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Pneumonia, thrombosis and vascular disease
Summary An enhanced risk of cardiovascular mortality has been observed after pneumonia. Epidemiological studies have shown that respiratory tract infections are associated with an increased risk of thrombotic‐related vascular disease such as myocardial infarction, ischemic stroke and venous thrombos...
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Published in: | Journal of thrombosis and haemostasis 2014-09, Vol.12 (9), p.1391-1400 |
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container_title | Journal of thrombosis and haemostasis |
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creator | Violi, F. Cangemi, R. Calvieri, C. |
description | Summary
An enhanced risk of cardiovascular mortality has been observed after pneumonia. Epidemiological studies have shown that respiratory tract infections are associated with an increased risk of thrombotic‐related vascular disease such as myocardial infarction, ischemic stroke and venous thrombosis. Myocardial infarction and stroke have been detected essentially in the early phase of the disease (i.e. within 48 h from hospital admission), with an incidence ranging from as low as 1% to as high as 11%. Age, previous cardiovascular events and high pneumonia severity index were independent predictors of myocardial infarction; clinical predictors of stroke were not identified. Deep venous thrombosis and pulmonary embolism may also occur after pneumonia but incidence and clinical predictors must be defined. The biological plausibility of such an association may be deduced by experimental and clinical studies, showing that lung infection is complicated by platelet aggregation and clotting system activation, as documented by up‐regulation of tissue factor and down‐regulation of activated protein C. The effect of antithrombotic drugs has been examined in experimental and clinical studies but results are still inconclusive. |
doi_str_mv | 10.1111/jth.12646 |
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An enhanced risk of cardiovascular mortality has been observed after pneumonia. Epidemiological studies have shown that respiratory tract infections are associated with an increased risk of thrombotic‐related vascular disease such as myocardial infarction, ischemic stroke and venous thrombosis. Myocardial infarction and stroke have been detected essentially in the early phase of the disease (i.e. within 48 h from hospital admission), with an incidence ranging from as low as 1% to as high as 11%. Age, previous cardiovascular events and high pneumonia severity index were independent predictors of myocardial infarction; clinical predictors of stroke were not identified. Deep venous thrombosis and pulmonary embolism may also occur after pneumonia but incidence and clinical predictors must be defined. The biological plausibility of such an association may be deduced by experimental and clinical studies, showing that lung infection is complicated by platelet aggregation and clotting system activation, as documented by up‐regulation of tissue factor and down‐regulation of activated protein C. The effect of antithrombotic drugs has been examined in experimental and clinical studies but results are still inconclusive.</description><identifier>ISSN: 1538-7933</identifier><identifier>ISSN: 1538-7836</identifier><identifier>EISSN: 1538-7836</identifier><identifier>DOI: 10.1111/jth.12646</identifier><identifier>PMID: 24954194</identifier><language>eng</language><publisher>England: Elsevier Limited</publisher><subject>Age Factors ; Anticoagulants - administration & dosage ; Blood Coagulation ; cardiovascular diseases ; Clinical Trials as Topic ; Fibrinolytic Agents - therapeutic use ; Humans ; Myocardial Infarction - complications ; Myocardial Infarction - epidemiology ; Patient Admission ; platelet activation ; Platelet Aggregation ; pneumonia ; Pneumonia - complications ; Pneumonia - epidemiology ; Protein C - metabolism ; Research Design ; Stroke - complications ; Stroke - epidemiology ; Thromboplastin - metabolism ; thrombosis ; Thrombosis - complications ; Thrombosis - epidemiology ; Treatment Outcome ; Vascular Diseases - complications ; Vascular Diseases - epidemiology</subject><ispartof>Journal of thrombosis and haemostasis, 2014-09, Vol.12 (9), p.1391-1400</ispartof><rights>2014 International Society on Thrombosis and Haemostasis</rights><rights>2014 International Society on Thrombosis and Haemostasis.