Analysis of cardiopulmonary findings in COVID-19 fatalities: High incidence of pulmonary artery thrombi and acute suppurative bronchopneumonia.
Identifieur interne : 000017 ( Main/Exploration ); précédent : 000016; suivant : 000018Analysis of cardiopulmonary findings in COVID-19 fatalities: High incidence of pulmonary artery thrombi and acute suppurative bronchopneumonia.
Auteurs : Claudia Grosse [Autriche] ; Alexandra Grosse [Autriche] ; Helmut J F. Salzer [Autriche] ; Martin W. Dünser [Autriche] ; Reinhard Motz [Autriche] ; Rupert Langer [Autriche]Source :
- Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology [ 1879-1336 ]
Descripteurs français
- KwdFr :
- Adulte d'âge moyen (MeSH), Artère pulmonaire (anatomopathologie), Autopsie (MeSH), Betacoronavirus (MeSH), Bronchopneumonie (anatomopathologie), Bronchopneumonie (virologie), Embolie pulmonaire (anatomopathologie), Embolie pulmonaire (virologie), Femelle (MeSH), Humains (MeSH), Incidence (MeSH), Infections à coronavirus (anatomopathologie), Infections à coronavirus (complications), Mâle (MeSH), Pandémies (MeSH), Pneumopathie virale (anatomopathologie), Pneumopathie virale (complications), Sujet âgé (MeSH), Sujet âgé de 80 ans ou plus (MeSH), Thrombose (anatomopathologie), Thrombose (virologie).
- MESH :
- anatomopathologie : Artère pulmonaire, Bronchopneumonie, Embolie pulmonaire, Infections à coronavirus, Pneumopathie virale, Thrombose.
- virologie : Bronchopneumonie, Embolie pulmonaire, Thrombose.
- complications : Adulte d'âge moyen, Autopsie, Betacoronavirus, Femelle, Humains, Incidence, Infections à coronavirus, Mâle, Pandémies, Pneumopathie virale, Sujet âgé, Sujet âgé de 80 ans ou plus.
English descriptors
- KwdEn :
- Aged (MeSH), Aged, 80 and over (MeSH), Autopsy (MeSH), Betacoronavirus (MeSH), Bronchopneumonia (pathology), Bronchopneumonia (virology), Coronavirus Infections (complications), Coronavirus Infections (pathology), Female (MeSH), Humans (MeSH), Incidence (MeSH), Male (MeSH), Middle Aged (MeSH), Pandemics (MeSH), Pneumonia, Viral (complications), Pneumonia, Viral (pathology), Pulmonary Artery (pathology), Pulmonary Embolism (pathology), Pulmonary Embolism (virology), Thrombosis (pathology), Thrombosis (virology).
- MESH :
- complications : Coronavirus Infections, Pneumonia, Viral.
- pathology : Bronchopneumonia, Coronavirus Infections, Pneumonia, Viral, Pulmonary Artery, Pulmonary Embolism, Thrombosis.
- virology : Bronchopneumonia, Pulmonary Embolism, Thrombosis.
- Aged, Aged, 80 and over, Autopsy, Betacoronavirus, Female, Humans, Incidence, Male, Middle Aged, Pandemics.
Abstract
Since its recognition in December 2019, coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has rapidly spread globally causing a pandemic that represents the greatest medical challenge in decades. The aim of the study was to evaluate the spectrum of cardiopulmonary pathology of COVID-19 based on (non-minimal invasive) autopsies performed on 14 COVID-19 decedents. Bilateral diffuse alveolar damage (DAD) was found in all patients. Superimposed acute bronchopneumonia was present in 11 of 14 (78.6%) patients and was considered the major cause of death in 2 patients. A key finding was the presence of thrombotic/thromboembolic vascular occlusions. We classified 5 types of pulmonary thrombi: 1. capillary microthrombi (11/14, 78.6%); 2. partially organized thrombi in mid-sized pulmonary arteries with complete vessel occlusion; 3. non-organized thrombi in mid-sized pulmonary arteries that did not completely fill out the vessel lumen and probably represented thromboemboli rather than thrombosis; 4. bone marrow emboli (1/14, 7.1%); and 5. septic pulmonary thromboemboli (1/14, 7.1%). Pulmonary thrombi in mid-sized arteries were noted in 5 of 14 (35.7%) patients, causing pulmonary infarction and/or pulmonary hemorrhage. All patients had evidence of chronic cardiac disease, including myocardial hypertrophy (13/14, 92.9%), mild to marked coronary artery atherosclerosis (14/14, 100%) and focal myocardial fibrosis (3/14, 21.4%). Acute myocardial infarction was found as concurrent cause of death in 3 (21.4%) patients, and significant cardiac hypertrophy (heart weight 750 g) was present in 1 (7.1%) patient with ATTR-positive cardiac amyloidosis. The autopsy findings confirm that COVID-19 is a systemic disease, with major involvement of the lungs, that increases the risk of cardiac and vascular complications including acute myocardial injury and thrombotic/thromboembolic events. Secondary acute bronchopneumonia is a common complication in patients with COVID-19 and may be the major cause of death.
