Reduction of body temperature with paracetamol in patients with acute stroke: randomised clinical trials are needed.
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Acetaminophen↗
Biomedical subjects
Ale Algra
Publications and source records attributed to Ale Algra.
Fibrinogen concentration and risk of ischemic stroke and acute coronary events in 5113 patients with transient ischemic attack and minor ischemic stroke.
BACKGROUND AND PURPOSE: Fibrinogen is an independent risk factor for coronary events in population-based studies and in patients with coronary heart disease, but there is uncertainty about prediction of stroke, particularly in secondary prevention. METHODS: We studied unpublished data from 3 prospective studies of patients with recent transient ischemic attack (TIA) or minor ischemic stroke: the United Kingdom TIA Aspirin (UK-TIA) trial (n=1860); the Dutch TIA trial (n=2960); and the Oxford TIA Study (n=293). By separate and pooled analysis, we used Cox models to determine the relationship between fibrinogen and risk of ischemic stroke and other vascular events during 23,272 patient-years of follow-up and adjusted for other risk factors. RESULTS: There was no significant heterogeneity in fibrinogen risk associations between studies. Fibrinogen predicted subsequent ischemic stroke, with a pooled hazard ratio (HR) for values above the median of 1.34 (95% CI, 1.13 to 1.60; P=0.001). The association tended to be stronger in patients with nonlacunar (HR=1.42; 95% CI, 1.13 to 1.78; P=0.002) than lacunar syndromes (HR=1.09; 95% CI, 0.80 to 1.49; P=0.58), but was not significantly so (P=0.18). There was no association with hemorrhagic stroke (adjusted HR=1.09; 95% CI, 0.55 to 2.17; P=0.81). Fibrinogen predicted acute coronary events (adjusted HR=1.42; 95% CI, 1.18 to 1.70; P<0.001) and all ischemic vascular events (adjusted HR=1.31; 95% CI, 1.15 to 1.49; P<0.001), but not nonvascular death (adjusted HR=1.24; 95% CI, 0.90 to 1.70; P=0.19). CONCLUSIONS: In patients with a previous TIA or ischemic stroke, risks of recurrent ischemic stroke and acute coronary events increase linearly with fibrinogen levels, but the relationships are weaker than in some previous population-based studies.
Aged↗
Underfunding of stroke research: a Europe-wide problem.
BACKGROUND AND PURPOSE: Previous studies in the United States and the United Kingdom have shown that stroke research is underfunded compared with coronary heart disease (CHD) and cancer research despite the high clinical and financial burden of stroke. We aimed to determine whether underfunding of stroke research is a Europe-wide problem. METHODS: Data for the financial year 2000 to 2001 were collected from 9 different European countries. Information on stroke, CHD, and cancer research funding awarded by disease-specific charities and nondisease-specific charity or government- funded organizations was obtained from annual reports, web sites, and by direct communication with organizations. RESULTS: There was marked and consistent underfunding of stroke research in all the countries studied. Stroke funding as a percentage of the total funding for stroke, CHD, and cancer was uniformly low, ranging from 2% to 11%. Funding for stroke was less than funding for cancer, usually by a factor of > or =10. In every country except Turkey, funding for stroke research was less than that for CHD. CONCLUSIONS: This study confirms that stroke research is grossly underfunded, compared with CHD and cancer, throughout Europe. Similar data have been obtained from the United States suggesting that relative underfunding of stroke research is likely to be a worldwide phenomenon.
Biomedical Research↗
Electrocardiographic abnormalities and serum magnesium in patients with subarachnoid hemorrhage.
BACKGROUND AND PURPOSE: ECG abnormalities and hypomagnesemia frequently occur after aneurysmal subarachnoid hemorrhage (SAH). Because hypomagnesemia is associated with several ECG abnormalities, we studied whether hypomagnesemia mediates ECG abnormalities after SAH. METHODS: We prospectively studied a consecutive series of 62 patients admitted within 72 hours after aneurysmal SAH. A standard 12-lead ECG and serum magnesium measurement were routinely performed at admission. The relationship between serum magnesium and ECG abnormalities was assessed with linear regression analysis and the Mann-Whitney test in case of dichotomized ECG abnormalities. RESULTS: Hypomagnesemia was present in 23 patients (37%), and 38 patients (61%) had a long QTc duration. Low serum magnesium was related to a long PR interval (P=0.001) and a shorter QTc interval (P=0.004). Adjustment for World Federation of Neurological Surgeons score, hydrocephalus, and the amount of cisternal and ventricular blood did not influence these relations. CONCLUSIONS: In patients with SAH, lower serum magnesium levels are related to less pronounced increase in the QTc interval. Although the direction of the relation was unexpected, decreased serum magnesium might be the missing link between SAH and ECG abnormalities.
