Impact of Infectious Burden on Extent and Long-Term Prognosis of Atherosclerosis

Espinola‐Klein, Christine; Rupprecht, Hans J.; Blankenberg, Stefan; Bickel, Christoph; Kopp, Helmut; Rippin, Gerd; Victor, Anja; Häfner, Gerd; Schlumberger, Wolfgang; Meyer, Jürgen

doi:10.1161/hc0102.101362

Cited by 270 publications

(129 citation statements)

References 34 publications

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“…Adults with HIV, tuberculosis, malaria, and periodontal disease also experience elevations of CRP and IL-6 that exceed the risk levels for heart attack and stroke (4,18,19). Elevated serum CRP has also related to past exposure to specific common pathogens (54)(55)(56).…”

Section: Discussionmentioning

confidence: 99%

Infection, inflammation, height, and longevity

Crimmins

Finch²

2005

Proc. Natl. Acad. Sci. U.S.A.

400

311

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Using historical data from cohorts born before the 20th century in four northern European countries, we show that increasing longevity and declining mortality in the elderly occurred among the same birth cohorts that experienced a reduction in mortality at younger ages. Concurrently, these cohorts also experienced increasing adult height. We hypothesize that both the decline in old-age mortality and the increase in height were promoted by the reduced burden of infections and inflammation. Thus, early growth and cardiovascular diseases of old age may share infectious and inflammatory causes rooted in the external environment.aging ͉ vascular disease ͉ mortality ͉ historical cohorts L ife expectancy has doubled during the last 250 years from preindustrial norms of 35-40 years (1, 2). Although all ages have benefited, the increases among the elderly began many decades after the increases at younger ages (3). We have hypothesized that the historical increase in life expectancy at the older ages was due in part to life-long reduction in exposure to chronic inflammation (4). It is well known that the survivors of birth cohorts with lowered early age mortality due to infections experienced lower mortality throughout adult life (5-8), a relationship we have characterized as the ''cohort morbidity phenotype'' (4). Others have proposed that mortality at young and old age is linked by improvements in nutrition and a reduction in organ damage due to infections (9,10). We add the reduction in lifelong exposure to inflammation to these explanations and develop in more detail the physiological mechanisms linking lifetime exposure to infections and late life health outcomes. We also consider inflammation as a possible link between childhood mortality and adult height (11).We argue that the demographic and economic revolutions beginning Ͼ200 years ago were accompanied by a physiological revolution, which occurred long before the benefits of modern medicine. The historical reduction in inflammation was an internal manifestation of the physiological revolution, which was also indexed by the historical increases in height. We propose a general model in which the reduction in lifelong levels of infections and inflammation reduced and delayed the atherosclerotic process and mortality due to heart disease and allowed increased height (Fig. 1). This heuristic model emphasizes the pathway from decreases in infection through reductions in inflammation but recognizes that other potential links include improvements in diet and nutrition and reductions in direct organ damage. Thus, our model considers a broader set of pathophysiological mechanisms linking health across the life course than presented heretofore.Extensive debate over the causes of the historical mortality decline has not resolved the relative roles of improved public health, vaccines, income, and nutrition (1, 12). However, all of these factors would have reduced exposure to, resistance to, or consequences of infections. The role we hypothesize for inflammation considers the ...

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Section: Discussionmentioning

confidence: 99%

Infection, inflammation, height, and longevity

Crimmins

Finch²

2005

Proc. Natl. Acad. Sci. U.S.A.

