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1.
Circulation ; 146(12): 892-906, 2022 Sep 20.
Article in English | MEDLINE | ID: covidwho-2089002

ABSTRACT

BACKGROUND: Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces a prothrombotic state, but long-term effects of COVID-19 on incidence of vascular diseases are unclear. METHODS: We studied vascular diseases after COVID-19 diagnosis in population-wide anonymized linked English and Welsh electronic health records from January 1 to December 7, 2020. We estimated adjusted hazard ratios comparing the incidence of arterial thromboses and venous thromboembolic events (VTEs) after diagnosis of COVID-19 with the incidence in people without a COVID-19 diagnosis. We conducted subgroup analyses by COVID-19 severity, demographic characteristics, and previous history. RESULTS: Among 48 million adults, 125 985 were hospitalized and 1 319 789 were not hospitalized within 28 days of COVID-19 diagnosis. In England, there were 260 279 first arterial thromboses and 59 421 first VTEs during 41.6 million person-years of follow-up. Adjusted hazard ratios for first arterial thrombosis after COVID-19 diagnosis compared with no COVID-19 diagnosis declined from 21.7 (95% CI, 21.0-22.4) in week 1 after COVID-19 diagnosis to 1.34 (95% CI, 1.21-1.48) during weeks 27 to 49. Adjusted hazard ratios for first VTE after COVID-19 diagnosis declined from 33.2 (95% CI, 31.3-35.2) in week 1 to 1.80 (95% CI, 1.50-2.17) during weeks 27 to 49. Adjusted hazard ratios were higher, for longer after diagnosis, after hospitalized versus nonhospitalized COVID-19, among Black or Asian versus White people, and among people without versus with a previous event. The estimated whole-population increases in risk of arterial thromboses and VTEs 49 weeks after COVID-19 diagnosis were 0.5% and 0.25%, respectively, corresponding to 7200 and 3500 additional events, respectively, after 1.4 million COVID-19 diagnoses. CONCLUSIONS: High relative incidence of vascular events soon after COVID-19 diagnosis declines more rapidly for arterial thromboses than VTEs. However, incidence remains elevated up to 49 weeks after COVID-19 diagnosis. These results support policies to prevent severe COVID-19 by means of COVID-19 vaccines, early review after discharge, risk factor control, and use of secondary preventive agents in high-risk patients.


Subject(s)
COVID-19 , Thrombosis , Vascular Diseases , Venous Thromboembolism , Venous Thrombosis , Adult , COVID-19/complications , COVID-19/epidemiology , COVID-19 Vaccines , Cohort Studies , Humans , SARS-CoV-2 , Thrombosis/complications , Thrombosis/epidemiology , Vascular Diseases/complications , Venous Thromboembolism/etiology , Venous Thrombosis/epidemiology , Wales/epidemiology
3.
J Cardiothorac Surg ; 17(1): 261, 2022 Oct 08.
Article in English | MEDLINE | ID: covidwho-2064824

ABSTRACT

Post-Acute COVID-19 syndrome (PACS) is considered to be one of the least understood post-infectious syndromes. We report a case of a 21-year-old female who had a history of SARS-CoV-2 infection and presented with a right atrioventricular thrombus associated with pulmonary embolism and thrombocytopenia. At the time of admission, she was not vaccinated against SARS-CoV-2, and her serological tests for IgG and IgM antibodies against SARS-CoV-2 were positive. The size of the thrombus measured approximately 6 × 8 × 4 cm, which also led to tricuspid valve insufficiency due to mechanical dilatation of the valve's ring. The right atrioventricular thrombus also extended up to the inferior vena cava, leading to mild congestive hepatomegaly. Moreover, during thrombectomy, the mass of the thrombus was attached to the interseptal right atrial wall. The histopathological assessment of the core mass revealed that it was a right atrial myxoma hidden inside that large thrombus. We suspect that the formation and propagation of the thrombus to that size occurs as a part of Post-Acute COVID-19 syndrome (PACS). This study reviews and discusses coronavirus disease 2019-relate to thrombus formation inside cardiac chambers in case of a cardiac tumor, like myxoma in the setting of post-acute phase COVID-19 syndrome.


