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1.
J Vasc Surg Venous Lymphat Disord ; 2022 Jan 25.
Article in English | MEDLINE | ID: covidwho-1650575

ABSTRACT

OBJECTIVE: To investigate the radiographic resolution of acute pulmonary embolism (PE) using contrast-enhanced computed tomography (CECT) examinations in patients diagnosed with acute PE while hospitalized with coronavirus disease 2019 (COVID-19) and to understand the mid-term and long-term implications of anticoagulation therapy. METHODS: We identified patients with acute PE per CECT and at least one follow-up CECT from March 11, 2020, to May 27, 2021, using a prospective registry of all hospitalized patients with COVID-19 infection receiving care within a multicenter Health System. Initial and follow-up CECT examinations were reviewed independently by two radiologists to evaluate for PE resolution. The Modified Miller Score was used to assess for thrombus burden at diagnosis and on follow-up. RESULTS: Of the 6070 hospitalized patients with COVID-19 infection, 5.7% (348/6070) were diagnosed with acute PE and 13.5% (47/348) had a follow-up CECT examination. The mean ± standard deviation time to follow-up imaging was 44 ± 48 days (range, 3-161 days). Of 47 patients, 47 (72.3%) had radiographic resolution of PE, with a mean time to follow-up of 48 ± 43 days (range, 6-239 days). All patients received anticoagulation monotherapy for a mean of 149 ± 95 days and this included apixaban (63.8%), warfarin (12.8%), and rivaroxaban (8.5%), among others. The mean Modified Miller Score at PE diagnosis and follow-up was 4.8 ± 4.2 (range, 1-14) and 1.4 ± 3.3 (range, 0-16; P < .0001), respectively. Nine patients (19%) died at a mean of 13 ± 8 days after follow-up CECT (range, 1-27 days) and at a mean of 28 ± 16 days after admission (range, 11-68 days). Seen of the nine deaths (78%) deaths were associated with progression of COVID-19 pneumonia. CONCLUSIONS: Hospitalized patients with COVID-19 have a clinically apparent 5.7% rate of developing PE. In patients with follow-up imaging, 72.3% had radiographic thrombus resolution at a mean of 44 days while on anticoagulation. Prospective studies of the natural history of PEs with COVID-19 that include systematic follow-up imaging are warranted to help guide anticoagulation recommendations.

2.
Thromb Res ; 207: 150-157, 2021 Oct 07.
Article in English | MEDLINE | ID: covidwho-1458757

ABSTRACT

BACKGROUND: The reported incidence of venous thromboembolism (VTE) in COVID-19 patients varies widely depending on patient populations sampled and has been predominately studied in hospitalized patients. The goal of this study was to assess the evolving burden of COVID-19 and the timing of associated VTE events in a systems-wide cohort. METHODS: COVID-19 PCR positive hospitalized and non-hospitalized patients ≥18 years of age tested between 1/1/2020 through 12/31/2020 were retrospectively analyzed using electronic medical records from multiple states across the Mayo Clinic enterprise. Radiology reports within 90 days before and after confirmed COVID-19 diagnosis were examined for VTE outcomes using validated Natural Language Processing (NLP) algorithms. RESULTS: A 29-fold increased rate of VTE compared to the pre-COVID-19 period was noted during the first week following the first positive COVID-19 test (RR: 29.39; 95% CI 21.77-40.03). The rate of VTE steadily decreased and returned to baseline by the 6th week. Among 366 VTE events, most occurred during (n = 243, 66.3%) or after (n = 111, 30.3%) initial hospitalization. Only 11 VTE events were identified in patients who did not require hospitalization (3.0% of total VTE events). VTE and mortality increased with advancing age with a pronounced increased each decade in older patients. CONCLUSION: We observed a profoundly increased risk of VTE within the first week after positive testing for COVID-19 that returned to baseline levels after 6 weeks. VTE events occurred almost exclusively in patients who were hospitalized, with the majority of VTE events identified within the first days of hospitalization.

3.
J Am Coll Cardiol ; 76(18): 2073-2075, 2020 11 03.
Article in English | MEDLINE | ID: covidwho-1382457
4.
Mayo Clin Proc Innov Qual Outcomes ; 5(2): 388-402, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1361507

