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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
Main Authors: Violi, F., Cangemi, R., Calvieri, C.
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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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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. 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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. 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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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