic therapy, her pain was reduced, the left hand became slightly warm, and distal pulses were feebly palpable. Moreover, the skin colour returned to near normal with improvement of pallor. Bleeding was well controlled at the catheter site. Doppler sounds revealed partial improvement of arterial flow. After evaluation of partial improvement, a low dose 1000 iu per hour of heparin (UFH)was infused intravenously for 24 hours. After 48 hours, repeat angiography via the inserted catheter at the site did not reveal any atherosclerotic plaque and confirm the thrombosis-dissolution. The latter practice demonstrated a good blood flowto the left upper distal limb leaving a little thrombus in the superficial palmer arch. [Formula presented] [Formula presented] [Formula presented] Conclusion(s): Catheter-based thrombus aspiration and thrombolytic therapy is primarily reserved for patients with acute viable limb ischemia. As observed in the presented case, thrombus aspiration and thrombolytic therapy is recommended to be considered as an alternative therapeutic method for patients with arterial thrombosis due to the rapid response, shorter treatment time and lower cost, compared to common and sometimes unsuccessful therapies.Copyright © 2023

Optical Coherence Tomography Guided Percutaneous Coronary Intervention of Spontaneous Recanalized Coronary Thrombus

Clinical Information Patient Initials or Identifier Number: 56 years old woman Relevant Clinical History and Physical Exam: A 56-years-old woman with underlying history of hyperlipidemia without medical treatment. She experienced effort precordial tightness and shortness of breath for 8 months after COVID-19 vaccination. She received exercise TI 201 myocardial perfusion scan showed myocardial ischemia. EKG found old anterior wall myocardial infarction. Echocardiogram showed left ventricle anterior wall hypokinesia, LVEF 38%. [Formula presented] Relevant Test Results Prior to Catheterization: Coronary angiogram found left anterior descending artery from proximal to middle 70~80% long diffuse stenosis with spontaneous recanalized coronary thrombus. Also left anterior descending artery diagonal 2 branch bifurcation was 70% stenosis with spontaneous recanalized coronary thrombus (Medina 1.1.1) [Formula presented] [Formula presented] Relevant Catheterization Findings: Coronary angiogram found left coronary artery middle and diagonal branch braided apperance. OCT found recanalized thrombi, high backscattered septa that divided the lumen into multiple small cavities, created "lotus root" appearance. [Formula presented] [Formula presented] Interventional Management Procedural Step: Left main coronary artery was engaged with EBU3.5/7F guiding catheter. We advanced Runthrough to LAD-D and second wire Sion to LAD-DB2 but can't advance. Then we used with Sasuke double lumen catheter and successful advance Pilot 50 to LAD-DB2 distal. OCT found multiple channels with LAD-D and DB2 branch wires are at different channels, so we used cutting balloon 2.5 x 10mm as unconventional method. OCT was rechecked again and successfully destroyed to multiple channel of SRCT between LAD and Diagonal 2 branch. Long diffuse dissection found after POBA so we deployed to LAD-DB2 branch with DES Synergy 2.5 x 16mm and advanced LAD-M bifurcation to Pantera LEO 3.0 x 20mm and done Mini-Crush technique. Deployed for main vessel LAD-P to M long diffuse lesion with DES Xience 2.75 x 48mm at 14atm. Then we rewire Fielder XTR to DB2 branch with the support of Sasuke but difficult to deliver to Diagonal 2 branch. POT with Pantera LEO 3.0 x 20mm to LAD stent proximal site. Then successfully advance Fielder XTR to DB2 branch. Final kissing balloon technique with Pantera 2.75 x 12mm to LAD main vessel and MINI TREK 1.5 x15mm to LAD-DB2. [Formula presented] [Formula presented] [Formula presented] Conclusion(s): This is a case of SRCT (Spontaneous Recannalized Coronary Thrombus) that was confirmed with OCT. For secure side branch patency, main trunk & side branch wire must be in same channel. Due to relatively unstable hemodynamic, we chose to use unconventional method with 2.5 x 10mm Wolverine cutting balloon. Relatively large side-branch diagonal branch, possible dissection at ostial diagonal branch, we chose upfront 2 stents, bifurcation stenting technique we used Mini-crush stenting. Some difficult when rewire to side branch and initial POT to main branch stent proximal and then successfully delivered. If without guidewire recross, unrescuable side-branch occlusion can be occurred.Copyright © 2023