Arrhythmias, Cardiac↗
Prevalence of the metabolic syndrome in patients with coronary heart disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm.
Metabolic syndrome patients are at increased risk for developing cardiovascular morbidity and mortality. The increasing prevalence of the metabolic syndrome in various asymptomatic populations has been well documented, however, limited information is available about the prevalence in manifest atherosclerotic vascular disease patients. The aim of this study is to determine the overall and gender-specific prevalence of the metabolic syndrome and its components in these patients. This cross-sectional survey of 1117 patients, aged 18-80 years, mean age 60+/-10 years, comprised patients with coronary heart disease (n=527), cerebrovascular disease (n=258), peripheral arterial disease (n=232) or abdominal aortic aneurysm (n=100). Metabolic syndrome was defined by Adult Treatment Panel III. The prevalence of the metabolic syndrome in the study population was 46%: 58% in PAD patients, 41% in CHD patients, 43% in CVD patients and 47% in AAA patients. Overall, women had a higher prevalence than men (56% versus 43%). Age did not influence the metabolic syndrome prevalence; crude odds ratios (crude OR) 1.00 (95% CI: 0.99-1.02). Our results demonstrate a high prevalence of the metabolic syndrome in patients with manifest atherosclerotic vascular disease. Screening for metabolic syndrome in patients with high risk for new vascular incidents may identify patients with even higher vascular risk and may direct anti-atherosclerotic treatment in order to prevent new vascular incidents in the same or another vascular bed.
Adolescent↗
The metabolic syndrome is associated with advanced vascular damage in patients with coronary heart disease, stroke, peripheral arterial disease or abdominal aortic aneurysm.
AIMS: The metabolic syndrome is associated with an increased risk of cardiovascular disease in patients without a cardiovascular history. We investigated whether the metabolic syndrome is related to the extent of vascular damage in patients with various manifestations of vascular disease. METHODS AND RESULTS: The study population of this cross-sectional survey consisted of 502 patients recently diagnosed with coronary heart disease (CHD), 236 with stroke, 218 with peripheral arterial disease (PAD) and 89 with abdominal aortic aneurysm (AAA). Metabolic syndrome was diagnosed according to Adult Treatment Panel III criteria. Carotid Intima Media Thickness (IMT), Ankle Brachial Pressure Index (ABPI) and albuminuria were used as non-invasive markers of vascular damage and adjusted for age and sex if appropriate. The prevalence of the metabolic syndrome in the study population was 45%. In PAD patients this was 57%; in CHD patients 40%, in stroke patients 43% and in AAA patients 45%. Patients with the metabolic syndrome had an increased mean IMT (0.98 vs 0.92mm, P-value <0.01), more often a decreased ABPI (14% vs 10%, P-value 0.06) and increased prevalence of albuminuria (20% vs 15%, P-value 0.03) compared to patients without this syndrome. An increase in the number of components of the metabolic syndrome was associated with an increase in mean IMT (P-value for trend <0.001), lower ABPI (P-value for trend <0.01) and higher prevalence albuminuria (P-value for trend <0.01). CONCLUSION: In patients with manifest vascular disease the presence of the metabolic syndrome is associated with advanced vascular damage.
Aortic Aneurysm, Abdominal↗
Classification of outcomes events in the Dutch TIA trial: prognostic value of accepted and rejected events.
