Biomedical subjects

A Algra

Publications and source records attributed to A Algra.

At least 55 records · Page 3Linked to original sources

PubMed2005

Troponin I in predicting cardiac or pulmonary complications and outcome in subarachnoid haemorrhage.

BACKGROUND: Patients with aneurysmal subarachnoid haemorrhage (SAH) are at risk of cardiac and pulmonary complications. Troponin I (cTnI), a reliable marker of myocardial injury, is frequently raised after SAH. AIMS: To investigate the additional value of (cTnI) in predicting cardiac or pulmonary complications and outcome in patients with SAH. METHODS: Admission cTnI was measured in a prospective series of patients admitted within 24 hours of SAH. By means of univariate and multivariate logistic regression models the additional prognostic value of raised cTnI (>0.3 microg/litre) was investigated compared with established prognosticators (clinical condition on admission, age, and amount of blood on admission computed tomography) for predicting the occurrence of pulmonary oedema, pulmonary gas exchange abnormalities, rhythm disturbances, inadequate cardiac performance, a combination of these complications, and poor outcome. Area under the operator characteristic curve (AUC-ROC) was used to assess additional prognostic value. RESULTS: Abnormal cTnI concentrations were found on admission in 35 of 68 patients. Abnormal cTnI concentrations and poor clinical condition independently predicted cardiac or pulmonary complications. After extending the model with World Federation of Neurological Surgeons scale and age in addition to abnormal cTnI, the AUC-ROC improved from 0.70 (95% confidence interval (CI), 0.57 to 0.83) to 0.83 (95% CI, 0.72 to 0.93). Abnormal cTnI also independently predicted poor outcome. The additional prognostic value of cTnI for poor outcome is limited. CONCLUSIONS: cTnI measurement is a powerful predictor for the occurrence of pulmonary and cardiac complications, but does not carry additional prognostic value for clinical outcome in patients with aneurysmal SAH.

Cerebral Angiography↗

PubMed2004

Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage.

BACKGROUND: Secondary ischaemia is a frequent complication after aneurysmal subarachnoid haemorrhage (SAH), and responsible for a substantial proportion of patients with poor outcome after SAH. The cause of secondary ischaemia is unknown, but hypovolaemia and fluid restriction are important risk factors. Therefore, volume expansion therapy (hypervolaemia) is frequently used in patients with SAH to prevent or treat secondary ischaemia. OBJECTIVES: To determine the effectiveness of volume expansion therapy for improving outcome in patients with aneurysmal SAH. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched September 2003). In addition we searched MEDLINE (1966 to January 2004) and EMBASE (1980 to January 2004) and contacted trialists to identify further published and unpublished studies. SELECTION CRITERIA: All randomised controlled trials of volume expansion therapy in patients with aneurysmal SAH. We also sought controlled trials based on consecutive groups of patients quasi-randomly allocated to treatment or control group and included these in the analysis if the two groups were well comparable with regard to major prognostic factors. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted the data and assessed trial quality. Trialists were contacted to obtain missing information. MAIN RESULTS: We identified three trials. One truly randomised trial and one quasi-randomised trial with comparable baseline characteristics for both groups were included in the analyses. Volume expansion therapy did not improve outcome (Relative Risk (RR) 1.0; 95% Confidence Interval (CI) 0.5 to 2.2), nor the occurrence of secondary ischaemia (RR 1.1; 95% CI 0.5 to 2.2). Hypervolaemia tended to increase the rate of complications (RR 1.8; 95% CI 0.9 to 3.7) In another quasi-randomised trial, outcome assessment was done only at the day of operation (7 to 10 days after SAH). In the period before operation, treatment resulted in a reduction of secondary ischaemia (RR 0.33; 95% CI 0.11 to 0.99) and case fatality (RR 0.20; 95% CI 0.07 to 1.2). REVIEWERS' CONCLUSIONS: The effects of volume expansion therapy have been studied properly in only two trials of patients with aneurysmal SAH, with very small numbers. At present, there is no sound evidence for the use of volume expansion therapy in patients with aneurysmal SAH.

Humans↗

PubMed2004

[Carotid endarterectomy indicated in asymptomatic stenosis].

Carotid endarterectomy (CE) is of proven value for patients with a high-grade symptomatic stenosis of the internal carotid artery (ICA). Recently, the Asymptomatic Carotid Atherosclerosis Study group showed that in patients with an asymptomatic ICA stenosis of more than 60%, CE caused an absolute risk reduction of perioperative death or stroke during 5 year follow-up of 5.4% (95% confidence interval: 3.0-7.8). Half of these strokes were disabling. The number needed to treat to save one patient from death within 30 days or stroke within in the following 5 years was 19. Further studies are needed to isolate a group of patients that will substantially benefit from the operation. CE is probably most effective in males under 75 years of age. A low surgical morbidity and mortality is an absolute prerequisite to justify CE for an asymptomatic ICA stenosis.

Age Factors↗

PubMed2004

Spinal dural arteriovenous fistulas: long-term follow-up of 44 treated patients.

To assess the long-term clinical course of 44 patients treated for a spinal dural arteriovenous fistula, patients were re-examined after a median follow-up of 5.7 years. In total, 70% of patients rated their activities of daily life as better or much better than before treatment. In most patients, gait disturbances and muscle strength had improved after treatment, with reduced disability; problems with micturition, defecation, and erection tended to remain unchanged.

Activities of Daily Living↗

PubMed2004

Prevention and treatment of glucocorticoid-induced osteoporosis with active vitamin D3 analogues: a review with meta-analysis of randomized controlled trials including organ transplantation studies.