Subject(s)
COVID-19 , Heart Neoplasms , Myxoma , Thrombosis , Adult , COVID-19/complications , Female , Heart Atria/pathology , Heart Neoplasms/complications , Humans , Immunoglobulin G , Immunoglobulin M , Myxoma/complications , Myxoma/diagnosis , Myxoma/surgery , SARS-CoV-2 , Thrombosis/complications , Vena Cava, Inferior , Young Adult
4.
Zh Nevrol Psikhiatr Im S S Korsakova ; 122(9): 128-131, 2022.
Article in Russian | MEDLINE | ID: covidwho-2056581

ABSTRACT

The literature reports that cerebral venous thrombosis (CVT) develops in 1-1.5% of patients with COVID-19. Recently, a new syndrome named vaccine-induced immune thrombotic thrombocytopenia (VITT) has been described. VITT is a rare side-effect of COVID-19 vaccination that also causes CVT. The article presents an overview of the above problem and a clinical case of a patient with CVT that developed within a month after the first component of the Sputnik V vaccination and COVID-19.


Subject(s)
COVID-19 , Intracranial Thrombosis , Thrombosis , Venous Thrombosis , COVID-19/complications , COVID-19 Vaccines , Humans , Intracranial Thrombosis/diagnostic imaging , Intracranial Thrombosis/etiology , Thrombosis/complications , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/drug therapy
5.
Clin Appl Thromb Hemost ; 28: 10760296221127276, 2022.
Article in English | MEDLINE | ID: covidwho-2053691

ABSTRACT

Background: We investigated the importance of lupus anticoagulant (LA) in patients with SARS-CoV-2. Methods: Medical records of 41 SARS-CoV-2 infected patients were reviewed. Patients were classified into two groups according to the frequency of positive LA test results: "LA (-)" and "LA (+) ≥1" (LA positive at least once). Statistical analysis was performed to determine the association between LA presence and change in LA test results and disease course according to both hospital days (HD) and days after diagnosis (DD). Results: The prevalence of LA was 51.2%. Averagely, the first change in LA test result occurred during DD 12-13 and between HD 9-10. The second change occurred on DD 15-16 and HD 13-14. The presence of LA was associated with severe disease (P = .004) but was not associated with thrombotic complications or mortality. The change of results from negative to positive or vice versa or the frequency of the changes was not associated with disease severity, thrombotic complications, or mortality. Conclusions: LA positivity can be regarded as one of the findings suggesting more serious SARS-CoV-2 infection.


Subject(s)
Antiphospholipid Syndrome , COVID-19 , Thrombosis , Antiphospholipid Syndrome/complications , COVID-19/complications , Humans , Lupus Coagulation Inhibitor , SARS-CoV-2 , Thrombosis/complications
6.
Int J Mol Sci ; 23(18)2022 Sep 14.
Article in English | MEDLINE | ID: covidwho-2039871

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic has claimed the lives of millions of people around the world. Severe vitamin D deficiency can increase the risk of death in people with COVID-19. There is growing evidence that acute kidney injury (AKI) is common in COVID-19 patients and is associated with poorer clinical outcomes. The kidney effects of SARS-CoV-2 are directly mediated by angiotensin 2-converting enzyme (ACE2) receptors. AKI is also caused by indirect causes such as the hypercoagulable state and microvascular thrombosis. The increased release of soluble urokinase-type plasminogen activator receptor (suPAR) from immature myeloid cells reduces plasminogen activation by the competitive inhibition of urokinase-type plasminogen activator, which results in low plasmin levels and a fibrinolytic state in COVID-19. Frequent hypercoagulability in critically ill patients with COVID-19 may exacerbate the severity of thrombosis. Versican expression in proximal tubular cells leads to the proliferation of interstitial fibroblasts through the C3a and suPAR pathways. Vitamin D attenuates the local expression of podocyte uPAR and decreases elevated circulating suPAR levels caused by systemic inflammation. This decrease preserves the function and structure of the glomerular barrier, thereby maintaining renal function. The attenuated hyperinflammatory state reduces complement activation, resulting in lower serum C3a levels. Vitamin D can also protect against COVID-19 by modulating innate and adaptive immunity, increasing ACE2 expression, and inhibiting the renin-angiotensin-aldosterone system. We hypothesized that by reducing suPAR levels, appropriate vitamin D supplementation could prevent the progression and reduce the severity of AKI in COVID-19 patients, although the data available require further elucidation.


