A systemic review of the risk factors for cervical artery dissection.
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Humans↗
Biomedical subjects
Florian Buggle
Publications and source records attributed to Florian Buggle.
Inflammatory response after acute ischemic stroke.
BACKGROUND AND PURPOSE: This study aimed to characterize the time course of inflammatory parameters after acute ischemic stroke. METHODS: We serially determined high sensitivity C-reactive protein (CRP), fibrinogen, and leukocyte counts at 10 time points between days 1 and 90 after ischemic stroke and in control subjects. RESULTS: CRP did not significantly change, whereas fibrinogen increased after stroke. At all time points, CRP and fibrinogen were higher than in healthy control subjects, but not risk factor control subjects. The leukocyte count declined after stroke and was significantly elevated as compared to both control groups only on day 1 but not later. NIHSS levels were positively correlated with CRP and fibrinogen at all time points. Larger infarcts were associated with a higher CRP and leukocyte counts on day 90. Treatment with aspirin was associated with lower values for all three inflammatory parameters in the subacute phase after ischemia. CONCLUSIONS: The course after stroke was different between the parameters of inflammation. Only the leukocytes followed the paradigm of an acute phase response.
Aged↗
Influenza vaccination is associated with a reduced risk of stroke.
BACKGROUND AND PURPOSE: Vascular death rates and hospitalizations for stroke are increased during influenza epidemics. Influenza vaccination may prevent stroke. We investigated whether influenza vaccination is associated independently with reduced odds of stroke and whether effects are confined to stroke subgroups and winter seasons and shared by other vaccinations. METHODS: During 18 months, we performed standardized interviews assessing vaccination status, risk factors, health-related behavior, and socioeconomic factors in 370 consecutive patients with ischemic or hemorrhagic stroke or transient ischemic attack (TIA) and 370 age- and sex-matched control subjects selected randomly from the population. RESULTS: Influenza vaccination during the last vaccination campaign was less common in patients (19.2%) than control subjects (31.4%; P<0.0001). After adjustment for vascular risk factors, education, health-related behavior and other factors, influenza vaccination (odds ratio [OR], 0.46; 95% CI, 0.28 to 0.77) but not other combined recent vaccinations (OR, 0.80; 95% CI, 0.42 to 1.43) were associated with reduced odds of stroke/TIA. Significant effects were found in men, older subjects (>65 years), subjects with previous vascular diseases, and regarding ischemic stroke; nonsignificant trends existed in women, younger subjects, and regarding hemorrhagic stroke. In etiologic subgroups of cerebral ischemia, similar effects were found. No protective effects were found during summer months; however, results also varied considerably between both winter seasons examined. CONCLUSIONS: These results support the hypothesis that influenza vaccination may be associated with reduced stroke risk. However, residual confounding cannot be excluded, and interventional studies are required to evaluate the role of influenza vaccination in stroke prevention.
Age Factors↗
Association between cerebral ischemia and cytotoxin-associated gene-A-bearing strains of Helicobacter pylori.
BACKGROUND AND PURPOSE: Studies on Helicobacter pylori infection and risk of ischemic stroke yielded variable results. Infection with more virulent H. pylori strains, such as cytotoxin-associated gene-A (CagA)-bearing strains, may be of particular relevance for ischemic diseases. We investigated whether H. pylori and CagA seropositivity are independent risk factors for cerebral ischemia or its etiologic subtypes. METHODS: We determined IgG antibodies against H. pylori and CagA protein (enzyme immunoassays) in 190 patients with acute cerebral ischemia and in 229 age- and sex-matched control subjects selected randomly from the general population. RESULTS: CagA seropositivity was more common in patients (114/190; 60.0%) than in control subjects (99/229; 43.2%; odds ratio, 1.97; 95% CI, 1.33 to 2.91; P<0.001). This result remained significant after adjustment for age, sex, vascular risk factors and diseases, and childhood and adult social status (odds ratio, 1.84; 95% CI, 1.13 to 3.00; P=0.015). Subgroup analyses yielded similar results in all etiologic stroke subtypes. In contrast, H. pylori seropositivity in general was not associated with increased risk of stroke or its etiologic subtypes. CONCLUSIONS: Our results support the hypothesis of an association between infection with CagA-positive H. pylori strains and acute cerebral ischemia.
Adult↗
Leukocyte count as an independent predictor of recurrent ischemic events.
