Infections Cause Stroke

The vast majority of studies have found associations between infections and cerebrovascular disease (stroke). The pathogens implicated include bacteria such as Chlamydia pneumoniae, Helicobacter pylori, and dental pathogens; and viruses. People in less wealthy classes are more to be infected; and smokers are more likely to be in the less wealthy classes. Therefore, the stage is set for confounding by infection, which is not elimi nated by adjusting for proxy variables.

All of the anti-smokers' studies blaming smoking for causing strokes, including the Surgeon General reports and the SAMMEC, simply ignore the role of infection and stonewall the issue of confounding by infection. Therefore, they are not reputable studies, and supposed authorities who use them as such are guilty of fraud and deceit.

Association between cerebral infaction and increased serum bacterial antibody levels in young adults. J Syrjanen, VV Valtonen, M Iivanainen, T Hovi, M Malkamadi, PH Makela. Acta Neurol Scand 1986 Mar;73(3):273-278.

Preceding infection as an important risk factor for ischaemic brain infarction in young and middle aged patients. J Syrjanen, VV Valtonen, M Iivanainen, M Kaste, JK Huttunen. Br Med J (Clin Res Ed) 1988 Apr 23;296(6630):1156-1160.

Anticardiolipin response and its association with infections in young and middle-aged patients with cerebral infarction. J Syrjanen, O Vaarala, M Iivanainen, T Palosuo, VV Valtonen, K Aho. Acta Neurol Scand 1988 Nov;78(5):381-386.

Dental infections in association with cerebral infarctions in young and middle-aged men. J Syrjanen, J Peltola, V Valtonen, M Iivanainen, M Kaste, JK Huttunen. J Intern Med 1989 Mar;225(3):179-184.

Infection as a risk factor for infarction and atherosclerosis. VV Valtonen. Ann Med 1991;23(5):539-543. (Review).

Immunohematologic characteristics of infection-associated cerebral infarction. SF Ameriso, VL Wong, FP Quismorio, M Fisher. Stroke 1991 Aug;22(8):1004-1009.

Infection as a risk factor for cerebral infarction. J Syrjanen. Eur Heart J 1993 Dec;14 Suppl K:17-19. (Review).

Cytomegalovirus/herpesvirus and carotid atherosclerosis: the ARIC Study. PD Sorlie, E Adam, SL Melnick, A Folsom, T Skelton, LE Chambless, R Barnes, JL Melnick. J Med Virol 1994 Jan;42(1):33-37. "The case-control odds ratio for CMV antibodies was 1.55 (P=.03)," before "adjustment."

Recent infection as a risk factor for cerebrovascular ischemia. AJ Grau, F Buggle, S Heindl, C Steicjhen-Wiehn, T Banerjee, M Maiwald, M Rohlfs, H Suhr, W Fiehn, H Becher, W Hache. Stroke 1995 Mar;26(3):373-379.

Prospective relations between Helicobacter pylori infection, coronary heart disease, and stroke in middle aged men. PH Whincup, MA Mendall, IJ Perry, DP Strachan, M Walker. Heart 1996 Jun;75(6):568-572.

[Infectious diseases as a cause and risk factor for cerebrovascular ischemia]. AJ Grau, F Buggle, W Hacke. Nervenarzt 1996 Aug;67(8):639-649.

Cohort study of cytomegalovirus infection as a risk factor for carotid intimal-medial thickening, a measure of subclinical atherosclerosis. FJ Nieto, E Adam, P Sorlie, H Farzadegan, JL Melnick, GW Comstock, M Szklo. Circulation 1996 Sep 1;94(5):922-927. "The results from this first population-based cohort study of CMV infection and carotid IMT are compatible with the hypothesis of a causal role of CMV in atherosclerosis."

Impairments of the protein C system and fibrinolysis in infection-associated stroke. RF Macko, SF Ameriso, A Gruber, JH Griffin, JA Fernendez, R Barndt, FP Quismorio, JM Weiner, M Fisher. Stroke 1996 Nov;27(11):2005-2011.