</rights><rights>Copyright © 2014 International Society on Thrombosis and Haemostasis</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4216-520463a26a91d5ed896e099efea1d06d6a586f0cac2f4ecffee238ad1505e1c53</citedby><cites>FETCH-LOGICAL-c4216-520463a26a91d5ed896e099efea1d06d6a586f0cac2f4ecffee238ad1505e1c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24954194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Violi, F.</creatorcontrib><creatorcontrib>Cangemi, R.</creatorcontrib><creatorcontrib>Calvieri, C.</creatorcontrib><title>Pneumonia, thrombosis and vascular disease</title><title>Journal of thrombosis and haemostasis</title><addtitle>J Thromb Haemost</addtitle><description>Summary
An enhanced risk of cardiovascular mortality has been observed after pneumonia. Epidemiological studies have shown that respiratory tract infections are associated with an increased risk of thrombotic‐related vascular disease such as myocardial infarction, ischemic stroke and venous thrombosis. Myocardial infarction and stroke have been detected essentially in the early phase of the disease (i.e. within 48 h from hospital admission), with an incidence ranging from as low as 1% to as high as 11%. Age, previous cardiovascular events and high pneumonia severity index were independent predictors of myocardial infarction; clinical predictors of stroke were not identified. Deep venous thrombosis and pulmonary embolism may also occur after pneumonia but incidence and clinical predictors must be defined. The biological plausibility of such an association may be deduced by experimental and clinical studies, showing that lung infection is complicated by platelet aggregation and clotting system activation, as documented by up‐regulation of tissue factor and down‐regulation of activated protein C. The effect of antithrombotic drugs has been examined in experimental and clinical studies but results are still inconclusive.</description><subject>Age Factors</subject><subject>Anticoagulants - administration & dosage</subject><subject>Blood Coagulation</subject><subject>cardiovascular diseases</subject><subject>Clinical Trials as Topic</subject><subject>Fibrinolytic Agents - therapeutic use</subject><subject>Humans</subject><subject>Myocardial Infarction - complications</subject><subject>Myocardial Infarction - epidemiology</subject><subject>Patient Admission</subject><subject>platelet activation</subject><subject>Platelet Aggregation</subject><subject>pneumonia</subject><subject>Pneumonia - complications</subject><subject>Pneumonia - epidemiology</subject><subject>Protein C - metabolism</subject><subject>Research Design</subject><subject>Stroke - complications</subject><subject>Stroke - epidemiology</subject><subject>Thromboplastin - metabolism</subject><subject>thrombosis</subject><subject>Thrombosis - complications</subject><subject>Thrombosis - epidemiology</subject><subject>Treatment Outcome</subject><subject>Vascular Diseases - complications</subject><subject>Vascular Diseases - epidemiology</subject><issn>1538-7933</issn><issn>1538-7836</issn><issn>1538-7836</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNp10MtKAzEUBuAgiq2XhS8gA25UnDb3TpZS1CoFXdR1SJMzdMpcatJR-vbGTutCMJuTxcd_Dj9CFwQPSHzD5XoxIFRyeYD6RLAsHWVMHu7_irEeOglhiTFRguJj1KNcCU4U76PbtxraqqkLc5esF76p5k0oQmJql3yaYNvS-MQVAUyAM3SUmzLA-W6eovfHh9l4kk5fn57H99PUckpkGjdwyQyVRhEnwGVKAlYKcjDEYemkEZnMsTWW5hxsngNQlhlHBBZArGCn6LrLXfnmo4Ww1lURLJSlqaFpgyZCEjXiGVeRXv2hy6b1dbxuqxgVIsNR3XTK-iYED7le-aIyfqMJ1j8F6lig3hYY7eUusZ1X4H7lvrEIhh34KkrY_J-kX2aTLvIb5sh4eA</recordid><startdate>201409</startdate><enddate>201409</enddate><creator>Violi, F.</creator><creator>Cangemi, R.</creator><creator>Calvieri, C.