DOI: 10.1016/j.carpath.2020.107263
PubMed: 32784110
PubMed Central: PMC7365076
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Betacoronavirus (MeSH)</term>
<term>Bronchopneumonia (pathology)</term>
<term>Bronchopneumonia (virology)</term>
<term>Coronavirus Infections (complications)</term>
<term>Coronavirus Infections (pathology)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Incidence (MeSH)</term>
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<term>Pneumonia, Viral (pathology)</term>
<term>Pulmonary Artery (pathology)</term>
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<term>Thrombosis (pathology)</term>
<term>Thrombosis (virology)</term>
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<term>Artère pulmonaire (anatomopathologie)</term>
<term>Autopsie (MeSH)</term>
<term>Betacoronavirus (MeSH)</term>
<term>Bronchopneumonie (anatomopathologie)</term>
<term>Bronchopneumonie (virologie)</term>
<term>Embolie pulmonaire (anatomopathologie)</term>
<term>Embolie pulmonaire (virologie)</term>
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<term>Humains (MeSH)</term>
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<term>Thrombose</term>
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<term>Pneumonia, Viral</term>
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<term>Thrombosis</term>
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<front><div type="abstract" xml:lang="en">Since its recognition in December 2019, coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has rapidly spread globally causing a pandemic that represents the greatest medical challenge in decades. The aim of the study was to evaluate the spectrum of cardiopulmonary pathology of COVID-19 based on (non-minimal invasive) autopsies performed on 14 COVID-19 decedents. Bilateral diffuse alveolar damage (DAD) was found in all patients. Superimposed acute bronchopneumonia was present in 11 of 14 (78.6%) patients and was considered the major cause of death in 2 patients. A key finding was the presence of thrombotic/thromboembolic vascular occlusions. We classified 5 types of pulmonary thrombi: 1. capillary microthrombi (11/14, 78.6%); 2. partially organized thrombi in mid-sized pulmonary arteries with complete vessel occlusion; 3. non-organized thrombi in mid-sized pulmonary arteries that did not completely fill out the vessel lumen and probably represented thromboemboli rather than thrombosis; 4. bone marrow emboli (1/14, 7.1%); and 5. septic pulmonary thromboemboli (1/14, 7.1%). Pulmonary thrombi in mid-sized arteries were noted in 5 of 14 (35.7%) patients, causing pulmonary infarction and/or pulmonary hemorrhage. All patients had evidence of chronic cardiac disease, including myocardial hypertrophy (13/14, 92.9%), mild to marked coronary artery atherosclerosis (14/14, 100%) and focal myocardial fibrosis (3/14, 21.4%). Acute myocardial infarction was found as concurrent cause of death in 3 (21.4%) patients, and significant cardiac hypertrophy (heart weight 750 g) was present in 1 (7.1%) patient with ATTR-positive cardiac amyloidosis. The autopsy findings confirm that COVID-19 is a systemic disease, with major involvement of the lungs, that increases the risk of cardiac and vascular complications including acute myocardial injury and thrombotic/thromboembolic events. Secondary acute bronchopneumonia is a common complication in patients with COVID-19 and may be the major cause of death.</div>
</front>
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<Title>Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology</Title>
<ISOAbbreviation>Cardiovasc Pathol</ISOAbbreviation>
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<ArticleTitle>Analysis of cardiopulmonary findings in COVID-19 fatalities: High incidence of pulmonary artery thrombi and acute suppurative bronchopneumonia.</ArticleTitle>
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<Abstract><AbstractText>Since its recognition in December 2019, coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has rapidly spread globally causing a pandemic that represents the greatest medical challenge in decades. The aim of the study was to evaluate the spectrum of cardiopulmonary pathology of COVID-19 based on (non-minimal invasive) autopsies performed on 14 COVID-19 decedents. Bilateral diffuse alveolar damage (DAD) was found in all patients. Superimposed acute bronchopneumonia was present in 11 of 14 (78.6%) patients and was considered the major cause of death in 2 patients. A key finding was the presence of thrombotic/thromboembolic vascular occlusions. We classified 5 types of pulmonary thrombi: 1. capillary microthrombi (11/14, 78.6%); 2. partially organized thrombi in mid-sized pulmonary arteries with complete vessel occlusion; 3. non-organized thrombi in mid-sized pulmonary arteries that did not completely fill out the vessel lumen and probably represented thromboemboli rather than thrombosis; 4. bone marrow emboli (1/14, 7.1%); and 5. septic pulmonary