Acute infection as a risk factor for ischemic stroke. LY Bova, NM Bornstein, AD Korczyn. Stroke 1996 Dec;27(12):2204-2206.

Association of Chlamydial infection with cerebrovascular disease. MLJ Wimmer, R Sandmann-Strupp, P Saikku, RL Haberl. Stroke 1996 Dec;27(12):2207-2210.

Association between acute cerebrovascular ischemia and chronic and recurrent infection. AJ Grau, F Buggle, C Ziegler, W Schwarz, J Meuser, A-J Tasman, A Buhler, C Benesch, H Becher, W Hacke. Stroke 1997 Sep;28(9):1724-1729.

Helicobacter pylori infection: a risk factor for ischaemic cerebrovascular disease and carotid atheroma. HS Markus, MA Mendall. J Neurol Neurosurg Psychiatry 1998 Jan;64(1):104-107.

Recent bacterial and viral infection is a risk factor for cerebrovascular ischemia: clinical and biochemical studies. AJ Grau, F Buggle, H Becher, E Zimmermann, M Spiel, T Fent, M Maiwald, E Werle, M Zorn, H Hengel, W Hacke. Neurology 1998 Jan;50(1):196-203.

Chlamydia pneumoniae antibody titers are significantly associated with acute stroke and transient cerebral ischemia. The West Birmingham Stroke Project. PJ Cook, D Honeybourne, GYH Lip, DG Beevers, R Wise, P Davies. Stroke 1998 Feb;29(2):404-410.

Role of infection as a risk factor for atherosclerosis, myocardial infarction, and stroke. KJ Mattila, VV Valtonen, MS Nieminen, S Asikainen. Clin Infect Dis 1998 Mar;26(3):719-734.

Bacterial infections and atherosclerosis. JB Muhlestein. J Investig Med 1998 Oct;46(8):396-402. (Review).

Prospective study of herpes simplex virus, cytomegalovirus, and the risk of myocardial infarction and stroke. PM Ridker, CH Hennekens, MJ Stampfer, F Wang. Circulation 1998 Dec 22/29;98(25):2796-2799.

Chlamydia pneumoniae but not cytomegalovirus antibodies are associated with future risk of stroke and cardiovascular disease: a prospective study in middle-aged to elderly men with treated hypertension. B Fagerberg, J Gnarpe, H Gnarpe, S Agewall, J Wikstrand. Stroke 1999 Feb;30(2):299-305.

Association of cervical artery dissection with recent infection. AJ Grau, T Brandt, F Buggle, E Orberk, J Mytilineos, E Werle, Conradt, M Krause, R Winter, W Hacke. Arch Neurol 1999 Jul;56(7):851-856.

Preceding infection as a risk factor of stroke in the young. D Nagaraja, R Christopher, M Tripathi, MV Kumar, ER Valli, SA Patil. J Assoc Physicians India 1999 Jul;47(7):673-675.

Lack of association of infectious agents with risk of future myocardial infarction and stroke. Definitive evidence disproving the infection/coronary artery disease hypothesis? SE Epstein, J Zhu. Circulation 1999 Sep 28;100(13):1366-1368. (Editorial).

Association of periodontal infections with atherosclerotic and pulmonary diseases. FA Scannapieco, RJ Genco. J Periodontal Res 1999 Oct;34(7):340-345. (Review).

Chlamydia pneumoniae antibodies and high lipoprotein(a) levels do not predict ischemic cerebral infarctions: results from a nested case-control study in northern Sweden. CA Glader, B Stegmayr, J Boman, H Stenlund, L Weinehall, G Hallmans, GH Dahlen. Stroke 1999 Oct;30(10):2013-2018.

Multiple infections in carotid atherosclerotic plaques. B Chiu. Am Heart J 1999 Nov;138(5 Pt 2):S534-S536.

[Infection, atherosclerosis and acute ischemic cerebrovascular disease]. A Grau, F Buggle. Rev Neurol 1999 Nov 1-15;29(9):847-851. (Review).