ABSTRACT

OBJECTIVE: To evaluate differences in thromboinflammatory biomarkers between patients with severe coronavirus disease 2019 (COVID-19) infection/death and mild infection. PATIENTS AND METHODS: MEDLINE, Cochrane Central Register of Controlled Trials, EMBASE, EBSCO, Web of Science, and CINAHL databases were searched for studies comparing thromboinflammatory biomarkers in COVID-19 among patients with severe COVID-19 disease or death (severe/nonsurvivors) and those with nonsevere disease or survivors (nonsevere/survivors) from January 1, 2020, through July 11, 2020. Inclusion criteria were (1) hospitalized patients 18 years or older comparing severe/nonsurvivors vs nonsevere/survivors and (2) biomarkers of inflammation and/or thrombosis. A random-effects model was used to estimate the weighted mean difference (WMD) between the 2 groups of COVID-19 severity. RESULTS: We included 75 studies with 17,052 patients. The severe/nonsurvivor group was older, had a greater proportion of men, and had a higher prevalence of hypertension, diabetes, cardiac or cerebrovascular disease, chronic kidney disease, malignancy, and chronic obstructive pulmonary disease. Thromboinflammatory biomarkers were significantly higher in patients with severe disease, including D-dimer (WMD, 0.60; 95% CI, 0.49 to 0.71; I 2 =83.85%), fibrinogen (WMD, 0.42; 95% CI, 0.18 to 0.67; I 2 =61.88%; P<.001), C-reactive protein (CRP) (WMD, 35.74; 95% CI, 30.16 to 41.31; I 2 =85.27%), high-sensitivity CRP (WMD, 62.68; 95% CI, 45.27 to 80.09; I 2 =0%), interleukin 6 (WMD, 22.81; 95% CI, 17.90 to 27.72; I 2 =90.42%), and ferritin (WMD, 506.15; 95% CI, 356.24 to 656.06; I 2 =52.02%). Moderate to significant heterogeneity was observed for all parameters (I 2 > 25%). Subanalysis based on disease severity, mortality, and geographic region of the studies revealed similar inferences. CONCLUSION: Thromboinflammatory biomarkers (D-dimer, fibrinogen, CRP, high-sensitivity CRP, ferritin, and interleukin 6) and marker of end-organ damage (high-sensitivity troponin I) are associated with increased severity and mortality in COVID-19 infection.

5.
Mayo Clin Proc ; 96(7): 1718-1726, 2021 07.
Article in English | MEDLINE | ID: covidwho-1213418

ABSTRACT

OBJECTIVE: To determine the difference in the rate of thromboembolic complications between hospitalized coronavirus disease 2019 (COVID-19)-positive compared with COVID-19-negative patients. PATIENTS AND METHODS: Adult patients hospitalized from January 1, 2020, through May 8, 2020, who had COVID-19 testing by polymerase chain reaction assay were identified through electronic health records across multiple hospitals in the Mayo Clinic enterprise. Thrombotic outcomes (venous and arterial) were identified from the hospital problem list. RESULTS: We identified 3790 hospitalized patients with COVID-19 testing across 19 hospitals, 102 of whom had positive test results. The median age was lower in the COVID-positive patients (62 vs 67 years; P=.03). The median duration of hospitalization was longer in COVID-positive patients (8.5 vs 4 days; P<.001) and more required intensive care unit care (56.9% [58 of 102] vs 26.8% [987 of 3688]; P<.001). Comorbidities, including atrial fibrillation/flutter, heart failure, chronic kidney disease, and malignancy, were observed less frequently with COVID-positive admissions. Any venous thromboembolism was identified in 2.9% of COVID-positive patients (3 of 102) and 4.6% of COVID-negative patients (168 of 3688). The frequency of venous and arterial events was not different between the groups. The unadjusted odds ratio (OR) for COVID-positive-patients for any venous thromboembolism was 0.63 (95% CI, 0.19 to 2.02). A multivariable logistic regression model evaluated death within 30 days of hospital discharge; neither COVID positivity (adjusted OR, 1.12; 95% CI, 0.54 to 2.34) nor thromboembolism (adjusted OR, 0.90; 95% CI, 0.60 to 1.32) was associated with death. CONCLUSION: Early experience in patients with COVID-19 across multiple academic and regional hospitals representing different US regions demonstrates a lower than previously reported incidence of thrombotic events. This incidence was not higher than a contemporary COVID-negative hospitalized comparator.


Subject(s)
COVID-19/complications , Hospitalization/statistics & numerical data , Intensive Care Units/statistics & numerical data , SARS-CoV-2 , Thrombosis/etiology , Aged , COVID-19/epidemiology , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Pandemics , Retrospective Studies , Thrombosis/epidemiology , United States/epidemiology
6.
Mayo Clin Proc ; 96(2): 274-276, 2021 02.
Article in English | MEDLINE | ID: covidwho-1065452
7.
J Thromb Thrombolysis ; 51(4): 985-988, 2021 May.
Article in English | MEDLINE | ID: covidwho-1053058

ABSTRACT

OBJECTIVES: Infection with the SARS-COV2 virus (COVID-19) may be complicated by thrombotic diathesis. This complication often involves the pulmonary microcirculation. While macrovascular thrombotic complications of the lung may include pulmonary artery embolism, pulmonary artery thrombus in situ has also been hypothesized. Pulmonary vein thrombosis has not been described in this context. METHODS/RESULTS: Herein, we provide a case of an otherwise healthy male who developed an ischemic stroke with left internal carotid thrombus. Further imaging revealed pulmonary emboli with propagation through the pulmonary veins into the left atrium. This left atrial thrombus provides a source of atypical "paradoxic arterial embolism". CONCLUSIONS: Thrombotic outcomes in the setting of severe COVID 19 pneumonia may include macrovascular venous thromboembolism, microvascular pulmonary vascular thrombosis and arterial thromboembolism. Pulmonary vein, herein described, provides further mechanistic pathway for potential arterial embolic phenomenon.