Subject(s)
Acute Kidney Injury , COVID-19 , Thrombosis , Acute Kidney Injury/drug therapy , Acute Kidney Injury/etiology , Angiotensin-Converting Enzyme 2 , Angiotensins , COVID-19/complications , COVID-19/drug therapy , Fibrinolysin , Humans , Plasminogen , Receptors, Urokinase Plasminogen Activator , SARS-CoV-2 , Thrombosis/complications , Urokinase-Type Plasminogen Activator , Versicans , Vitamin D , Vitamins
7.
Thromb Res ; 219: 95-101, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2031708

ABSTRACT

BACKGROUND: COVID-19 patients carry an increased rate of thrombosis. It is controversial to which extent thrombi in the pulmonary arterial tree really contribute to disease severity with hypoxemia secondary to microvascular/lung parenchymal damage with viral alveolitis considered to play the main role in critical disease. OBJECTIVES: The primary objective was to compare post-mortem lung disease from fatal COVID-19 pneumonia in patients with macroscopically evident pulmonary arterial tree thrombosis and patients without, by characterizing the immunohistochemical nature of thrombi, and by comparing clinical and laboratory features of these patients with other COVID-19 patients who died but without evidence of pulmonary arterial thrombosis (controls). PATIENTS AND METHODS: 13 COVID-19 pneumonia cases (mean age ± standard deviation: 74 ± 6.5 years) with macroscopically visible pulmonary arterial thrombosis were compared to 14 controls. Hematoxylin and Eosin stained slides were reviewed choosing those with visible pulmonary thrombi which were further characterized by immunohistochemistry, in particular for the inflammatory infiltrates. Ante mortem serum markers relevant to pulmonary embolism were evaluated in both groups. RESULTS: Twenty arterial thrombi (5 cases with multiple thrombi) were selected for study and were composed by white blood cells (WBC) [median, IQR range: 10 % (5-12.25)], mainly neutrophils [58 % (35.2-64.5)]. Cases with thrombosis showed significantly higher levels of platelet count [median, IQR range: 195000/mmc (157750-274,500) vs 143,500 (113000-175,250), p = 0.011], LDH [854 U/L (731-1315) vs 539 (391.5-660), p = 0.003] at admission, and D-dimer at ICU transfer [25,072 FEU (6951-50,531) vs 1024 (620-5501), p = 0.003]. CONCLUSIONS: Immunothrombotically driven arterial thrombi in COVID-19 patients are associated with D-Dimer and LDH elevations, thus linking inflammation, coagulopathy and organ damage in fatal COVID-19.


Subject(s)
COVID-19 , Hypertension, Pulmonary , Thrombosis , Biomarkers , COVID-19/complications , Eosine Yellowish-(YS) , Hematoxylin , Humans , Lung , SARS-CoV-2 , Thrombosis/complications
8.
Rom J Morphol Embryol ; 63(1): 39-48, 2022.
Article in English | MEDLINE | ID: covidwho-2026773