thromboemboli (1/14, 7.1%). Pulmonary thrombi in mid-sized arteries were noted in 5 of 14 (35.7%) patients, causing pulmonary infarction and/or pulmonary hemorrhage. All patients had evidence of chronic cardiac disease, including myocardial hypertrophy (13/14, 92.9%), mild to marked coronary artery atherosclerosis (14/14, 100%) and focal myocardial fibrosis (3/14, 21.4%). Acute myocardial infarction was found as concurrent cause of death in 3 (21.4%) patients, and significant cardiac hypertrophy (heart weight 750 g) was present in 1 (7.1%) patient with ATTR-positive cardiac amyloidosis. The autopsy findings confirm that COVID-19 is a systemic disease, with major involvement of the lungs, that increases the risk of cardiac and vascular complications including acute myocardial injury and thrombotic/thromboembolic events. Secondary acute bronchopneumonia is a common complication in patients with COVID-19 and may be the major cause of death.</AbstractText>
<CopyrightInformation>Copyright © 2020. Published by Elsevier Inc.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Grosse</LastName>
<ForeName>Claudia</ForeName>
<Initials>C</Initials>
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<Author ValidYN="Y"><LastName>Salzer</LastName>
<ForeName>Helmut J F</ForeName>
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<AffiliationInfo><Affiliation>Department of Pulmonology, Kepler University Hospital, Krankenhausstrasse 9, 4041 Linz, Austria.</Affiliation>
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<Author ValidYN="Y"><LastName>Motz</LastName>
<ForeName>Reinhard</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Institute of Pathology and Microbiology, Johannes Kepler University Linz, Altenberger Strasse 69, 4040 Linz, Austria.</Affiliation>
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<Author ValidYN="Y"><LastName>Langer</LastName>
<ForeName>Rupert</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Institute of Pathology and Microbiology, Johannes Kepler University Linz, Altenberger Strasse 69, 4040 Linz, Austria.</Affiliation>
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<Month>07</Month>
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<MeshHeading><DescriptorName UI="D011651" MajorTopicYN="N">Pulmonary Artery</DescriptorName>
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<MeshHeading><DescriptorName UI="D011655" MajorTopicYN="N">Pulmonary Embolism</DescriptorName>
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<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D013927" MajorTopicYN="N">Thrombosis</DescriptorName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
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</MeshHeading>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autopsy</Keyword>
<Keyword MajorTopicYN="N">COVID-19</Keyword>
<Keyword MajorTopicYN="N">Cardiopulmonary pathology</Keyword>
<Keyword MajorTopicYN="N">Coronavirus</Keyword>
<Keyword MajorTopicYN="N">Diffuse alveolar damage</Keyword>
<Keyword MajorTopicYN="N">SARS-CoV-2</Keyword>
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</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year>
<Month>06</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2020</Year>
<Month>07</Month>
<Day>09</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2020</Year>
<Month>07</Month>
<Day>12</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2020</Year>
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<Day>14</Day>
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<PubMedPubDate PubStatus="medline"><Year>2020</Year>
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<PubMedPubDate PubStatus="entrez"><Year>2020</Year>
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<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">32784110</ArticleId>
<ArticleId IdType="pii">S1054-8807(20)30067-3</ArticleId>
<ArticleId IdType="doi">10.1016/j.carpath.2020.107263</ArticleId>
<ArticleId IdType="pmc">PMC7365076</ArticleId>
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<affiliations><list><country><li>Autriche</li>
</country>
</list>
<tree><country name="Autriche"><noRegion><name sortKey="Grosse, Claudia" sort="Grosse, Claudia" uniqKey="Grosse C" first="Claudia" last="Grosse">Claudia Grosse</name>
</noRegion>
<name sortKey="Dunser, Martin W" sort="Dunser, Martin W" uniqKey="Dunser M" first="Martin W" last="Dünser">Martin W. Dünser</name>
<name sortKey="Grosse, Alexandra" sort="Grosse, Alexandra" uniqKey="Grosse A" first="Alexandra" last="Grosse">Alexandra Grosse</name>
<name sortKey="Langer, Rupert" sort="Langer, Rupert" uniqKey="Langer R" first="Rupert" last="Langer">Rupert Langer</name>
<name sortKey="Motz, Reinhard" sort="Motz, Reinhard" uniqKey="Motz R" first="Reinhard" last="Motz">Reinhard Motz</name>
<name sortKey="Salzer, Helmut J F" sort="Salzer, Helmut J F" uniqKey="Salzer H" first="Helmut J F" last="Salzer">Helmut J F. Salzer</name>
</country>
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