OBJECTIVE: In large multicentre clinical trials adjudication of outcome events most often is done centrally. Some of these events would eventually be judged not to meet the criteria and hence would be rejected. If the classification procedures work correctly one would expect a higher risk of future vascular events after an 'accepted' rather than after a 'rejected event. In the present study we aimed at testing the adequacy of a classification procedure in a trial of patients with a transient ischemic attack (TIA) or minor ischemic stroke by comparing the further outcome between patients in whom a possible event was either rejected or accepted for the final analysis in this trial. RESEARCH DESIGN AND METHODS: The vascular outcome events were analysed in 3150 patients with TIA or minor stroke who participated in the Dutch TIA trial. We identified the patients with a first 'accepted' or 'rejected' non-fatal stroke or myocardial infarction (MI). In these two groups of patients we determined the occurrence of the subsequent vascular events (vascular death, stroke or MI). The incidence was compared with survival analysis techniques. RESULTS: Among 308 patients with a first nonfatal 'accepted' event in 81 (26.3%) a new vascular event occurred; among the 51 patients with a 'rejected' event there were 12 (23.5%) such events. The hazard ratio for new vascular events was 1.22 (95% CI 0.67-2.22). After multivariate adjustment for age, type of qualifying event, history of smoking, angina pectoris and myocardial infarction, and Rankin score > or = 3, the hazard ratio was 1.49 (95% CI 0.78-2.84). CONCLUSION: our study suggested that the adjudication process of outcome events in the Dutch TIA trial was done correctly because a trend towards a higher recurrence rate of vascular events among patients with 'accepted' outcome events was found.
Aged↗
Side of brain infarction and long-term risk of sudden death in patients with symptomatic carotid disease.
BACKGROUND AND PURPOSE: Current publications suggest increased risk of sudden death in experimental animals with acute right insular lesions and in patients with recent right-sided brain infarction, particularly if the insula is involved. METHODS: Using 3 different time definitions, we related long-term risk of sudden death to presence and side of brain infarction on the baseline brain scan and handedness in 2885 patients with symptomatic carotid disease. RESULTS: In 1295 patients without brain infarction, 5-year risk of sudden death was 5.3% (24-hour definition); in those with left-sided infarction (n=471), 8.8%; in those with right-sided infarction (n=477), 6.0%; and in those with bilateral infarction (n=535), 9.7%. After accounting for differences of other risk factors (eg, previous myocardial infarction) in Cox regression, adjusted hazard ratios (HRs) compared with no infarction were as follows: left-sided HR, 1.45 (95% confidence interval [CI], 1.00 to 2.10); right-sided HR, 0.96 (95% CI, 0.62 to 1.47); and bilateral HR, 1.40 (95% CI, 0.98 to 2.00). Insular infarction occurred in 41 patients; none died suddenly. Left-handed or ambidextrous patients (n=183) had a lower risk of sudden death than right-handers; the adjusted HR for left-handed or ambidextrous patients was 0.24 (95% Cl, 0.07 to 0.70). These results were essentially the same for the 10- and 60-minute definitions of sudden death. CONCLUSIONS: In the long-term, left-sided, not right-sided, brain infarction is associated with increased risk of sudden death. Left-handed or ambidextrous patients have a lower risk of sudden death than right-handed patients, suggesting a role for the brain.
Aged↗
Effect of second- and third-generation oral contraceptives on the protein C system in the absence or presence of the factor VLeiden mutation: a randomized trial.
A plausible mechanism to explain thrombotic risk differences associated with the use of second- and third-generation oral contraceptives (OCs), particularly in carriers of factor V(Leiden), is still lacking. In a double-blind trial, 51 women without and 35 women with factor V(Leiden) were randomized to either a second- (30 microg ethinylestradiol/150 microg levonorgestrel) or third- (30 microg ethinylestradiol/150 microg desogestrel) generation OC. After 2 cycles of use and a wash-out of 2 cycles, the participants continued with the corresponding progestagen-only preparation. Hemostatic variables that probe the activity of the anticoagulant protein C system were determined. Compared with levonorgestrel, desogestrel-containing OCs significantly decreased protein S and increased activated protein C (APC) resistance in both groups. OCs with desogestrel had the most pronounced effects in carriers of factor V(Leiden). Progestagen-only preparations caused changes of anticoagulant parameters opposite to those of combined OCs, which in a number of cases were more pronounced with levonorgestrel. Our data show that progestagens in combined OCs counteract the thrombotic effect of the estrogen component. The higher thrombotic risk associated with third-generation OCs compared with second-generation OCs may be explained by the fact that desogestrel appeared less antithrombotic than levonorgestrel, especially in women with factor V(Leiden).