400

311

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“…A pathogenetic role for infections in atherosclerosis is suggested by the detection of pathogens in the arterial vessels and by more or less strong association between atherosclerosis and serological responses to pathogens, such as cytomegalovirus, herpes simplex virus, Haemophilus influenzae, Chlamydia pneumoniae, or Helicobacter pylori, or between the extent of atherosclerosis and the infectious burden (2,(5)(6)(7)(8)(9)(10)(11)(12)(13). However, the role of cell-mediated immunity and the functional status of pathogenspecific T cells within atherosclerotic lesions remain poorly characterized.…”

mentioning

confidence: 99%

T helper type 1 lymphocytes drive inflammation in human atherosclerotic lesions

Benagiano

Azzurri

Ciervo

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

145

124

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Atherosclerotic lesions are infiltrated by macrophages and T lymphocytes, potentially reactive to pathogens. We studied in vivo activated T lymphocytes that infiltrate atherosclerotic plaques of Helicobacter pylori-infected patients with or without anti-Chlamydia pneumoniae antibodies. In all atherosclerotic lesions, T helper type 1 (Th1) cells were predominant. C. pneumoniae-specific T cells were detected only in the plaques of anti-C. pneumoniae seropositive patients, whereas H. pylori-specific T cells were found in the gastric mucosa but not in the plaques of the same patients. Plaque-derived Th1 cells expressed cytotoxicity, proapoptotic activity, and help for monocyte tissue factor production. Although multifactorial, atherosclerosis can be regarded as a Th1-driven immunopathological condition.

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“…On the other hand, many recent reports indicate that chronic inflammatory reaction to transfusion-transmitted infections promotes atherosclerotic vascular changes [18,19,20,21,22,23,24,25]. Helicobacter pylori , Chlamydia pneumoniae , herpes simplex virus, CMV and HCV have been reported to be pathogens of atherosclerosis [18, 19, 25].…”

Section: Discussionmentioning

confidence: 99%

“…Another mechanism could be chronic inflammation caused by various infectious agents transmitted by transfusion. This mechanism has been considered as a risk factor for atherosclerosis [18,19,20,21,22,23,24,25]. If so, one may wonder whether the risks of mortality from other stroke or cardiovascular diseases (CVD) may also be elevated by transfusion.…”

Section: Introductionmentioning

confidence: 99%

History of Blood Transfusion before 1990 Is a Risk Factor for Stroke and Cardiovascular Diseases: The Japan Collaborative Cohort Study (JACC Study)

Yamada

Iso²,

Wada³

et al. 2005

Cerebrovasc Dis

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Background: We have previously shown novel evidence that history of blood transfusion is a risk factor for mortality from subarachnoid hemorrhage. This study was conducted to assess history of transfusion as a risk factor for other hemorrhagic stroke or ischemic stroke and cardiovascular diseases. Study Design and Methods: A total of 88,312 Japanese participants (36,823 men and 51,489 women), aged 40–79 years, without history of stroke, heart disease or cancer, completed a questionnaire including history of transfusion under the JACC Study from 1988 to 1990. Participants were followed up annually until deceased, or when they moved away from the surveyed community, or at the end of 1999. The underlying causes of death were determined according to the International Classification of Diseases, 10th revision (ICD-10). Results: Total follow-up person-years were 871,437 (males 359,437, females 512,000). During this 10-year period, 309 died from intracerebral hemorrhage, 587 from ischemic stroke and 472 from coronary heart disease. The multivariate relative risks of a transfusion history were 2.16 (95% CI 1.42–3.27, p < 0.001) for intracerebral hemorrhage, 1.63 (95% CI 1.18–2.27, p = 0.004) for ischemic stroke and 1.66 (95% CI 1.17–2.36, p = 0.005) for coronary heart disease, after adjustment for conventional cardiovascular risk factors. Conclusion: A transfusion history was associated with increased mortality from stroke and coronary heart disease.

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Impact of Infectious Burden on Extent and Long-Term Prognosis of Atherosclerosis

Cited by 270 publications

References 34 publications

Infection, inflammation, height, and longevity

Infection, inflammation, height, and longevity

T helper type 1 lymphocytes drive inflammation in human atherosclerotic lesions

History of Blood Transfusion before 1990 Is a Risk Factor for Stroke and Cardiovascular Diseases: The Japan Collaborative Cohort Study (JACC Study)

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