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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of reported associations between increased bleeding tendency and systemically decreased alpha 2-antiplasmin in patients with systemic amyloid deposition we studied alpha 2-antiplasmin, fibrinogen, C-reactive protein and blood levels of locally produced endothelial hemostasis factors in the acute and quiescent phase in 16 patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D). None of the factors measured in the quiescent phase of the disease was abnormal. In the acute phase, shortly after a stroke, only factor VIII:Ag was evidently elevated. We concluded that systemic abnormalities in the part of the fibrinolysis system studied are not likely to be responsible for multifocal and recurrent cerebral hemorrhages in HCHWA-D. The role of an elevated factor VIII:Ag level in the acute phase is unclear.
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PMID:Hereditary cerebral hemorrhage with amyloidosis-Dutch type: a study of fibrinolysis. 161 71

Antibodies to cardiolipin were measured in 100 consecutive patients with first ever stroke, on admission and at three and six months after the acute event. One hundred healthy, age- and sex-matched, British elderly individuals were also screened for antibodies to cardiolipin as a control group. Elevated levels of anticardiolipin antibody (i.e. 5 SD above the laboratory control mean) were present in none of the control group, but in 21 per cent of the patients with stroke. Thirteen of these 21 patients (62 per cent) died within three months, compared to 17 (21.5 per cent) of the seventy-nine patients without elevated levels of anticardiolipin antibodies (p less than 0.001). Six of the eight survivors with persistently elevated anticardiolipin antibodies had significant residual disability following stroke (Barthel score 0-9) compared to 11 of the 62 without (p less than 0.001). Two patients with initially raised anticardiolipin antibodies who became independent at six months showed a progressive decline in the level of these antibodies to normal. The presence of high levels of anticardiolipin antibody did not correlate with other recognized prognostic indices of stroke, except for incontinence. No correlation was noted between levels of antibody to cardiolipin, antinuclear factor, antibody to double-stranded DNA and C-reactive protein, either in the stroke patients or in the elderly control population. Hypertension was significantly more common in the patients with high anticardiolipin antibodies than in the rest of the patients in the stroke population (p = 0.33). There was no correlation between levels of anticardiolipin antibody and age. Anticardiolipin antibody may be considered as an independent prognostic marker for both mortality and clinical outcome after acute stroke.
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PMID:Antibodies to cardiolipin in stroke: association with mortality and functional recovery in patients without systemic lupus erythematosus. 192 75

The well-known coagulation inhibitors antithrombin and protein C, and the more recently described inhibitors, heparin cofactor II and extrinsic pathway inhibitor, were measured in plasma during a 7-day observation period, from patients with pneumonia (n = 13), and in stroke patients with infarction (n = 9) and haemorrhage (n = 9). In patients with pneumonia, elevated fibrinopeptide A levels and subnormal antithrombin and protein C levels suggested some degree of consumption of the inhibitors. Later, an increase was observed for all the inhibitors, but was most conspicuous for heparin cofactor II which reached high normal values. C-reactive protein, initially markedly elevated, decreased rapidly. This finding suggests that heparin cofactor II might act as a delayed acute phase reactant. In stroke patients only small, not statistically significant, changes occurred during the observation period, except for heparin cofactor II which increased in patients with haemorrhagic stroke.
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PMID:Coagulation inhibitor levels in pneumonia and stroke: changes due to consumption and acute phase reaction. 247 68

The clinical features and course of aortitis syndrome were studied in 11 women older than 40 years of age. The patients were Japanese women, mean age 57 +/- 6 years old, who were followed for 6.9 +/- 3.8 years. Data from 24 young patients were used for comparison. In the older patients, systemic hypertension (73%), calcification of the aorta (73%), left ventricular hypertrophy (92%) and cardiomegaly (82%) were frequent, whereas the erythrocyte sedimentation rate was normal in 5 patients and only slightly accelerated in 6. C-reactive protein was positive in 2. The incidence of cardiac involvement and inflammatory signs was significantly different from findings in the young patients. Aortic regurgitation (AR) (55%) was significantly more frequent and renal artery stenosis was not observed. Other arterial lesions revealed a pattern similar to those seen in the young patients. An irregular luminal surface, kinking and calcification were present in the lesions in the older patients. The survival rate at 5 years was 80%. Five of 6 patients with AR had congestive heart failure, 4 of whom died. One died after a stroke. Thus, aortitis syndrome in older patients has a long course. There is usually an associated AR, renal artery stenosis is rare and other arterial lesions do not change a great deal. The prognosis may be good, but depends on the association of AR.
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PMID:Clinical features and course of aortitis syndrome in Japanese women older than 40 years. 614 41