Association of endotoxemia with carotid atherosclerosis and cardiovascular disease: prospective results from the Bruneck Study. CJ Wiedermann, S Kiechl, S Dunzendorfer, P Schratzberger, G Egger, F Oberhollenzer, J Willeit. J Am Coll Cardiol 1999 Dec;34(7):1975-81. "Notably, smokers with low endotoxin levels and nonsmokers did not differ in their atherosclerosis risk, whereas smokers with high levels almost invariably developed new lesions." [Note the anti-smoker contortions. What about nonsmokers with high levels? And does this purport that nonsmokers never develop new lesions?]

Fever and infection soon after ischemic stroke. AJ Grau, F Buggle, P Schnitzler, M Spiel, C Lichy, W Hacke. J Neurol Sci 1999 Dec 15;171(2):115-120.

Previous infection and other risk factors for acute cerebrovascular ischaemia: attributable risks and the characterisation of high risk groups. H Becher, A Grau, K Steindorf, F Buggle, W Hacke. J Epidemiol Biostat 2000;5(5):277-283.

[The relationship between immunological parameters with etiopathogenesis and clinical course of stroke]. A Czlonkowska, G Gromadzka. Neurol Neurochir Pol 2000;34(3 Suppl):13-26.

Frequency of coexistence of cytomegalovirus and Chlamydia pneumoniae in atherosclerotic plaques. HB Qavi, JL Melnick, E Adam, ME DeBakey. Cent Eur J Public Health 2000 May;8(2):71-73. CMV and/or C pneumoniae DNA were found in 71% of 17 carotid atherosclerotic plaques.

Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis. DJ Lanska, RJ Kryscio. Stroke 2000 Jun;31(6):1274-1282.

Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis: a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae. YG Song, HM Kwon, JM Kim, BK Hong, DS Kim, AJ Huh, KH Chang, HY Kim, TS Kang, BK Lee, DH Choi, YS Jang, HS Kim. Yonsei Med J 2000 Jun;41(3):219-327.

Chlamydia pneumoniae and the risk of first ischemic stroke: The Northern Manhattan Stroke Study. MS Elkind, IF Lin, JT Grayston, RL Sacco. Stroke 2000 Jul;31(7):1521-1525.

Infections, immunity, and atherosclerosis: associations of antibodies to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus with immune reactions to heat-shock protein 60 and carotid or femoral atherosclerosis. M Mayr, S Kiechl, J Willeit, G Wick, Q Xu. Circulation 2000 Aug 22;102(8):833-839.

Chlamydia pneumoniae DNA in non-coronary atherosclerotic plaques and circulating leukocytes. M Berger, B Schroder, G Daeschlein, W Schneider, A Busjahn, I Buchwalow, FC Luft, H Haller. J Lab Clin Med 2000 Sep;136(3):194-200.

Are morphological or functional changes in the carotid artery wall associated with Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, or herpes simplex virus infection? C Espinola-Klein, HJ Rupprecht, S Blankenberg, C Bickel, H Kopp, G Rippin, G Hafner, U Pfeifer, J Meyer. Stroke 2000 Sep;31(9):2127-2133.

Recent infection as a risk factor for intracerebral and subarachnoid hemorrhages. AK Kunze, A Annecke, F Wigger, C Lichy, F Buggle, H Schnippering, P Schnitzler, AJ Grau. Cerebrovasc Dis 2000 Sep-Oct;10(5):352-358.

Identification of periodontal pathogens in atheromatous plaques. VI Haraszthy, JJ Zambon, M Trevisan, M Zeid, RJ Genco. J Periodontol 2000 Oct;71(10):1554-1560.

[Chlamydia pneumoniae antibody titers in patients with acute ischemic stroke]. N Kawashima, J Kawada. Rinsho Shinkeigaku 2000 Nov;40(11):1063-1068.

Activated coagulation/fibrinolysis system and platelet function in acute thrombotic stroke patients with increased C-reactive protein levels. H Tohgi, S Konno, S Takahashi, D Koizumi, R Kondo, H Takahashi. Thromb Res 2000 Dec 1;100(5):373-379.