ABSTRACT

Cortisol is a key element in acute stress including a severe infection. However, in coronavirus-associated disease, 20% of subjects experience hypocortisolemia due to direct or immune damage of pituitary and adrenal glands. One extreme form of adrenal insufficiency is found in 2∕3 of cases with viral and post-viral adrenal infarction (AI) (with∕without adrenal hemorrhage) that is mostly associated with a severe coronavirus disease 2019 (COVID-19) infection; it requires prompt glucocorticoid intervention. Some reports are incidental findings at computed tomography (CT)∕magnetic resonance imaging (MRI) scans for non-adrenal complications like pulmonary spreading and others are seen on post-mortem analysis. This is a review of PubMed-accessible, English papers focusing on AI in addition to the infection, between March 1, 2020 and November 1, 2021. Exclusion criteria were acute adrenal insufficiency without the histopathological (HP) and∕or imaging report of adrenal enlargement, necrosis, etc., respective adrenal failure due to pituitary causes, or non-COVID-19-related adrenal events. We identified a total of 84 patients (different levels of statistical evidence), as follows: a retrospective study on 51 individuals, two post-mortem studies comprising nine, respectively 12 patients, a case series of five subjects, seven single-case reports. HP aspects include necrosis associated with ischemia, cortical lipid degeneration (+/- focal adrenalitis), and infarcts at the level of adrenal cortex, blood clot into vessels, acute fibrinoid necrosis in arterioles and capsules, as well as subendothelial vacuolization. Collateral potential contributors to adrenal damage are thrombotic events, coagulation anomalies, antiphospholipid syndrome, endothelial dysfunction, severe COVID-19 infection with multiorgan failure, etc. Clinical picture is variable from acute primary adrenal insufficiency to asymptomatic or mild evolution, even a retrospective diagnostic; it may be a part of long COVID-19 syndrome; glucocorticoid therapy for non-adrenal considerations might mask cortisol deficient status due to AI∕hemorrhage. Despite its rarity, the COVID-19-associated AI/hemorrhage represents a challenging new chapter, a condition that is essential to be recognized due to its gravity since prompt intervention with glucocorticoid replacement is lifesaving.


Subject(s)
Adrenal Insufficiency , COVID-19 , Thrombosis , Adrenal Glands , Adrenal Insufficiency/complications , COVID-19/complications , Glucocorticoids , Hemorrhage/complications , Humans , Hydrocortisone , Infarction/complications , Necrosis/complications , Retrospective Studies , Thrombosis/complications
9.
Turk Kardiyol Dern Ars ; 50(6): 466-469, 2022 09.
Article in English | MEDLINE | ID: covidwho-2025175

ABSTRACT

Coronavirus disease 2019 is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 virus. Hypoxic respiratory failure, multiorgan dysfunction, septic shock, thrombosis, and thromboembolic complications have been associated with the severe acute respiratory syndrome coronavirus 2 infection. We report the presentation of the severe acute respiratory syndrome coronavirus 2 infection with acute upper extremity ischemia and mesenteric ischemia clinic. We also report that this patient had an aortic arch mural thrombus as a possible source of thromboembolism, and we emphasize that the aorta should also be carefully evaluated in thromboembolic patients with coronavirus disease 2019.


Subject(s)
Arterial Occlusive Diseases , COVID-19 , Thromboembolism , Thrombosis , Arterial Occlusive Diseases/complications , COVID-19/complications , Humans , SARS-CoV-2 , Thromboembolism/etiology , Thrombosis/complications , Thrombosis/diagnostic imaging
11.
Indian J Gastroenterol ; 41(3): 313-318, 2022 06.
Article in English | MEDLINE | ID: covidwho-1971854

ABSTRACT

Involvement of the gastrointestinal (GI) system in corona virus disease-19 (COVID-19) in form of diarrhea, loss of taste, nausea, and anorexia is common and associated with poor prognosis. COVID-19 is also associated with a hypercoagulable state that mainly involves the pulmonary vasculature. However, GI complications involving thrombosis are observed infrequently. We report two COVID-19 patients who had two different causes of acute abdomen. The first patient was a 49-year-old male diagnosed with an aortic thrombus along with a splenic infarct. He was diagnosed early and successfully managed with anticoagulants. The second patient was a 30-year-old male who developed pain in the abdomen and was found to have features suggestive of peritonitis. A contrast-enhanced computerized tomography (CECT) scan of the abdomen revealed dilated bowel loops. Immediate exploratory laparotomy was performed; he was found to have jejunal perforation with gangrene. Histopathological examination of the resected specimen showed inflammatory cells with edema and thrombotic vessels. However, he succumbed to sepsis and multiorgan failure. Therefore, it is important to investigate cases of acute abdomen in COVID-19 thoroughly and whenever indicated CT angiogram should be obtained.