There are approximately 20,000 excess deaths from cardiovascular disease each winter in England and Wales. The reasons for the excess have not been fully elucidated. For one year, we studied 96 men and women aged 65-74 living in their own homes in order to examine seasonal variation in plasma fibrinogen and factor VII clotting activity (FVIIc), and to investigate relationships with infection and other cardiovascular-disease risk factors. Both fibrinogen and FVIIc plasma values were greater in winter with estimated winter-summer differences (confidence intervals) of 0.13 (0.05-0.20) g/L for fibrinogen and 4.2 (1.2-7.1)% of standard for FVIIc. These differences could account for 15% and 9% increases in ischaemic heart disease risk in winter respectively. After adjustment for confounding by season, fibrinogen was strongly related to neutrophil count (p < 0.0001), C-reactive protein (p < 0.0001), alpha 1-antichymotrypsin (p < 0.0001), and self-reported cough (p < 0.0001) and coryza (p = 0.0004), but not to ambient temperature. Therefore, we suggest that seasonal variation in fibrinogen might be induced by winter respiratory infections via activation of the acute phase response. Seasonal variations in the cardiovascular risk factors fibrinogen and FVIIc provide further possible explanations for the marked seasonal variation in death from ischaemic heart disease and stroke in the elderly.
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PMID:Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease. 790 26

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked for using an enzyme-linked immunosorbent assay (ELISA) in 19 patients with giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meeting Bird's criteria) and in three patients with isolated polymyalgia rheumatica. IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two patients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG antiphospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients with anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinical (n = 2) or histologic (n = 4) evidence of giant cell arteritis. None of the three patients with polymyalgia rheumatica but no giant cell arteritis had anti-cardiolipin or anti-beta 2 glycoprotein I antibodies. The VDRL was negative in the 14 patients who had this test. Tests for lupus anticoagulant were performed routinely, always with negative results. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the erythrocyte sedimentation rate (p < 0.006) and for serum C-reactive protein (p < 0.03) and fibrinogen values (p = 0.05), and a trend toward higher platelet counts, as compared to those who tested negative for anticardiolipin antibody. The mean daily prednisone dose at the time of sampling was significantly lower in giant cell arteritis patients with anti-cardiolipin antibodies (p < 0.05); this difference may account for the apparent correlation between anti-cardiolipin antibodies and laboratory markers for inflammation. These data, as well as findings from serial measurements, suggest that anti-cardiolipin antibodies are present early in the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg prednisone per day. In this study, only one patient without anticardiolipin antibodies developed a cerebrovascular accident. Positive tests for anti-cardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomitant giant cell arteritis, which is usually symptomatic.
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PMID:Antibodies to cardiolipin and beta 2 glycoprotein I in patients with polymyalgia rheumatica and giant cell arteritis. 873 42

Proinflammatory cytokines play an eminent role in pathophysiology of infection and inflammation. Their actual clinical importance is, however, uncertain. In this study, we tested the hypothesis that inflammatory cytokines could be useful in detection of infections in high-risk patients. We prospectively studied the diagnostic value of determination of concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and the 55- and 75-kd soluble TNF receptors (sTNFR-p55 and sTNFR-p75) in detection of nosocomial infections in 52 patients with acute ischemic stroke, as an exemplary high-risk group, and compared these findings to those of conventional inflammatory indicators of inflammation (C-reactive protein and leukocyte count). After 1 week of hospitalization, 27% of the patients had minor or moderately severe nosocomial infections. This subpopulation exhibited significantly increased concentrations of IL-6 and sTNFR-p55 but not of IL-1beta, TNF-alpha, or sTNFR-p75. As expected, levels of C-reactive protein and leukocytes were increased in infected patients. The sensitivity and specificity for detection of nosocomial infections at day 7 of hospitalization was highest for IL-6, followed by C-reactive protein and the leukocyte count. The data suggest that the proinflammatory cytokine IL-6, in addition to its considerable pathophysiologic importance in systemic inflammation, may be valuable in detection of infections in high-risk patients.
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PMID:Proinflammatory cytokines: indicators of infection in high-risk patients. 939 Jun 42

