Predictive Role of Blood Cellular Indices and Their Relationship with Endogenous Glycosaminoglycans as Determinants of Inflammatory Biomarkers in Pulmonary Embolism.

INTRODUCTION: In this study, we profiled the levels of blood cellular indices, endogenous glycosaminoglycans (GAGs) and inflammatory biomarkers in a cohort comprised of pulmonary embolism (PE) patients, to determine their inter-relationships. Identification of this relationship may provide insight to the complex pathophysiology of PE and the predictive role of blood cellular indices in acute PE patients. MATERIALS AND METHODS: Plasma samples from PE patients and healthy controls were analyzed for thrombo-inflammatory biomarkers (IL-2, IL-4, IL-6, IL-8, IL-10, VEGF, IFN-É£, TNF-α, IL-1α, IL-1ß, MCP-1, EGF, D-dimer, CRP and MMP-9) using biochip array and ELISA methods. The endogenous GAG levels were quantified using a fluorescence quenching method. The data regarding the blood cellular indices were collected through the review of patient medical records and analyzed to demonstrate their relationship. RESULTS: The levels of inflammatory biomarkers and endogenous GAGs were elevated in acute PE patients compared to controls (P < .05). Most of the blood cellular indices have shown significant differences in acute PE patients compared to controls (P < .05). The levels of inflammatory biomarkers, endogenous GAGs and the blood cellular indices have shown significant associations in correlation and multivariable analysis. While NLR, PLR and SII were significantly predicting the 30-day mortality, PNR, ELR and EMR were not sufficient to predict 30-day mortality in acute PE. CONCLUSION: Our results show that the increased thrombo-inflammatory response is associated with the release of GAGs and the changes in blood cellular indices. The predictive role of the blood cellular indices for mortality is dependent on their relationship with the inflammatory response.

Neurological Complications of Pulmonary Embolism: a Literature Review.

PURPOSE OF REVIEW: The present review discusses in-depth about neurological complications following acute venous thromboembolism (VTE). RECENT FINDINGS: Intracranial hemorrhage, acute ischemic cerebrovascular events, and VTE in brain tumors are described as central nervous system (CNS) complications of PE, while peripheral neuropathy and neuropathic pain are reported as peripheral nervous system (PNS) sequelae of PE. Syncope and seizure are illustrated as atypical neurological presentations of PE. Mounting evidence suggests higher risk of venous thromboembolism (VTE) in patients with neurological diseases, but data on reverse, i.e., neurological sequelae following VTE, is underexplored. The present review is an attempt to explore some of the latter issues categorized into CNS, PNS, and atypical complications following VTE.

The Relevance of Anti-PF4 Antibody Isotypes and Endogenous Glycosaminoglycans and their Relationship with Inflammatory Biomarkers in Pulmonary Embolism Patients.

INTRODUCTION: Previous studies have shown that inflammation may contribute to the interplay of endogenous glycosaminoglycans (GAGs) and anti-PF4 antibodies. In this study, we quantified the levels of anti-PF4 antibody isotypes and endogenous GAGs together with inflammatory biomarkers in pulmonary embolism (PE) patients to determine whether there is a relationship in between. Identification of this relationship may provide insight to the complex pathophysiology of PE and HIT and may also be useful for development of potential prognostic, diagnostic and therapeutic interventions. MATERIALS AND METHODS: Plasma samples from PE patients (n: 210) were analyzed for anti-PF4 antibody isotypes and various thrombo-inflammatory cytokines utilizing commercially available biochip array and ELISA methods. The endogenous GAG levels in PE patients' plasma were quantified using a fluorescence quenching method. The collected data analyzed to demonstrate the relationship between various parameters. RESULTS: The endogenous GAG levels were increased in the PE group (P < .05). The levels of anti-PF4 antibody isotypes were higher in varying levels in comparison to the normal group (P < .05). Inflammatory cytokines have shown varying levels of increase with IL-6, IL-8 and IL-10 showing the most pronounced values. Mortality outcome was related to increased GAGs and some of the cytokines. CONCLUSION: In this study, we demonstrated increased levels of anti-PF4 antibody isotypes, endogenous GAGs, and inflammatory biomarkers in a large patient cohort in PE. The levels of the endogenous GAGs and inflammatory biomarkers were associated with PE severity and mortality. More studies are needed to understand this complex pathophysiology.

Acute submassive pulmonary embolism after SARS-CoV-2 infection: a case report of reinfection or prolonged hypercoagulable state.

BACKGROUND: Coronavirus disease 19 (COVID-19) reinfection has been a topic of discussion with data still emerging. Viral antibodies are known to develop upon initial infection; however, it is unclear the amount of protection this confers against reinfection. Additionally, COVID-19-associated coagulopathy (CAC) is a well-documented phenomenon; however, there are no high-quality studies to support the treatment of outpatients beyond standard indications of venous thromboembolism (VTE) prophylaxis. This case describes a patient with either COVID-19 reinfection or prolonged course of CAC resulting in pulmonary embolism (PE). CASE SUMMARY: A 40-year-old healthy man presented with fever and cough. He tested positive for COVID-19 and was sent home to self-quarantine. His symptoms resolved and repeat COVID-19 testing returned negative. Two months later, he developed dyspnoea on exertion and syncope. Computed tomography with PE protocol demonstrated acute bilateral PE, and repeat COVID-19 testing returned positive. He was escalated to catheter-directed thrombolysis, but prior to the procedure went into cardiopulmonary arrest. Cardiopulmonary resuscitation was initiated and full-dose systemic alteplase was administered. Cardiothoracic surgery was consulted for consideration of veno-arterial extracorporeal membrane oxygenation; however, return of spontaneous circulation was unable to be achieved. DISCUSSION: This case raises the question of COVID-19 reinfection and prolonged risk of VTE due to CAC. We believe the patient was reinfected with COVID-19 provoking his PE; however, a single COVID-19 infection causing a prolonged course of CAC is possible. Until better data exists, decisions regarding outpatient prophylaxis must be individualized to weigh the risks of bleeding against the risk of thrombosis.

Paradoxical Embolism Causing Myocardial Infarction in a COVID-19 Patient Presenting With Pulmonary Embolism.

The presence of myocardial injury in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection is common. The cardiac complications of SARS-CoV2 infection are varied and distinguishing between them can be complicated.  A 55-year-old man with recent diagnosis of SARS-CoV2 infection presented with chest pain, syncope, and was found to have saddle pulmonary embolism (PE). Marked elevation in cardiac enzymes prompted a coronary angiogram which was normal. Cardiac MRI revealed late gadolinium enhancement (LGE) in the anterolateral wall consistent with myocardial infarction (MI). He was diagnosed with paradoxical embolism causing MI. The differential for elevated cardiac enzymes is wide in patients with SARS-CoV2 infection. This case illustrates that sometimes multiple diagnoses exist, and that a high index of suspicion is required to continue work-up.

Difficulties of Managing Submassive and Massive Pulmonary Embolism in the Era of COVID-19.

Acute pulmonary embolism (PE) is a potentially life-threatening manifestation of venous thromboembolic disease. Severe acute respiratory syndrome-coronavirus-2, a novel coronavirus that causes coronavirus disease-2019 (COVID-19), has been associated with an increased risk of thrombosis. We describe the therapeutic challenges of 3 patients presenting with PE and suspected or confirmed COVID-19. (Level of Difficulty: Beginner.).