Occlusive Explosion

Clinical Information Patient Initials or Identifier Number: A Relevant Clinical History and Physical Exam: 47yr old man, suffered a blast injury at the workplace after an O2 tank exploded while he was transferring liquid gas into a tank for welding purposes. The impact has caused him to temporary loss of consciousness. Upon awakening, he had severe chest pain associated with shortness of breath. On examination, superficial partial thickness injury on the chest wall, and lungs: reduced breath sound bi-basally, no murmur heard. BP:106/77mmHg, HR:100/min, SPO2 100% on HFM 15L/min. [Formula presented] [Formula presented] [Formula presented] Relevant Test Results Prior to Catheterization: Serial ECGs were done and showed dynamic changes in the anterior leads Bedside echo before invasive coronary angiograms shows mild LVSD, normal valves, and no pericardial effusion [Formula presented] [Formula presented] Relevant Catheterization Findings: Right radial approach 6F system Opitorque catheter for diagnostic angiogram LMS: smooth LAD: ATO mid LAD, DG1 prox ATO LCx: smooth RCA: smooth Impression: ATO to LAD and Diagonal 1 ( Dual ATO) [Formula presented] [Formula presented] [Formula presented] Interventional Management Procedural Step: Right radial coronary angiogram via 6F system EBU 3.0 engaged with good support Sion blue wired into LAD, export catheter delivered, and aspirated red thrombus Pre-dilated with Sapphire 3 SC 2.5x15mm @ 6-10ATM Flow established in LAD, however, decided to interrogate DG1 as it shows ATO BMW wired into the DG1 and pre-dilated with Sapphire 3 SC 2.0x15mm Noted nonflow limiting dissection and decided to stent DG1 with 2.25x34mm@12ATM, dissection sealed and TIMI III flow established Stented mid LAD with 2.5x30mm @12ATM just before LAD/DG1 bifurcation, then stented proximal LAD with 2.5x 26mm@ 12ATM. Post-dilated LAD with 2.75x15mm@ 14-20ATM TIMI II-III flow IV Tirofiban has been given a loading dose due to a high thrombus burden and sluggish flow [Formula presented] [Formula presented] [Formula presented] Conclusion(s): Myocardial infarction is a rare complication of blunt chest trauma. This case demonstrates how blast shock waves result in the dissection of the coronary vessel leading to total occlusion of the two vessels. It also promotes red thrombus within the coronary vessels. Percutaneous coronary intervention is the most suitable way to treat this condition. Intravascular imaging such as IVUS or OCT would be beneficial to demonstrate the physiology behind this MI and would also be helpful in planning and optimizing the lesions. Unfortunately, intravascular imaging was not used for this patient to reduce procedural time as he was treated during the height of the COVID pandemic.Copyright © 2023

Specific characteristics of STEMI in COVID-19 patients and their practical implications: A systematic review

Introduction: STEMI is one of the cardiac emergencies whose management has been mostly challenged by the COVID-19 pandemic. Patients presenting with the "lethal combo" of STEMI and concomitant SARS-CoV- 2 infection have faced dramatic issues related to need for self-isolation, systemic inflammation with multi-organ disease, and difficulties to obtain timely diagnosis and treatment. Method(s):We performed a systematic search of three electronic databases from February 1st 2020 to January 31st 2022. We included all studies reporting crude rates of in-hospital outcomes of STEMI patients with concomitant COVID-19. Result(s): A total of 9 observational studies were identified, mainly conducted during the first wave of the pandemic. STEMI patients with COVID -19 were more likely Afro-American and displayed higher rates of hypertension and diabetes with lower smoking prevalence. Associated comorbidities, including coronary artery disease, prior stroke and chronic kidney disease were also more common in those with SARS-CoV-2 infection. At coronary angiography, a higher thrombus burden in COVID-19 positive STEMI patients was highlighted, with up to 10-fold higher rates of stent thrombosis and greater need for glycoprotein IIb/IIa inhibitors and aspiration thrombectomy;this was not always associated with prolonged times from symptom onset to hospital admission and door-to-balloon. COVID-19 positive STEMI patients were less likely to receive coronary angiography and primary PCI, and more likely to be treated with fibrinolytics only. At the same time, patients with Covid-19 were more prone to present MINOCA. In-hospital mortality ranged from 15% to 40%, with consistent variability across different studies and subjects who tested positive for SARS-CoV- 2 did also present higher rates of cardiogenic shock, cardiac arrest, prolonged ICU stay, mechanical ventilation, major bleeding, and stroke. Conclusion(s): The coexistence of STEMI and COVID-19 was associated with increased in-hospital mortality and poor short-term prognosis. This was not entirely attributable to logistic issues determining delayed coronary revascularization, since patients' specific clinical and angiographic characteristics, including higher burden of cardiovascular risk factors and greater coronary thrombogenicity might have substantially contributed to this trend. (Figure Presented).

Histologic Assessment of Thromboemboli Due to Plaque Rupture, Plaque Erosion, or COVID-19 Microthrombi.

Plaque rupture, plaque erosion, and COVID-19 infection can cause acute coronary syndromes (ACS). We illustrate case examples demonstrating the distinctive and characteristic pathologic findings underlying each of these various causes of acute myocardial infarction. A deeper understanding of the pathophysiology of ACS is necessary for the development of newer agents and techniques to improve outcomes after ACS. (Level of Difficulty: Advanced.).