Traditional risk factors, e.g. hyperlipidemia, cigarette consumption, blood pressure, family history, and diabetes, predict < 50% of all future cardiovascular events. This paper reviews the use of novel hemostatic and thrombotic markers, such as intrinsic fibrinolysis and systemic micro-inflammation, for the prediction of the risk of arterial thrombotic disease. It has been hypothesized that relative abnormalities in the hemostatic and thrombotic systems are common on a population basis, and that they predispose certain individuals to clinically pathologic thrombosis. Abnormal levels of fibrinolytic parameters have been shown to predict future cardiovascular events, and tissue-type plasminogen activator antigen appears to be the most useful of these markers. Low-grade chronic inflammation may play an important role in atherogenesis. Of the newer inflammatory parameters, C-reactive protein has been the best studied and evidence suggests that elevated levels of C-reactive protein can predict the future risk of both myocardial infarction and stroke, both in healthy individuals and in patients with known coronary artery disease. Results from clinical trials to evaluate whether modification of novel risk factors results in a net clinical benefit are limited at present. However, novel markers will probably provide new directions in both thrombosis research and disease prevention.
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PMID:Intrinsic fibrinolytic capacity and systemic inflammation: novel risk factors for arterial thrombotic disease. 943 52

An increasing body of evidence has linked infections to atherosclerosis and thrombosis. Herpesviruses cause atherosclerosis in experimental animals. Herpesviruses can also be detected in atherosclerotic lesions in humans. Cytomegalovirus may play a role in arteriosclerosis in transplanted hearts, and this virus, together with tumor suppressor protein p53, can be found in restenosis lesions following angioplasty. Chlamydia pneumoniae and dental infections are associated with coronary heart disease in cross-sectional and longitudinal studies, and preceding respiratory infections are associated with ischemic stroke. Infections may favor formation of atherosclerosis and thrombosis by elevation of blood levels of fibrinogen, leukocytes, clotting factor, and cytokines and by alteration of the metabolism and functions of endothelial cells and monocyte macrophages. Low-grade infections may also be one of the causes of the inflammatory reaction observed in atherosclerotic lesions and acute ischemic symptoms, reflected in elevated levels of C-reactive protein. These observations warrant further studies in this field.
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PMID:Role of infection as a risk factor for atherosclerosis, myocardial infarction, and stroke. 952 51

Activation of blood coagulation and fibrinolysis has previously been detected in stroke patients. It is unknown, however, what factors contribute to the acceleration of coagulation reactions, especially in cases where no obvious predisposing factors exist. We therefore postulated and tested the hypothesis that in such patients monocytes may trigger the pathway leading to thrombosis by expressing tissue factor (TF). TF antigen was determined in 48 patients and 40 controls by flow cytometry using an indirect immunofluorescent technique. TF antigen expression was significantly increased on monocytes in young stroke patients in both the acute (p < 0.01) and chronic (p < 0.05) phases of the disease. The TF antigen also possessed functional activity, quantitated by a one-stage clotting assay. TF expression on monocytes was not associated with an elevation in C-reactive protein values. In both acute and chronic phases, blood coagulation activation markers, e.g. the thrombin-antithrombin complex and F1 + 2 fragments, were significantly elevated. However, in the acute phase D-dimer levels were similar to those in controls and were only elevated in the chronic phase of the disease (p < 0.05). In conclusion, in cerebral ischemia TF expression on monocytes suggests enhanced activation of blood coagulation and subsequent fibrinolysis.
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PMID:Monocytes express tissue factor in young patients with cerebral ischemia. 968 64


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