Mechanistic registry to study whether infection with Corona Virus Disease 2019 (COVID-19) accelerates atherosclerotic plaque progression

研究 2019 年冠状病毒病 (COVID-19) 感染是否加速动脉粥样硬化斑块进展的机制登记

• 批准号: 10482402
• 负责人: JAGAT NARULA
• 金额: $ 148.67万
• 依托单位: ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-02-01 至 2025-06-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10482402
• 关键词: 2019-nCoV; Acceleration; Acute; Anatomy; Angiography; Area; Arterial Fatty Streak; Atherosclerosis; Blood Vessels; COVID-19; COVID-19 mortality; COVID-19 patient; COVID-19 risk; COVID-19 treatment; Cardiac; Cardiology; Cause of Death; Cholesterol; Clinical; Coronary; Coronary Arteriosclerosis; Coronary artery; Data Collection; Deposition; Development; Diagnostic; Economics; Essential worker; Ethnic Origin; Event; Fatty acid glycerol esters; Growth; Immunology; Infection; Inflammation; Inflammatory; Inflammatory Response; Injury; Laboratories; Laboratory Markers; Link; Measurement; Measures; Methods; Multicenter Trials; Neighborhoods; New York City; Pathway interactions; Patients; Physicians; Population Density; Preventive; Preventive care; Process; Qualifying; Race; Registries; Reporting; Research Personnel; Residual state; Risk; Risk Assessment; Role; SARS-CoV-2 infection; SARS-CoV-2 infection history; Socioeconomic Factors; Stenosis; Testing; United States; Viral; Virus; Virus Diseases; X-Ray Computed Tomography; attenuation; coronary computed tomography angiography; coronavirus disease; cytokine; deprivation; ethnic diversity; experience; high risk; improved; indexing; inflammatory marker; inflammatory milieu; knowledge base; mortality; novel; participant enrollment; post SARS-CoV-2 infection; post-pandemic; promoter; psychosocial; racial diversity; remdesivir; socioeconomics; systemic inflammatory response; urban setting

Project Summary / Abstract The primary objective of the corona virus disease 2019 (COVID-19) (COVID-CT) registry is to determine if infection with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus which causes COVID-19, results in marked progression of coronary atherosclerotic plaque in patients with previously defined anatomic coronary artery disease (CAD). COVID-19 induces a pro-inflammatory cytokine release and pro- thrombotic processes that we hypothesize will accelerate atherosclerotic plaque progression. Coronary computed tomographic angiography (CCTA) is a robust noninvasive method uniquely capable of measuring angiographic stenosis and quantifying and characterizing atherosclerotic plaque. Our group has extensive experience in large multicenter trials and registries using CCTA to identify key atherosclerotic plaque features associated with progression and major CAD events. Moreover, we propose use of a novel CT marker of coronary artery inflammation - the perivascular fat attenuation index (FAI) – a marker highly predictive of acute CAD events and to assess serial changes in coronary inflammation. COVID-19 is rapidly becoming a leading cause of death with substantial evidence that pre-existing CAD increases risk of serious illness and mortality from COVID-19. By enrolling patients with high risk, atherosclerotic plaque, findings from the COVID-CT registry will inform this link between the inflammatory response sustained during COVID-19 to accelerated atherosclerotic plaque progression. If our hypotheses are confirmed, then clinicians and patients will have clear information that viral infections, such as SARS-CoV-2, alter the inflammatory milieu and accelerate progression of atherosclerosis. Importantly, a connection between COVID- 19 and CAD will broadly impact preventive risk assessment for the ~7 million patients infected with SARS-CoV- 2 and millions more yet to be tested in the United States. To date, evidence is lacking as to whether the COVID-19 results in marked atherosclerotic plaque progression among racially and ethnically diverse patients with CCTA-defined CAD who reside across a socioeconomically- diverse, urban setting. The present proposal constitutes a comprehensive approach assessing the clinical importance of atherosclerotic plaque progression following COVID-19. Currently, the implications of epicardial coronary injury following SARS-CoV-2 infection is unknown. Yet, the inflammatory pathway of atherosclerotic plaque progression is well studied and, as such, our hypotheses are supported by this knowledge base. The proposed COVID-19 registry is poised to provide an improved mechanistic understanding of the role of viral infection on alterations in atherosclerotic plaque.

项目概要/摘要 2019 年冠状病毒病 (COVID-19) (COVID-CT) 登记的主要目标是确定是否 感染严重急性呼吸综合征冠状病毒-2 (SARS-CoV-2)，该病毒会导致 COVID-19导致先前定义的患者冠状动脉粥样硬化斑块显着进展 解剖学冠状动脉疾病（CAD）。 COVID-19 诱导促炎细胞因子释放并促 我们假设血栓形成过程将加速动脉粥样硬化斑块的进展。冠状动脉 计算机断层扫描血管造影 (CCTA) 是一种强大的无创方法，能够独特地测量 血管造影狭窄以及量化和表征动脉粥样硬化斑块。我们集团拥有广泛的 使用 CCTA 识别关键动脉粥样硬化斑块特征的大型多中心试验和注册经验 与进展和主要 CAD 事件相关。此外，我们建议使用一种新型冠状动脉 CT 标记物 动脉炎症 - 血管周围脂肪衰减指数 (FAI) - 高度预测急性 CAD 事件的标志物 并评估冠状动脉炎症的连续变化。 COVID-19 正在迅速成为主要死亡原因，有大量证据表明先前存在 CAD 增加因 COVID-19 罹患严重疾病和死亡的风险。通过招募高风险、动脉粥样硬化患者 斑块，COVID-CT 登记的结果将告知持续的炎症反应之间的联系 在COVID-19期间加速动脉粥样硬化斑块的进展。如果我们的假设得到证实，那么 临床医生和患者将获得明确的信息，即 SARS-CoV-2 等病毒感染会改变 炎症环境并加速动脉粥样硬化的进展。重要的是，新冠病毒之间存在联系 19 和 CAD 将广泛影响约 700 万感染 SARS-CoV 的患者的预防风险评估 2 以及还有数百万人有待在美国进行测试。 迄今为止，尚缺乏证据表明 COVID-19 是否会导致明显的动脉粥样硬化斑块进展 患有 CCTA 定义的 CAD 的不同种族和族裔患者，他们居住在不同的社会经济地位 多样化的城市环境。本提案构成了评估临床效果的综合方法 COVID-19 后动脉粥样硬化斑块进展的重要性。目前，心外膜的影响 SARS-CoV-2 感染后的冠状动脉损伤尚不清楚。然而，动脉粥样硬化的炎症途径 斑块进展已得到充分研究，因此，我们的假设得到了该知识库的支持。这 拟议的 COVID-19 注册表旨在提供对病毒作用的更好的机制理解 感染对动脉粥样硬化斑块变化的影响。