Acute respiratory-tract infections and risk of first-time acute myocardial infarction

Meier, Christoph; Jick, Susan S.; Derby, Laura E.; Meier, CR; Jick, Susan S.; Derby, LE; Vasilakis, Catherine; Jick, Hershel

doi:10.1016/s0140-6736(97)11084-4

Cited by 351 publications

(254 citation statements)

References 26 publications

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“…Infectious diseases [26,27], including influenza [28], have been associated with an increased occurrence of acute cardiovascular events, in particular in patients with evidence of increased risk of cardiovascular disease. Several abnormalities induced by infections can favour acute cardiovascular events, including endothelial dysfunction, prothrombotic changes in the blood and direct damage to coronary plaques [29,30].…”

Section: Inflammation and Platelet Activationmentioning

confidence: 99%

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Lanza

Barone

Scalone

et al. 2010

Journal of Internal Medicine

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Section: Inflammation and Platelet Activationmentioning

confidence: 99%

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Lanza

Barone

Scalone

et al. 2010

Journal of Internal Medicine

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Section: Introductionmentioning

confidence: 99%

“…2,3,7,8 Acute respiratory infections in particular have been associated with an increased risk of myocardial infarction (MI). 7,8 Influenza epidemics have been associated with excess mortality attributed to cardiovascular disease, 9,10 although they have not been found to be associated with increased rates of hospitalizations for acute ischemic cardiac events. 11 Recent studies suggest that influenza vaccination may reduce the risk of recurrent MI, 12 primary cardiac arrest, 13 death from cardiovascular disease, 14 and hospitalization for ischemic heart disease.…”

Section: Introductionmentioning

confidence: 99%

Influenza Vaccination and Risk of Incident Myocardial Infarction

Heffelfinger¹,

Heckbert²,

Psaty³

et al. 2006

Human Vaccines

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Background: Several studies suggest that influenza vaccination may be associated with a decreased risk of acute cardiovascular events. We examined the association between influenza vaccination and risk of incident myocardial infarction (MI) in persons at least 65 years of age in a population-based case-control study.Methods: Case subjects were members of Group Health Cooperative (GHC), a health maintenance organization, with incident MI during 1992-1998. Control subjects were GHC members without a history of MI who were frequency matched to case subjects by age, sex, calendar year, and presence of treated hypertension. The medical records of 750 case subjects with MI and 1735 controls were reviewed.Results: Receipt of influenza vaccine was not associated with risk of incident MI during the months of November through March (odds ratio [OR]: 0.97, 95% confidence interval [CI]: 0.75-1.27) or April through September (OR: 0.97, 95% CI 0.75-1.26).Conclusions: This study does not provide evidence supporting an association of influenza vaccination and reduction in risk of myocardial infarction.

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“…Interestingly, recent clinical findings showed that acute respiratory infection is associated with an increased risk of acute myocardial infarction. 42 In a case-control study, previous use of tetracyclines or quinolones, antibiotics that are active against C pneumoniae, was associated with a lower incidence of firsttime acute myocardial infarction. 43 Both of these findings include the possibility but do not prove that C pneumoniae is associated with myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Chlamydia pneumoniae Proteins Induce Secretion of the 92-kDa Gelatinase by Human Monocyte– Derived Macrophages

Vehmaan-Kreula

Puolakkainen

Sarvas

et al. 2001

ATVB

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Abstract-Chlamydia pneumoniae, an intracellular Gram-negative respiratory bacterium, and macrophages are present in inflammatory tissue sites such as atherosclerotic lesions, where abnormal degradation of the extracellular matrix takes place. To evaluate the potential of C pneumoniae for participation in matrix destruction, we studied the effect of this bacterium on the production of 3 matrix-degrading metalloproteinases, 92-kDa gelatinase, interstitial collagenase-1, and stromelysin-1, and their natural inhibitor TIMP-1 (tissue inhibitor of metalloproteinases-1) by human monocyte-derived macrophages differentiated in vitro. Spontaneous production of collagenase and stromelysin by these cells was minimal and was not influenced by C pneumoniae. In contrast, the cells secreted substantial basal quantities of 92-kDa gelatinase, the secretion of which was stimulated (on average, 2.5-fold) by C pneumoniae. C pneumoniae regulated the expression of 92-kDa gelatinase by macrophages at the pretranslational level. Macrophages secreted only small quantities of TIMP-1. The chlamydial proteins Omp2, MOMP, and HSP60 were also found to participate in the induction of 92-kDa gelatinase by C pneumoniae. Denaturation of chlamydial proteins by boiling reduced 92-kDa gelatinase secretion only partially (by 35%), suggesting that the heat-stabile lipopolysaccharide molecules also stimulate secretion of the enzyme.The results show that production of 92-kDa gelatinase by human macrophages is selectively upregulated by C pneumoniae, which suggests that these bacteria, when present in a macrophage-containing inflammatory environment, actively participate in the destruction of the extracellular matrix.

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Acute respiratory-tract infections and risk of first-time acute myocardial infarction

Cited by 351 publications

References 26 publications

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Influenza Vaccination and Risk of Incident Myocardial Infarction

Chlamydia pneumoniae Proteins Induce Secretion of the 92-kDa Gelatinase by Human Monocyte– Derived Macrophages

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