BACKGROUND AND PURPOSE: Inflammatory markers predict first-time ischemic events. We investigated whether leukocyte and differential counts predict recurrent events and ischemic events in high-risk populations, and whether such events are preceded by acutely exacerbated inflammation. METHODS: We studied 18 558 patients with ischemic stroke, myocardial infarction, or peripheral arterial disease who participated in the trial of Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE), a study that compared the occurrence of ischemic stroke, myocardial infarction, or vascular death under randomized treatment with aspirin or clopidogrel. Leukocyte counts were frequently assessed during followup. RESULTS: Compared with the quartile with lowest leukocyte counts at baseline (<5.9x10(9)/L), patients in the top quartile (>8.2x10(9)/L) had higher risks for ischemic stroke (relative risk 1.30; P=0.007), myocardial infarction (relative risk 1.56, P<0.001), and vascular death (relative risk 1.51; P<0.001) after adjustment for other risk factors. Neutrophil counts contributed most to increased risk. Assessments of regression dilution effects based on replicate measurements show that these risk associations may underestimate the real associations by 30 to 50%. Treatment with aspirin or clopidogrel did not influence predictive effects by leukocytes. In the week before a recurrent event, but not at earlier time points, the leukocyte count was significantly increased over baseline levels (n=211; mean difference +0.46x10(9)/L; P=0.005). CONCLUSIONS: Leukocyte counts and mainly neutrophil counts are independently associated with ischemic events in these high-risk populations. An increase of leukocyte counts over baseline levels heralds a period of increased risk lasting about one week.
Aspirin↗
Periodontal disease as a risk factor for ischemic stroke.
BACKGROUND AND PURPOSE: Chronic infectious diseases may increase the risk of stroke. We investigated whether periodontal disease, including periodontitis and gingivitis, is a risk factor for cerebral ischemia. METHODS: We performed a case-control study with 303 patients examined within 7 days after acute ischemic stroke or transient ischemic attack, 300 population controls, and 168 hospital controls with nonvascular and noninflammatory neurological diseases. All subjects received a complete clinical and radiographic dental examination. The individual mean clinical attachment loss measured at 4 sites per tooth served as the main indicator for periodontitis. RESULTS: Patients had higher clinical attachment loss than population (P<0.001) and hospital (P=0.010) controls. After adjustment for age, sex, number of teeth, vascular risk factors and diseases, childhood and adult socioeconomic conditions, and lifestyle factors, the risk of cerebral ischemia increased with more severe periodontitis. Subjects with severe periodontitis (mean clinical attachment loss >6 mm) had a 4.3-times-higher (95% confidence interval, 1.85 to 10.2) risk of cerebral ischemia than subjects with mild or without periodontitis (<or=3 mm). Severe periodontitis was a risk factor in men but not women and in younger (<60 years) but not older subjects. Periodontitis increased the risk of cerebral ischemia caused by large-artery atherosclerosis, cardioembolism, and cryptogenic etiology. Gingivitis and severe radiologic bone loss were also independently associated with the risk of cerebral ischemia, whereas caries was not. CONCLUSIONS: Our study indicates that periodontal disease, a treatable condition, is an independent risk factor for cerebral ischemia in men and younger subjects.
Acute Disease↗
The association of gingivitis and periodontitis with ischemic stroke.
OBJECTIVES: The aim of this study was to assess the associations of different periodontal parameters with cerebral ischemia. METHODS: In a case-control study, 303 consecutive patients with ischemic stroke or transient ischemic attack, and 300 representative population controls received a complete clinical and radiographic dental examination. Patients were examined on average 3 days after ischemia. The individual mean clinical attachment loss measured at four sites per tooth was used as indicator variable for periodontitis. RESULTS: Patients had higher clinical attachment loss than population (p<0.001). After adjustment for age, gender, number of teeth, vascular risk factors and diseases, childhood and adult socioeconomic conditions and lifestyle factors, a mean clinical attachment loss >6 mm had a 7.4 times (95% confidence interval 1.55-15.3) a gingival index >1.2 a 18.3 times (5.84-57.26) and a radiographic bone loss a 3.6 times (1.58-8.28) higher risk of cerebral ischemia than subjects without periodontitis or gingivitis, respectively. CONCLUSION: Periodontitis is an independent risk factor for cerebral ischemia and acute exacerbation of inflammatory processes in the periodontium might be a trigger for the event of cerebral ischemia.
Adolescent↗
Platelet function under aspirin, clopidogrel, and both after ischemic stroke: a case-crossover study.