Detection of Helicobacter pylori in human carotid atheosclerotic plaques. SF Ameriso, EA Fridman, RC Leiguarda, GE Sevlever. Stroke 2001 Feb;32(2):385-391.

Chronic infections and the risk of carotid atherosclerosis: prospective results from a large population study. S Kiechl, G Egger, M Mayr, CJ Wiedermann, E Bonora, F Oberhollenzer, M Muggeo, Q Xu, G Wick, W Poewe, J Willeit. Circulation 2001 Feb 27;103(8):1064-1070. "[A]ny chronic infection versus none," odds ratio 4.08 (2.42-6.85), P<0.0001.

An association between an antibody against Chlamydia pneumoniae and common carotid atherosclerosis. R Kawamoto, T Doi, H Tokunaga, I Konishi. Intern Med 2001 Mar;40(3):208-213.

Enhanced progression of early carotid atherosclerosis is related to Chlamydia pneumoniae (Taiwan acute respiratory) seropositivity. D Sander, K Winbeck, J Klingelhofer, T Etgen, B Conrad. Circulation 2001 Mar 13;103(10):1390-1395.

Presence of Chlamydia pneumoniae in human symptomatic and asymptomatic carotid atherosclerotic plaque. R LaBiche, D Koziol, TC Quinn, C Gaydos, S Azhar, G Ketron, S Sood, TJ DeGraba. Stroke 2001 Apr;32(4):855-860. "[H]igh serum anti-chlamydial IgA levels (>/=1:128) were associated with occurrence of symptomatic disease (P=0.03; odds ratio, 2.86; 95% CI, 1.12 to 7.28)."

Chlamydia pneumoniae in atherosclerotic carotid artery plaques: high prevalence among heavy smokers. N Dobrilovic, L Vadlamani, M Meyer, CB Wright. Am Surg 2001 Jun;67(6):589-593.

Increased CD8(+) T cells associated with Chlamydia pneumoniae in symptomatic carotid plaque. ZD Nadareishvili, DE Koziol, B Szekely, C Ruetzler, R LaBiche, R McCarron, TJ DeGraba. Stroke 2001 Sep;32(9):1966-1972.

Chlamydia pneumoniae in atherosclerotic middle cerebral artery. D Virok, Z Kis, L Karai, L Intzedy, K Burian, A Szabo, B Ivanyi, E Gonczol. Stroke 2001 Sep;32(9):1973-1976. CP was found in 5/15 atherosclerotic cerebral arteries vs 0/4 otherwise healthy victims of trauma.

The significance of Chlamydia pneumoniae in symptomatic carotid stenosis. C Katsenis, E Kouskouni, L Kolokotronis, D Rizos, P Dimakakos. Angiology 2001 Sep;52(9):615-619.

C-reactive protein levels and viable Chlamydia pneumoniae in carotid artery atherosclerosis. SC Johnston, LM Messina, WS Browner, MT Lawton, C Morris, D Dean. Stroke 2001 Dec 1;32(12):2748-2752. 18/48 (38%) carotid endarterectomy specimens had viable C pneumoniae; and C-reactive protein levels were higher in these patients.