Adolescent↗
Antifibrinolytic therapy for aneurysmal subarachnoid hemorrhage: a major update of a cochrane review.
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Antifibrinolytic Agents↗
Antiplatelet therapy in aneurysmal subarachnoid hemorrhage: a systematic review.
BACKGROUND AND PURPOSE: Observational studies suggest that platelet inhibitors reduce the risk of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage and thereby have a beneficial effect on clinical outcome. Robust evidence, however, is lacking. We performed a systematic meta-analysis to determine whether antiplatelet therapy has a beneficial effect after SAH. METHODS: We searched Medline and the Cochrane Library to identify all randomized controlled trials of antiplatelet drugs versus control and calculated relative risks with corresponding 95% confidence intervals (CIs) for poor outcome (dependence or death), the occurrence of DCI, and the occurrence of any intracranial hemorrhage. RESULTS: We included 5 trials totaling 699 patients. The overall relative risk for poor outcome was 0.87 (95% CI, 0.65 to 1.17); for the occurrence of DCI (reported in 3 of the 5 studies), 0.65 (95% CI, 0.47 to 0.89); and for the occurrence of intracranial hemorrhage, 1.19 (reported in 4 of the 5 studies) (95% CI, 0.76 to 1.85). CONCLUSIONS: Our data indicate that antiplatelet drugs reduce the risk of DCI in patients with subarachnoid hemorrhage. A randomized clinical trial is warranted to assess the effect on overall outcome.
Brain Ischemia↗
A 2-step strategy to reduce the need for methionine-loading tests to diagnose hyperhomocysteinemia.
An increased plasma homocysteine level may increase the risk of cardiovascular disease. The methionine-loading test is commonly used to detect additional subjects with hyperhomocysteinemia who have normal fasting levels of homocysteine but increased post-methionine-load levels. We developed a 2-step strategy to restrict the methionine-loading test to those subjects with intermediate fasting homocysteine levels to confirm the presence of hyperhomocysteinemia. Hyperhomocysteinemia was defined as a fasting plasma homocysteine level of 16.3 micro mol/L or greater in women and 18.8 micro mol/L or greater in men or an increase in plasma homocysteine level after methionine loading of more than 42.3 micro mol/L for both sexes. From the results in 201 patients, 50 years and younger, with manifest atherosclerosis who underwent a methionine-loading test, we derived cutoff points to define an intermediate group of patients who required a methionine-loading test for hyperhomocysteinemia to be ruled out. These cutoff points were validated in a different population of 275 cardiovascular patients of similar age. The prevalence of hyperhomocysteinemia was 30% in the derivation population and 24% in the validation population. To achieve a sensitivity of 90% in diagnosing hyperhomocysteinemia, we set cutoff points of 11.3 and 9.4 micro mol/L for men and women, respectively. When these cutoff points are applied, it is possible to avoid performing the methionine-loading test in 50% to 75% of subjects tested. With a 2-step strategy to diagnose hyperhomocysteinemia, a sensitivity of 90% for the diagnosis of hyperhomocysteinemia can be achieved, and the need for the methionine-loading test is reduced substantially, with 50% to 75% of subjects no longer needing it.
Adult↗
Functional health and well-being of relatively young women with peripheral arterial disease is decreased but stable after diagnosis.