BACKGROUND AND PURPOSE: Combined antiplatelet agents may offer additive protection over single drugs after stroke. We investigated whether platelet activation is reduced under combined aspirin and clopidogrel compared with each drug alone. METHODS: In a case-crossover study, 31 patients with previous atherothrombotic or lacunar stroke who were treated with aspirin (100 to 300 mg/d) received clopidogrel (75 mg/d) and both aspirin and clopidogrel for 4 weeks. Platelet function in whole blood was studied after each treatment period and in healthy control subjects to assess activation-dependent antigens CD62p and CD63 by flow cytometry and collagen/epinephrine (CEPI-CT) and collagen/ADP (CADP-CT) closure times with the platelet function analyzer PFA-100, which investigates platelet-related function under shear stress. RESULTS: CD62p expression and CD63 expression were not different under the 3 treatment regimens. CD63 but not CD62p expression was lower in control subjects than in stroke patients regardless of the antiplatelet treatment (P<0.05). CEPI-CT was prolonged under aspirin and aspirin plus clopidogrel compared with clopidogrel monotherapy (P<0.0001). CADP-CT was longer under combination therapy than under aspirin (P=0.0009) or clopidogrel (P=0.0074) or in control subjects (P=0.0010), mainly because of strong prolongation in a patient subgroup (28%). CONCLUSIONS: CD63 expression reflecting the release of platelet lysosomes is consistently increased after stroke and incompletely suppressed by treatment with aspirin, clopidogrel, or both. The strong prolongation of CADP-CT under combined aspirin and clopidogrel in a patient subgroup may indicate a lower risk of thrombosis but also a higher risk of hemorrhage. The predictive value of platelet activation parameters requires investigation in prospective studies.
Antigens, CD↗
Lack of evidence for pulmonary venous thrombosis in cryptogenic stroke: a magnetic resonance angiography study.
BACKGROUND: Even after extensive evaluation, the etiology of ischemic stroke remains undefined in a considerable proportion of cases, suggesting that causes of stroke may exist that have not yet been established. We tested the hypothesis that pulmonary venous thrombosis (PVT) is a potential source of brain embolism in patients with cryptogenic stroke. SUMMARY OF REPORT: Within 7 days after mild to moderately severe ischemic stroke or transient ischemic attack, 18 patients (9 women, 9 men; mean age, 48 years) were studied in whom the etiology remained undefined despite complete workup. All patients received high-resolution pulmonary venography with the use of multiple-bolus, multiphase, 3-dimensional, gadolinium-enhanced MR angiography (MRA). Overall quality of the MRA was good in 14 and insufficient in 4 patients, mainly as a result of breathing artifacts. Visualization of the main and segmental veins and evaluability of their patency were good for most right pulmonary veins but often inadequate for left pulmonary veins, particularly for those in the left lower lobe. There was no evidence for PVT in any of the sufficiently visualized pulmonary veins. CONCLUSIONS: The results do not support the hypothesis of PVT as a contributor to the etiology of ischemic stroke. However, the study was limited regarding scan volume, spatial discrimination, patient selection, and delay between ischemia and MRA. Therefore, further investigations, including postmortem studies, are needed to resolve the question of whether PVT may contribute to ischemic stroke.
Adult↗
Course of platelet activation markers after ischemic stroke.
BACKGROUND AND PURPOSE: The aim of this study was to evaluate the time course of platelet activation after ischemic stroke and to investigate whether platelet activation and inflammation are correlated with each other. METHODS: We serially determined expression of p-selectin (CD62p) and lysosome-associated membrane protein (CD63) by platelets using flow cytometry at 10 time points between days 1 and 90 in patients after ischemic stroke (n=50), in healthy subjects (n=30), and in risk factor control subjects (n=20). Furthermore, we correlated leukocyte count, C-reactive protein, and fibrinogen levels with platelet activation markers. RESULTS: CD62p and CD63 expression was higher on day 1 after stroke than in both control groups (P<0.005 for both). CD62p expression rapidly declined, whereas CD63 expression remained significantly elevated until day 90. Stroke severity and different medication for secondary stroke prevention did not influence CD62p or CD63 expression. Platelet activation markers and inflammatory parameters were not correlated with each other at any time point after stroke. CONCLUSIONS: The initial increase in both CD62p and CD63 expression by platelets is followed by a differential regulation of both parameters after stroke. The rapid decrease in CD62p expression may be caused by shedding from the cell surface. Its persistent elevation makes CD63 a good candidate for studies on predictors for stroke recurrence. Our findings suggest that the expression of CD62p and CD63 by platelets is regulated independently from inflammatory indexes.
Aged↗