Active and passive smoking, chronic infections, and the risk of carotid atherosclerosis: prospective results from the bruneck study. S Kiechl, P Werner, G Egger, F Oberbollenzer, M Mayr, Q Xu, W Poewe, J Willett. Stroke 2002 Sep;33(9):2170-2176. The bottom line of this study is that "Remarkably [sic], current and ex-smokers faced an increased atherosclerosis risk only in the presence of chronic infections (odds ratios [95% CIs], 3.3 [1.8 to 6.2] and 3.4 [1.8 to 6.3]; P<0.001 each)." The same held true for passive smoking as well. This is only "remarkable" to deluded true believers of the lie that smoking causes heart disease. It is not remarkable to those who realize that the anti-smokers have purposely used defective studies all along, to falsely blame smoking for heart disease that is really caused by infection. In addition, "current, past, and nonsmokers without infections did not differ substantially in their estimated risk burden." Despite this, the deluded authors cling to their ossified prejudices by claiming that "the pro-atherogenic effects of cigarette smoking are mediated in part by the chronic infections found in smokers" [sic - these infections are also found in non-smokers, who have NO reduced risk of heart disease; they merely succomb a few years later, which is best attributable to less exposure to the relevant infections.] - and they ludicrously proclaim that "A better understanding of the pathogenetic mechanisms of smoking [sic - rather than the pathogenetic mechanisms of INFECTION, as any rational person would conclude!] may offer novel clues for disease prevention supplementary to the primary goal of achieving long-term abstinence." And then, the vile and despicable American Heart Association proclaims in its viciously dishonest press release that "Cigarette smoking turns the entire body into a breeding ground for infection." (Science Daily Sep. 6, 2002.)

Impact of infectious burden on progression of carotid atherosclerosis. C Espinola-Klein, HJ Rupprecht, S Blankenberg, C Bickel, H Kopp, A Victor, G Hafner, W Prellwitz, W Schlumberger, J Meyer. Stroke 2002 Nov;33(11):2581-2586. "Elevated IgA antibodies against C. pneumoniae (P<0.04) and IgG antibodies against Epstein-Barr virus (P<0.01) and herpes simplex virus type 2 (P<0.04) were associated with progression of atherosclerosis... Infectious burden, divided into 0 to 3, 4 to 5, and 6 to 8 seropositives, was significantly associated with progression of atherosclerosis, with odds ratios of 1.8 (95% confidence interval, 1.1 to 2.9) for 4 to 5 and 3.8 (95% CI, 1.6 to 8.8) for 6 to 8 compared with 0 to 3 seropositives after adjustment."

Increased risk of atherosclerosis is confined to CagA-positive Helicobacter pylori strains: prospective results from the Bruneck study. M Mayr, S Kiechl, MA Mendall, J Willeit, G Wick, Q Xu. Stroke. 2003 Mar;34(3):610-615. "Common carotid artery intima-media thickness-both absolute values and changes between 1995 and 2000-were significantly enhanced in subjects seropositive to CagA but not in those infected with CagA-negative H pylori strains. There was a clear dose-response relation between anti-CagA antibodies and both intima-media thickness and atherosclerosis risk. Notably, the risk of atherosclerosis associated with CagA seropositivity was amplified by elevated C-reactive protein levels."

AAN: Chlamydia Pneumoniae a Risk Factor for Stroke. By Charlene Laino. Doctor's Guide 2003 Apr 7. Re MS Elkind et al, Antibodies to Chlamydia Pneumoniae Are Associated with Risk of Ischemic Stroke, presented at the 55th Annual Meeting of the American Academy of Neurology. Of 218 patients with their first stroke, "[P]atients with high IgG levels were 60% more likely to have had a stroke than those with normal levels, and individuals with IgA titers were 50% more likely to have had a stroke." The effect was stronger using higher cutoff levels.

Association of serum-soluble heat shock protein 60 with carotid atherosclerosis: clinical significance determined in a follow-up study. Q Xiao, K Mandal, G Schett, M Mayr, G Wick, F Oberhollenzer, J Willeit, S Kiechl, Q Xu. Stroke 2005 Dec;36(12):2571-6. "RESULTS: sHSP60 levels measured in 1995 and 2000 were highly correlated (r=0.40; P<0.001), indicating consistency over a 5-year period. Circulating HSP60 levels were significantly correlated with antilipopolysaccharide and anti-HSP60 antibodies. It was also elevated in subjects with chronic infection (top quintile group of HSP60, among subjects with and without chronic infection: 23.8% versus 17.0%; P=0.003 after adjustment for age and sex). HSP60 levels were significantly associated with early atherogenesis, both in the entire population (multivariate odds ratio, for a comparison between quintile group V versus I+II: 2.0 [1.2 to 3.5] and the subgroup free of atherosclerosis at the 1995 baseline: 3.8 [1.6 to 8.9]). The risk of early atherogenesis was additionally amplified when high-sHSP60 and chronic infection were present together."