OBJECTIVE: This study was undertaken to investigate the extent to which health-related quality of life (HQOL) is reduced in young women with peripheral arterial disease (PAD) compared with age-matched and gender-matched control subjects. Moreover, potential determinants of HQOL in young women with PAD were studied, ie, traditional cardiovascular risk factors, location of stenosis and time since diagnosis. METHODS: This was a population-based case-control study. Subjects were 208 young (<50 years) women with PAD diagnosed at angiography and 471 population-based age-matched and gender-matched control subjects. All participants completed the RAND-36 questionnaire, which produces a HQOL profile. The questionnaire contains 36 items that assess 8 domains of HQOL. Each domain is given a mean score ranging from 0 to 100, with higher scores indicative of better quality of life. RESULTS: PAD had a deleterious effect on HQOL in young women. Ability to deal with the physical requirements of daily life was affected, and physical capabilities limited activity to a considerable extent. Mean differences observed for 2 domains, ie, Physical functioning and Role-physical, were -25.1 (95% confidence interval [CI], -28.8,-21.4) and -22.5 (95% CI, -28.9,-16.0). Within the group of young women with PAD, HQOL did not depend on age, smoking, hypercholesterolemia, or education. However, women with hyperglycemia, hypertension, or increased body mass index scored lower on 1 or more domains of RAND-36. Location of stenosis was also related to HQOL; patients with more proximal stenosis scored slightly higher on the domain Physical functioning, compared with women with more distal stenosis. Time (0-10 years) between diagnosis (1990-1999) and when RAND-36 was filled out (2000) is related to score on the Mental health domain; score increases over time. Scores on the other 7 domains of HQOL showed no significant relation to duration of disease. CONCLUSION: Quality of life in young women with PAD was statistically significant diminished for all domains of RAND-36 in comparison with HQOL in healthy age-matched control subjects. HQOL of patients with recently diagnosed PAD is comparable to that of patients in whom the diagnosis was made several years previously. Effective therapy might stabilize, albeit not improve, quality of life in this specific patient population.
Adult↗
Hyperhomocysteinemia and risk for peripheral arterial occlusive disease in young women.
OBJECTIVE: Few studies to date have examined the relationship between hyperhomocysteinemia and peripheral arterial occlusive disease (PAOD) in young women. In this study we assessed hyperhomocysteinemia as a risk factor for PAOD in young women. In addition, we evaluated the effect of joint exposure to hyperhomocysteinemia and traditional risk factors. METHODS: Two hundred twenty women, ages 18 to 49 years, with PAOD and 629 healthy women (control group) from a population-based case-control study filled out the same structured questionnaire and donated venous blood samples for determination of plasma homocysteine levels. Hyperhomocysteinemia was defined as nonfasting total plasma homocysteine level above the 90th percentile of the control range. RESULTS: Young women with hyperhomocysteinemia had a 2.5-fold (95% confidence interval [CI], 1.7-3.9) increased risk for PAOD. When presence of hyperhomocysteinemia was combined with presence of a traditional risk factor, relative risk strongly increased in smokers (odds ratio [OR], 18.9; 95% CI, 8.3-42.9) and in women with hypertension (OR, 10.3; 95% CI, 5.4-19.8), hypercholesterolemia (OR, 8.5; 95% CI, 4.2-17.1), and diabetes (OR, 8.9; 95% CI, 1.7-46.9). CONCLUSIONS: Hyperhomocysteinemia is a risk factor for PAOD in young women. There is a strong synergistic effect between hyperhomocysteinemia and all traditional vascular risk factors. Our findings may have implications for risk management in these young women.
Adolescent↗
Prothrombotic coagulation defects and cardiovascular risk factors in young women with acute myocardial infarction.
We investigated the effect of prothrombotic coagulation defects in combination with smoking and other conventional risk factors on the risk of myocardial infarction in young women. In 217 women with a first myocardial infarction before the age of 50 years and 763 healthy control women from a population-based case-control study, factor V Leiden and prothrombin 20210A status were determined. Data on major cardiovascular risk factors and oral contraceptive use were combined with the presence or absence of these prothrombotic mutations, and compared between patients and controls. The overall odds ratio for myocardial infarction in the presence of a coagulation defect was 1.1 [95% confidence interval (CI) 0.6-1.9]. The combination of a prothrombotic mutation and current smoking increased the risk of myocardial infarction 12-fold (95% CI 5.7-27) compared with non-smokers without a coagulation defect. Among women who smoked cigarettes, factor V Leiden presence versus absence increased the risk of myocardial infarction by 2.0 (95% CI 0.9-4.6), and prothrombin 20210A presence versus absence had an odds ratio of 1.0 (95% CI 0.3-3.5). We conclude that factor V Leiden and prothrombin 20210A do not add substantially to the overall risk of myocardial infarction in young women. However, in women who smoke, the presence of factor V Leiden increased the risk of myocardial infarction twofold.