</creator><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201409</creationdate><title>Pneumonia, thrombosis and vascular disease</title><author>Violi, F. ; Cangemi, R. ; Calvieri, C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4216-520463a26a91d5ed896e099efea1d06d6a586f0cac2f4ecffee238ad1505e1c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Age Factors</topic><topic>Anticoagulants - administration & dosage</topic><topic>Blood Coagulation</topic><topic>cardiovascular diseases</topic><topic>Clinical Trials as Topic</topic><topic>Fibrinolytic Agents - therapeutic use</topic><topic>Humans</topic><topic>Myocardial Infarction - complications</topic><topic>Myocardial Infarction - epidemiology</topic><topic>Patient Admission</topic><topic>platelet activation</topic><topic>Platelet Aggregation</topic><topic>pneumonia</topic><topic>Pneumonia - complications</topic><topic>Pneumonia - epidemiology</topic><topic>Protein C - metabolism</topic><topic>Research Design</topic><topic>Stroke - complications</topic><topic>Stroke - epidemiology</topic><topic>Thromboplastin - metabolism</topic><topic>thrombosis</topic><topic>Thrombosis - complications</topic><topic>Thrombosis - epidemiology</topic><topic>Treatment Outcome</topic><topic>Vascular Diseases - complications</topic><topic>Vascular Diseases - epidemiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Violi, F.</creatorcontrib><creatorcontrib>Cangemi, R.</creatorcontrib><creatorcontrib>Calvieri, C.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Violi, F.</au><au>Cangemi, R.</au><au>Calvieri, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pneumonia, thrombosis and vascular disease</atitle><jtitle>Journal of thrombosis and haemostasis</jtitle><addtitle>J Thromb Haemost</addtitle><date>2014-09</date><risdate>2014</risdate><volume>12</volume><issue>9</issue><spage>1391</spage><epage>1400</epage><pages>1391-1400</pages><issn>1538-7933</issn><issn>1538-7836</issn><eissn>1538-7836</eissn><abstract>Summary
An enhanced risk of cardiovascular mortality has been observed after pneumonia. Epidemiological studies have shown that respiratory tract infections are associated with an increased risk of thrombotic‐related vascular disease such as myocardial infarction, ischemic stroke and venous thrombosis. Myocardial infarction and stroke have been detected essentially in the early phase of the disease (i.e. within 48 h from hospital admission), with an incidence ranging from as low as 1% to as high as 11%. Age, previous cardiovascular events and high pneumonia severity index were independent predictors of myocardial infarction; clinical predictors of stroke were not identified. Deep venous thrombosis and pulmonary embolism may also occur after pneumonia but incidence and clinical predictors must be defined. The biological plausibility of such an association may be deduced by experimental and clinical studies, showing that lung infection is complicated by platelet aggregation and clotting system activation, as documented by up‐regulation of tissue factor and down‐regulation of activated protein C. The effect of antithrombotic drugs has been examined in experimental and clinical studies but results are still inconclusive.</abstract><cop>England</cop><pub>Elsevier Limited</pub><pmid>24954194</pmid><doi>10.1111/jth.12646</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Age Factors Anticoagulants - administration & dosage Blood Coagulation cardiovascular diseases Clinical Trials as Topic Fibrinolytic Agents - therapeutic use Humans Myocardial Infarction - complications Myocardial Infarction - epidemiology Patient Admission platelet activation Platelet Aggregation pneumonia Pneumonia - complications Pneumonia - epidemiology Protein C - metabolism Research Design Stroke - complications Stroke - epidemiology Thromboplastin - metabolism thrombosis Thrombosis - complications Thrombosis - epidemiology Treatment Outcome Vascular Diseases - complications Vascular Diseases - epidemiology |
title | Pneumonia, thrombosis and vascular disease |
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