Subject(s)
Abdomen, Acute , COVID-19 , Thrombosis , Abdomen, Acute/etiology , Adult , Anticoagulants , COVID-19/complications , Humans , Male , Middle Aged , Thrombosis/complications , Thrombosis/etiology , Tomography, X-Ray Computed/methods
12.
Thromb Res ; 217: 73-75, 2022 09.
Article in English | MEDLINE | ID: covidwho-1956355
13.
Tomography ; 8(4): 1836-1850, 2022 07 15.
Article in English | MEDLINE | ID: covidwho-1939006

ABSTRACT

INTRODUCTION: Coronavirus SARS-CoV-2, the causative agent of COVID-19, primarily causes a respiratory tract infection that is not limited to respiratory distress syndrome, but it is also implicated in other body systems. Systemic complications were reported due to an exaggerated inflammatory response, which involves severe alveolar damage in the lungs and exacerbates the hypercoagulation that leads to venous thrombosis, ischemic attack, vascular dysfunction and infarction of visceral abdominal organs. Some complications are related to anticoagulant drugs that are administrated to stabilize hypercoagulability, but increase the risk of bleeding, hematoma and hemorrhage. The aim of this study is to report the diagnostic role of CT in the early diagnosis and management of patients with severe COVID-19 complications through the most interesting cases in our experience. MATERIAL AND METHODS: The retrospective analysis of patients studied for COVID-19 in our institution and hospitals, which are part of the university training network, was performed. CASES: Pneumomediastinum, cortical kidney necrosis, splenic infarction, cerebral ischemic stroke, thrombosis of the lower limb and hematomas are the most major complications that are reviewed in this study. CONCLUSIONS: Since the onset of the COVID-19 pandemic, the CT imaging modality with its high sensitivity and specificity remains the preferred imaging choice to diagnose early the different complications associated with COVID-19, such as thrombosis, ischemic stroke, infarction and pneumomediastinum, and their management, which significantly improved the outcomes.


Subject(s)
COVID-19 , Ischemic Stroke , Mediastinal Emphysema , Stroke , Thrombosis , COVID-19/complications , COVID-19/diagnostic imaging , Humans , Infarction/complications , Mediastinal Emphysema/complications , Pandemics , Retrospective Studies , SARS-CoV-2 , Stroke/etiology , Thrombosis/complications
14.
PLoS One ; 17(7): e0269466, 2022.
Article in English | MEDLINE | ID: covidwho-1933333

ABSTRACT

BACKGROUND: Coronavirus disease-2019 (COVID-19) is associated with thromboembolism. Antiphospholipid antibody (APLa) formation is one of the mechanisms. Vitamin D deficiency has been associated with thrombosis in antiphospholipid antibody syndrome. OBJECTIVE: Measure APLa and vitamin D in hospitalized COVID-19 patients with and without thrombosis to evaluate if thromboembolism is associated with concomitant APLa and vitamin D deficiency. METHODS: Case-control study. Hospitalized COVID-19 patients with a thromboembolic event (ischemic stroke, myocardial infarction, deep venous thrombosis/pulmonary embolism, Cases n = 20). Controls (n = 20): Age, sex-matched without thromboembolic events. Patients with autoimmune disorders, antiphospholipid antibody syndrome, thrombophilia, anticoagulation therapy, prior thromboembolism, chronic kidney disease 3b, 4, end-stage renal disease, and malignancy were excluded. Given the limited current literature on the role of concomitant antiphospholipid antibodies and vitamin D deficiency in causing venous and/or arterial thrombosis in hospitalized COVID-19 patients, we enrolled 20 patients in each arm. Anti-cardiolipin IgG/IgM, beta-2 glycoprotein-1 IgG/IgM, lupus anticoagulant and vitamin D levels were measured in both groups. RESULTS: Cases were 5.7 times more likely to be vitamin D deficient (OR:5.7, 95% CI:1.3-25.6) and 7.4 times more likely to have any one APLa (OR:7.4, 95% CI: 1.6-49.5) while accounting for the effects of sex. Patients with both APLa and vitamin D deficiency had significantly more thrombosis compared to patients who were antibody positive without vitamin D deficiency (100% vs 47.4%; p = 0.01). CONCLUSIONS: Thrombosis in COVID-19 was associated with concomitant APLa and vitamin D deficiency. Future studies in COVID-19 should assess the role of vitamin D in reducing thrombosis.