Adult↗
Hypomagnesemia after aneurysmal subarachnoid hemorrhage.
OBJECTIVE: Hypomagnesemia frequently occurs in hospitalized patients, and it is associated with poor outcome. We assessed the frequency and time distribution of hypomagnesemia after aneurysmal subarachnoid hemorrhage (SAH) and its relationship to the severity of SAH, delayed cerebral ischemia (DCI), and outcome after 3 months. METHODS: Serum magnesium was measured in 107 consecutive patients admitted within 48 hours after SAH. Hypomagnesemia (serum magnesium <0.70 mmol/L) at admission was related to clinical and initial computed tomographic characteristics by means of the Mann-Whitney U test. Hypomagnesemia at admission and during the DCI onset period (Days 2-12) was related to the occurrence of DCI and hypomagnesemia at admission, and hypomagnesemia that occurred any time during the first 3 weeks after SAH was related to outcome. RESULTS: Hypomagnesemia at admission was found in 41 patients (38%) and was associated with more cisternal (P = 0.006) and ventricular (P = 0.005) blood, a longer duration of unconsciousness (P = 0.007), and a worse World Federation of Neurosurgical Societies scale score at admission (P = 0.001). The crude hazard ratio for DCI with hypomagnesemia at admission was 2.4 (95% confidence interval, 1.0-5.6), and after multivariate adjustment it was 1.9 (95% confidence interval, 0.7-4.7). The hazard ratio of hypomagnesemia from Days 2 to 12 for patients with DCI was 3.2 (range, 1.1-8.9) after multivariate adjustment. The crude odds ratio for poor outcome (Glasgow Outcome Scale score, 1-3) with hypomagnesemia at admission was 2.5 (range, 1.1-5.5). Hypomagnesemia at admission did not contribute to the prediction of outcome in the multivariate model. CONCLUSION: Hypomagnesemia is frequently present after SAH and is associated with severity of SAH. Hypomagnesemia occurring between Days 2 and 12 after SAH predicts DCI.
Aged↗
Sudden death.
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Autonomic Nervous System↗
Novel risk factors for peripheral arterial disease in young women.
PURPOSE: To investigate traditional and novel risk factors (homocysteine and C-reactive protein levels, and exposure to infections) for peripheral arterial disease in young women. SUBJECTS AND METHODS: In a multicenter, population-based, case-control study, 212 young women (mean [+/- SD] age, 48.2 +/- 7.0 years) with peripheral arterial disease and 475 healthy control women (mean age, 45.5 +/- 8.1 years) completed a standardized questionnaire and provided blood samples. Peripheral arterial disease was angiographically confirmed if a stenotic lesion (more than 50% reduction of the lumen) was present in at least one major peripheral artery. Hyperhomocysteinemia was defined as a nonfasting plasma homocysteine level exceeding the 90th percentile of the control group. History of infectious diseases was determined by questionnaire. RESULTS: Elevated C-reactive protein levels were associated with an increased likelihood of peripheral arterial disease (odds ratio [OR] = 3.9; 95% confidence interval [CI]: 1.8 to 8.5 for women in the third quartile; OR = 3.1; 95% CI: 1.4 to 6.8 for women in the fourth quartile; both comparisons with women in the first quartile). Hyperhomocysteinemia was not associated with a significantly increased risk of peripheral arterial disease (OR = 1.6; 95% CI: 0.9 to 3.0). A history of chickenpox, shingles, mumps, pneumonia, chronic bronchitis, peptic ulcer, or periodontitis was independently related to peripheral arterial disease, with adjusted odds ratios varying from 1.7 (95% CI: 1.0 to 3.1) for mumps to 3.4 (95% CI: 1.5 to 7.7) for peptic ulcer. The risk of peripheral arterial disease increased with the number of these infections; exposure to five or more infections increased the odds 3.7-fold (95% CI: 1.7 to 8.2). This association was not affected by the level of C-reactive protein. CONCLUSION: Our results do not support a strong relation between homocysteine and peripheral arterial disease in young women. However, an elevated C-reactive protein level and several types of symptomatic infection were associated with peripheral arterial disease.
Arteriosclerosis↗