Subject(s)
COVID-19 , Carotid Artery Thrombosis , Ischemic Stroke , Pulmonary Embolism , Pulmonary Veno-Occlusive Disease , Brain/diagnostic imaging , COVID-19/blood , COVID-19/complications , COVID-19/physiopathology , Carotid Artery Thrombosis/complications , Carotid Artery Thrombosis/diagnosis , Diagnosis, Differential , Heart Atria/diagnostic imaging , Heart Atria/pathology , Hemiplegia/diagnosis , Hemiplegia/etiology , Humans , Ischemic Stroke/diagnosis , Ischemic Stroke/etiology , Ischemic Stroke/physiopathology , Lung/diagnostic imaging , Male , Middle Aged , Pulmonary Embolism/diagnostic imaging , Pulmonary Embolism/etiology , Pulmonary Veno-Occlusive Disease/complications , Pulmonary Veno-Occlusive Disease/diagnosis , Pulmonary Veno-Occlusive Disease/physiopathology , SARS-CoV-2/pathogenicity , Tomography, X-Ray Computed/methods
8.
Shock ; 55(6): 700-716, 2021 06 01.
Article in English | MEDLINE | ID: covidwho-998566

ABSTRACT

ABSTRACT: There is increasing evidence that novel coronavirus disease 2019 (COVID-19) leads to a significant coagulopathy, a phenomenon termed "COVID-19 associated coagulopathy." COVID-19 has been associated with increased rates of both venous and arterial thromboembolic events, a source of significant morbidity and mortality in this disease. Further evidence suggests a link between the inflammatory response and coagulopathy associated with COVID-19. This presents a unique set of challenges for diagnosis, prevention, and treatment of thrombotic complications. In this review, we summarize and discuss the current literature on laboratory coagulation disruptions associated with COVID-19 and the clinical effects of thromboembolic events including pulmonary embolism, deep vein thrombosis, peripheral arterial thrombosis, and acute ischemic stroke in COVID-19. Endothelial injury and augmented innate immune response are implicated in the development of diffuse macro- and microvascular thrombosis in COVID-19. The pathophysiology of COVID-19 associated coagulopathy is an important determinant of appropriate treatment and monitoring of these complications. We highlight the importance of diagnosis and management of dysregulated coagulation in COVID-19 to improve outcomes in COVID-19 patients with thromboembolic complications.


Subject(s)
Blood Coagulation Disorders , Blood Coagulation/immunology , COVID-19 , Immunity, Innate , SARS-CoV-2/immunology , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/immunology , Blood Coagulation Disorders/pathology , Blood Coagulation Disorders/therapy , COVID-19/complications , COVID-19/pathology , COVID-19/therapy , Humans , Ischemic Stroke/complications , Ischemic Stroke/metabolism , Ischemic Stroke/pathology , Pulmonary Embolism/etiology , Pulmonary Embolism/immunology , Pulmonary Embolism/pathology , Pulmonary Embolism/therapy , Thrombosis/etiology , Thrombosis/immunology , Thrombosis/pathology , Thrombosis/therapy
9.
Mayo Clin Proc ; 95(11): 2467-2486, 2020 11.
Article in English | MEDLINE | ID: covidwho-735313

ABSTRACT

A higher risk of thrombosis has been described as a prominent feature of coronavirus disease 2019 (COVID-19). This systematic review synthesizes current data on thrombosis risk, prognostic implications, and anticoagulation effects in COVID-19. We included 37 studies from 4070 unique citations. Meta-analysis was performed when feasible. Coagulopathy and thrombotic events were frequent among patients with COVID-19 and further increased in those with more severe forms of the disease. We also present guidance on the prevention and management of thrombosis from a multidisciplinary panel of specialists from Mayo Clinic. The current certainty of evidence is generally very low and continues to evolve.


Subject(s)
Anticoagulants/therapeutic use , COVID-19/drug therapy , Practice Guidelines as Topic , SARS-CoV-2 , Thrombosis/prevention & control , COVID-19/complications , COVID-19/epidemiology , Humans , Minnesota , Thrombosis/etiology
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