Subject(s)
Antiphospholipid Syndrome , COVID-19 , Thromboembolism , Thrombosis , Vitamin D Deficiency , Antibodies, Anticardiolipin , Antibodies, Antiphospholipid , Antiphospholipid Syndrome/complications , COVID-19/complications , Case-Control Studies , Humans , Immunoglobulin G , Immunoglobulin M , Thromboembolism/complications , Thrombosis/complications , Vitamin D , Vitamin D Deficiency/complications
15.
J Thromb Thrombolysis ; 54(1): 29-32, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1914001

ABSTRACT

Seated immobility thromboembolism syndrome (SIT) is the association of prolonged seated immobility with increased risk of venous thromboembolism (VTE). The advent of COVID-19 resulted in implementation of lockdowns to curb its spread. This resulted in compulsory work from home and minimization of outdoor activities. Consequently, this would have likely led to increased prolonged sitting and reduced mobility. Few case reports and studies have observed an increase in VTE incidence during the lockdown period. We likewise performed a clinical audit of our weekly thrombosis clinic cases and revealed three cases of VTE associated with prolonged sitting during Singapore's COVID-19 lockdown. Notably, all had other minor VTE risk factors in addition to prolonged sitting. All cases had intermediate-high risk pulmonary embolism and were given extended anticoagulation. With the pandemic still ongoing, periodic lockdown and quarantine measures may continue to be imposed. While the overall VTE risk conferred by prolonged seated immobility associated with lockdown measures is likely to be small, this risk can be easily mitigated and possibly prevented by simply staying mobile.


Subject(s)
COVID-19 , Pulmonary Embolism , Thrombosis , Venous Thromboembolism , COVID-19/epidemiology , Communicable Disease Control , Humans , Pandemics , Pulmonary Embolism/etiology , Pulmonary Embolism/prevention & control , Risk Factors , Thrombosis/complications , Venous Thromboembolism/complications , Venous Thromboembolism/prevention & control
16.
Arch Med Res ; 53(4): 341-351, 2022 06.
Article in English | MEDLINE | ID: covidwho-1889228

ABSTRACT

AIM OF THE STUDY: Development of thrombocytopenia and thrombosis after administration of the ChAdox1 nCoV-19 (AstraZeneca-Oxford) vaccine has recently been described. This new condition is called vaccine-induced immune thrombotic thrombocytopenia (VITT). Our objective was to summarize case reports on VITT with/without D-dimer increments in AstraZeneca-Oxford vaccinated individuals. DATA SOURCES: MEDLINE, PubMed, and Scopus databases were searched. STUDY SELECTION: Case series, case reports, letters to the editor; and abstracts of AstraZeneca-Oxford vaccinated patients with a clinical profile of thrombocytopenia (platelet count <150X10 3 /dL) and D-dimer determination, with or without thrombosis, and/or bleeding, and/or antibodies against platelet factor 4 (aPF4), were included. DATA EXTRACTION: Baseline risk factors, symptoms, physical signs; laboratory results, imaging findings, treatment; and outcome in patients with VITT reported in case series, were examined. DATA SYNTHESIS: Patients who developed VITT were more likely to be young women (ages 21 to 77) given the AstraZeneca-Oxford vaccine 5-14 days prior to presentation. Patients' signs, symptoms, and imaging findings were consistent with cerebral venous sinus thrombosis, or deep veins, lung, and other sites. Laboratory findings showed thrombocytopenia, low fibrinogen, and elevated D-dimer levels, while aPF4 was positive in most assays performed. Treatment was non-heparin anticoagulants, IV immunoglobulin, and steroids, as recommended by medical guidelines. CONCLUSIONS: Vaccine-induced immune thrombotic thrombocytopenia is a rare complication with high morbidity, related to administration of the AstraZeneca-Oxford vaccine. Clinicians should prepare for early identification of patients with suspicious symptoms, and prompt treatment initiated to avoid catastrophic events. D-dimer determination is useful for surveillance of cases with suspected VITT.