Detection of Chlamydia pneumoniae and Helicobacter pylori in atherosclerotic plaques of carotid artery by polymerase chain reaction. M Kaplan, SS Yavuz, B Cinar, V Koksal, MS Kut, F Yapici, H Gercekoglu, MM Demirtas. Int J Infect Dis 2006 Mar;10(2):116-123. "C. pneumoniae DNA was detected in 16 of 52 (30.8%) atherosclerotic plaques and 1 of 52 (1.9%) macroscopically healthy ascending aorta wall specimens (P < 0.001). H. pylori DNA was detected in 9 of 52 (17.3%) atherosclerotic plaques and none of the controls (P = 0.003)."

Seropositivity to Chlamydia pneumoniae is associated with risk of first ischemic stroke. MS Elkind, ML Tondella, DR Feikin, BS Fields, S Homma, MR Di Tullio. Stroke 2006 Mar;37(3):790-5. "Elevated C pneumoniae IgA titers were associated with increased risk of ischemic stroke after adjusting for hypertension, diabetes mellitus, current cigarette use, atrial fibrillation, and levels of high-density lipoprotein and low-density lipoprotein (adjusted OR, 1.5; 95% CI, 1.0 to 2.2)." [Note- UN-adjusted odds ratios should be presented, because adjustment is a fraud -cast.]

Elevated levels of anti-Chlamydia pneumoniae IgA and IgG antibodies in young adults with ischemic stroke. B Piechowski-Jóźwiak, A Mickielewicz, Z Gaciong, H Berent, H Kwieciński. Acta Neurol Scand 2007 Sep;116(3):144-149. 94 patients (<55 years) with ischemic stroke and 103 controls. "Mean IgA and IgG indices were higher in stroke patients vs controls (IgA: 1.40 vs 0.56; P < 0.001; IgG: 0.85 vs. 0.78; P < 0.003). The IgA seropositivity was associated with stroke risk (11.92; 5.94-23.92; P < 0.001) as well as IgG seropositivity was (2.31; 1.15-4.61; P < 0.016). Seropositivity assessed with combined IgA and IgG indices was associated with increased stroke risk (OR 9.35; 95% CI 4.78-18.29; P < 0.0001). After controlling for age and sex, the IgA seropositivity yielded a significantly adjusted OR for stroke (8.95; 4.44-18.07; P < 0.002), while IgG seropositivity did not (0.85; 0.53-1.63)."

Piechowski-Jóźwiak - Acta Neurol Scand 2007 abstract / PubMed

Chlamydia pneumoniae seropositivity in aetiological subtypes of brain infarction and carotid atherosclerosis: a case control study. S Alamowitch, J Labreuche, PJ Touboul, F Eb, P Amarenco; GENIC Investigators. J Neurol Neurosurg Psychiatry 2008 Feb;79(2):147-151. 483 brain infarction cases and 483 controls. "IgA seropositivity increased the BI risk in patients without hypertension (adjusted OR 2.79, 95% CI 1.15 to 6.74)."

Mechanisms

Emergence of a CD4+CD28- granzyme B+, cytomegalovirus-specific T cell subset after recovery of primary cytomegalovirus infection. EM van Leeuwen, EB Remmerswaal, MT Vossen, AT Rowshani, PM Wertheim-van Dillen, RA van Lier, IJ ten Berge. J Immunol 2004 Aug 1;173(3):1834-1841. "In this study, we show that in primary CMV infections, CD4(+)CD28(-) T cells emerge just after cessation of the viral load, indicating that infection with CMV triggers the formation of CD4(+)CD28(-) T cells. In line with this, we found these cells only in CMV-infected persons [emphasis added]. CD4(+)CD28(-) cells had an Ag-primed phenotype and expressed the cytolytic molecules granzyme B and perforin. Importantly, CD4(+)CD28(-) cells were to a large extent CMV-specific because proliferation was only induced by CMV-Ag, but not by recall Ags such as purified protein derivative or tetanus toxoid. CD4(+)CD28(-) cells only produced IFN-gamma after stimulation with CMV-Ag, whereas CD4(+)CD28(+) cells also produced IFN-gamma in response to varicella-zoster virus and purified protein derivative. Thus, CD4(+)CD28(-) T cells emerge as a consequence of CMV infection."