Subject(s)
COVID-19 , ChAdOx1 nCoV-19 , Fibrin Fibrinogen Degradation Products , Thrombocytopenia , Thrombosis , Adult , Aged , COVID-19/prevention & control , ChAdOx1 nCoV-19/adverse effects , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Middle Aged , Thrombocytopenia/chemically induced , Thrombocytopenia/diagnosis , Thrombosis/chemically induced , Thrombosis/complications , Young Adult
17.
Ann Vasc Surg ; 84: 6-11, 2022 Aug.
Article in English | MEDLINE | ID: covidwho-1872929

ABSTRACT

BACKGROUND: COVID-19 was initially identified as an acute respiratory disease, but it was quickly recognized that multiple organ systems could be affected. Venous thrombosis and pulmonary embolism have been well reported. However, there is a paucity of data on COVID-19-related arterial thrombosis. We examined the incidence, characteristics, treatment, and outcome in patients with acute COVID-19-related arterial thrombosis in a large health maintenance organization (HMO). METHODS: A retrospective multicenter case review was performed from March 2020 to March 2021. Cases were identified through a questionnaire sent to vascular surgeons. Patient characteristics, imaging, treatment, and outcome were reviewed. Successful revascularization was defined as restoration of blood flow with viability of the end organ and absence of death within 30 days. Limb salvage was defined as prevention of major amputation (transtibial or transfemoral) and absence of death in 30 days. RESULTS: There were 37,845 patients admitted with COVID-19 complications during this time. Among this group, 26 patients (0.07%) had COVID-19-related arterial thrombosis. The mean age was 61.7 years (range, 33-82 years) with 20 men (77%) and 6 women (23%). Ethnic minorities comprised 25 of 26 cases (96%). Peripheral arterial disease (PAD) was present in 4 of 26 (15%), active smoking in 1 of 26 (3.8%), and diabetes in 19 of 26 (73%) cases. Most patients developed acute arterial ischemia in the outpatient setting, 20 of 26 (77%). Of the outpatients, 6 of 20 (30%) had asymptomatic COVID-19 and 14 of 20 (70%) had only mild upper respiratory symptoms. Distribution of ischemia was as follows: 23 patients had at least one lower extremity ischemia, one patient had cerebral and lower extremity, one had mesenteric and lower extremity, and one had upper extremity ischemia. Revascularization was attempted in 21 patients, of which 12 of 21 (57%) were successful. Limb salvage was successful in 13 of 26 (50%) patients. The overall mortality was 31% (8/26). CONCLUSIONS: Our experience in a large HMO revealed that the incidence of COVID-19-related arterial thrombosis was low. The actual incidence is likely to be higher since our method of case collection was incomplete. The majority of arterial thrombosis occurred in the outpatient setting in patients with asymptomatic or mild/moderate COVID-19 respiratory disease. Acute ischemia was the inciting factor for hospitalization in these cases. Acute lower extremity ischemia was the most common presentation, and limb salvage rate was lower than that expected when compared to ischemia related to PAD. Arterial thrombosis associated with COVID-19 portends a significantly higher mortality. Education of primary care providers is paramount to prevent delayed diagnosis as most patients initially developed ischemia in the outpatient setting and did not have a high cardiovascular risk profile.