Elevated pro-inflammatory CD4+CD28- lymphocytes and stroke recurrence and death. ZG Nadareishvili, H Li, V Wright, D Maric, S Warach, JM Hallenbeck, J Dambrosia, JL Barker, AE Baird. Neurology 2004 Oct 26;63(8):1446-1451. 106 patients followed for one year; 10 recurrent strokes and 17 deaths occurred. "Stroke recurrence/death rates were significantly associated with increasing CD4+CD28- counts, rising from 14.2% in patients with CD4+CD28- levels of <1.0 to 48.1% for those with CD4+CD28- counts of >8.0% (p = 0.003, Cochran linear test of trend). Higher CD4+CD28- counts were also present in patients with a history of prior stroke (p = 0.03). After adjustment for age, admission NIH Stroke Scale score, prior stroke, and atrial fibrillation, CD4+CD28- counts of >8.0% were associated with a cumulative hazard ratio of 5.81 (95% CI: 1.58 to 21.32) for stroke recurrence or death."

Chlamydia pneumoniae in foci of "early" calcification of the tunica media in arteriosclerotic arteries: an incidental presence? YV Bobryshev, RS Lord, D Tran. Am J Physiol Heart Circ Physiol 2006 Apr;290(4):H1510-9. In carotid artery segments obtained by endarterectomy from 60 patients, "Medial calcification occurred in 10 of 17 (58.8%) C. pneumoniae double-positive arterial specimens, but no medial calcification was observed in any of 22 C. pneumoniae double-negative arterial specimens. Electron microscopy indicated C. pneumoniae in smooth muscle cells (SMCs) in foci of medial calcification. Medial SMCs showing damage to the cytoplasm and basement membrane contained the structures with the appearance of elementary, reticulate, and aberrant bodies of C. pneumoniae."

Unchecked CD70 expression on T cells lowers threshold for T cell activation in rheumatoid arthritis. WW Lee, ZZ Yang, G Li, CM Weyand, JJ Goronzy. J Immunol 2007 Aug 15;179(4):2609-2615. Expression of CD70 was the most striking difference between CD4(+)CD28(-) and CD4(+)CD28(+) T cells; and "CD70 on bystander CD4(+)CD28(-) T cells functioned by lowering the threshold for T cell activation."

New Test For C-Reactive Protein Identifies Patients With 11-Fold Higher Risk For Stroke

New Blood Test May Improve Risk Assessment for Ischemic Stroke in Middle Aged Adults. DGNews, Nov. 29, 2005. Re: C Ballantyne, R Hoogeveeen, H Bang, et al. Lipoprotein-associated phospholipase A2, high-sensitivity C-Reactive Protein, and Risk for Incident Ischemic Stroke in Middle-aged Men and Women in the Atherosclerosis Risk in Communities (ARIC) Study. Arch Intern Med 2005;165:1-7. "Individuals with the highest levels of both Lp-PLA2 and CRP had an 11.38-fold (95% CI 3.13-41.41) increased risk of suffering an ischemic stroke during the study, compared to individuals with the lowest levels of Lp-PLA2 and CRP. Notably, LDL-cholesterol levels did not differ between incident stroke cases and non-cases and, in fully adjusted models, LDL-cholesterol, HDL-cholesterol and triglycerides were not associated with increased risk for stroke consistent with previous reports."

Varicella Zoster Virus May Be An Underdiagnosed Cause of Stroke

Although herpes zoster is common in the elderly, none of these studies has considered its possible role in stroke.

See Also:

cast 03-08-08