Subject(s)
Arterial Occlusive Diseases , COVID-19 , Peripheral Arterial Disease , Thrombosis , Amputation/adverse effects , Arterial Occlusive Diseases/diagnostic imaging , Arterial Occlusive Diseases/epidemiology , Arterial Occlusive Diseases/surgery , COVID-19/complications , Female , Health Maintenance Organizations , Humans , Ischemia/diagnostic imaging , Ischemia/etiology , Ischemia/therapy , Limb Salvage/adverse effects , Lower Extremity/blood supply , Male , Middle Aged , Peripheral Arterial Disease/diagnostic imaging , Peripheral Arterial Disease/epidemiology , Peripheral Arterial Disease/therapy , Retrospective Studies , Risk Factors , Thrombosis/complications , Thrombosis/diagnostic imaging , Thrombosis/therapy , Treatment Outcome
19.
BMJ Case Rep ; 15(5)2022 May 19.
Article in English | MEDLINE | ID: covidwho-1854258

ABSTRACT

COVID-19 represents a global health emergency, causing significant morbidity and mortality. Multiple vaccines have been distributed worldwide to control the spread of this pandemic. Several reports of thrombosis and thrombocytopaenia have been described after vaccination. These have been termed vaccine-induced immune thrombocytopaenia and thrombosis (VITT). We report a fatal case of VITT after receiving the first dose of Ad26.COV2.S vaccine. A man in his 30s developed thrombocytopaenia, massive haemoperitoneum due to spleen rupture and extensive portal and femoral vein thrombosis. The patient rapidly developed multiple organ failure and died. We attributed this condition to the vaccine due to the temporal relationship, presence of thrombosis and thrombocytopaenia, high levels of platelet factor 4 antibodies and exclusion of other diagnoses. Healthcare providers should be aware of such rare but fatal complications of COVID-19 immunisation, as early diagnosis of VITT may improve prognosis by allowing timely appropriate treatment.


Subject(s)
COVID-19 , Purpura, Thrombocytopenic, Idiopathic , Thrombocytopenia , Thrombosis , Vaccines , Ad26COVS1 , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Humans , Male , Purpura, Thrombocytopenic, Idiopathic/chemically induced , Purpura, Thrombocytopenic, Idiopathic/complications , Thrombocytopenia/chemically induced , Thrombocytopenia/diagnosis , Thrombosis/complications , Vaccination/adverse effects , Vaccines/adverse effects
20.
Stroke ; 53(7): 2411-2419, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1840696

ABSTRACT

The main burden of SARS-CoV-2 falls on the lungs but neurological manifestations, the most disabling of which are strokes and which correlate with disease severity, are common. We proffer a novel mechanism for acute COVID-19 stroke whereby pulmonary vein clots developing within the characteristic pulmonary intravascular thrombotic lesions can embolize to the brain. Appreciation of this mechanism requires an understanding of the tricompartmental model of lung parenchyma oxygenation (the alveolus, the bronchial artery, and the pulmonary artery), all of which are compromised in COVID-19. Of these 3 sources, the bronchial artery plays a crucial role in COVID-19 stroke because the unique collaterals from bronchial artery to pulmonary vein which exist under normal physiological conditions (and which maintain venous patency when the pulmonary artery is blocked by embolus) are occluded, thus leading to venular thrombosis in the presence of hypercoagulability. Dislodgement of clots from this source translocates the pathology to the brain and is a disease mechanism, formerly rare, which may account for many cases of large vessel occlusion stroke in COVID-19. This mechanism extends the concept of cardioembolic stroke from endocardium retrogradely into the pulmonary circulation with which the left cardiac chambers lie in direct continuity, and which is an accepted stroke mechanism under other circumstances such as lung lobectomy, where surgical ligation of the pulmonary vein creates a blind sac from which thrombi can embolize. The proposed model is supported by postmortem studies which have demonstrated venular thrombosis and by case reports of pulmonary vein thrombosis in COVID-19. This concept provides a more plausible cause for COVID-19 associated large vessel occlusion stroke than other putative mechanisms, such as cerebral endotheliitis, cytokine storm, and hypercoagulopathy, although it is acknowledged that the latter mechanism contributes to the genesis of pulmonary vein clots. Recognizing that extrapulmonary manifestations including stroke arise within thrombosed pulmonary veins is key to understanding of neurological manifestations of SARS-CoV-2 infection.


Subject(s)
COVID-19 , Ischemic Stroke , Stroke , Thrombosis , COVID-19/complications , Humans , Lung/diagnostic imaging , SARS-CoV-2 , Stroke/etiology , Thrombosis/complications , Venules
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