The aim of this review with meta-analysis was to determine if there is a rationale to use activated forms of vitamin D3 to treat or prevent glucocorticoid-induced osteoporosis, and to compare the effect of active vitamin D3 metabolites with that of other anti-osteoporosis therapies. We performed a systemic search using MEDLINE/PubMed (1966-2003). Animal studies and clinical trials involving humans with data on therapy to treat or prevent glucocorticoid-induced osteoporosis with active vitamin D3 analogues were included. Animal studies and basic research studies with active vitamin D3 were reviewed (qualitative review). Meta-analysis (quantitative review) on clinical trials (including organ transplantation studies) was performed with percent change in lumbar spine bone mineral density or bone mineral content as the primary outcome measure; the secondary outcome measure was incidence of vertebral fractures. Fifty-four articles were found. Animal and basic research studies showed that active vitamin D3 analogues can inhibit bone loss during treatment with glucocorticoids. Concerning the effect on bone mineral density, the pooled effect size of active vitamin D3 analogues compared with no treatment, placebo, plain vitamin D3 and/or calcium was 0.35 (95% confidence interval (CI) 0.18, 0.52). Compared with bisphosphonates, the pooled effect size was -1.03 (95% CI -1.71, -0.36). The pooled estimate of the relative risk for vertebral fractures of active vitamin D3 analogues compared with no treatment, placebo, plain vitamin D3 and/or calcium was 0.56 (95% CI 0.34, 0.92) and compared with bisphosphonates it was 1.20 (95% CI 0.32, 4.55). Active vitamin D3 analogues not only preserve bone during glucocorticoid therapy more effectively than no treatment, placebo, plain vitamin D3 and/or calcium, but are also more effective in decreasing the risk of vertebral fractures. Bisphosphonates, however, are more effective in preserving bone and decreasing the risk of vertebral fractures than active vitamin D3 analogues.

Animals↗

PubMed2004

Characteristics of intracranial aneurysms in patients with familial subarachnoid hemorrhage.

BACKGROUND: Compared with sporadic aneurysms, familial aneurysms rupture at an earlier age and are more often located at the middle cerebral artery. Other characteristics of familial aneurysms may also differ from sporadic aneurysms. The authors compared the size of ruptured aneurysms and the number of aneurysms between patients with familial subarachnoid hemorrhage (SAH) and those with sporadic SAH. METHODS: The authors included all patients with familial SAH admitted to the University Medical Center Utrecht (UMCU) and their first-degree relatives with proven aneurysmal SAH, including admissions elsewhere. As reference group the authors used a consecutive series of patients with sporadic SAH admitted to the UMCU from December 1995 to March 1997. Criteria for sporadic SAH were absence of a positive family history and exclusion of aneurysms in first-degree relatives by means of MR angiography. The authors dichotomized sizes of aneurysms into small (</=10 mm) and large (>10 mm). Size and number of aneurysms between patients with familial SAH and sporadic SAH were compared with relative risks (RR) with corresponding 95% CI. RESULTS: The authors found 58 patients with familial SAH (48 with information on aneurysm size) and 88 patients with sporadic SAH. Twenty of 48 patients with familial SAH (41%) had large aneurysms, versus 17 (19%) with sporadic SAH (RR 2.1, 95% CI 1.2 to 3.6). Fifteen of 58 patients with familial SAH (26%) had multiple aneurysms, versus 9 (10%) with sporadic SAH (RR 2.5, 95% CI 1.2 to 5.4). CONCLUSIONS: Familial aneurysms are generally larger at time of rupture and more likely to be multiple than sporadic aneurysms. The development of large and multiple aneurysms may be related to genetic factors that determine defects of the arterial wall.

Academic Medical Centers↗

PubMed2004

Risk of intracerebral hemorrhage in patients with arterial versus cardiac origin of cerebral ischemia on aspirin or placebo: analysis of individual patient data from 9 trials.

BACKGROUND AND PURPOSE: Patients who are anticoagulated after cerebral ischemia have a 19-fold-higher risk of intracerebral hemorrhage (ICH) if they had an arterial rather than a cardiac source. To determine whether this excess risk of ICH was due to the underlying disease (cerebral ischemia of arterial versus cardiac origin) or whether it depended on the antithrombotic regimen, we studied the risk of ICH in arterial versus cardiac origin of cerebral ischemia in patients who received aspirin or no antithrombotic drugs. METHODS: Individual patient data of patients who received aspirin or placebo after cerebral ischemia were obtained from 9 clinical trials. Presence of atrial fibrillation was considered evidence of a cardiac source. Otherwise, events were considered of arterial origin. Cox proportional-hazards modeling was used for univariate and multivariate analyses. RESULTS: Fifty-four ICHs occurred in 16 625 patient-years in the aspirin-treated patients, and 7 ICHs occurred in 4317 patient-years in those on placebo. After multivariate adjustment for age, sex, current smoking, history of hypertension and diabetes, and aspirin dose (aspirin-treated patients only), the hazard ratio for ICH in patients with an arterial versus a cardiac source was 0.74 (95% confidence interval, 0.30 to 1.82) for aspirin-treated patients and 4.34 (95% confidence interval, 0.35 to 54) for placebo-randomized patients. CONCLUSIONS: Our findings do not confirm the previous finding of an excess risk of ICH in patients with cerebral ischemia of arterial origin. Therefore, it seems that having cerebral ischemia of arterial origin by itself is not associated with an increased risk of ICH, but only in combination with high-intensity anticoagulation.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2004

Folate, homocysteine levels, methylenetetrahydrofolate reductase (MTHFR) 677C --> T variant, and the risk of myocardial infarction in young women: effect of female hormones on homocysteine levels.

In young women data are limited about the association between myocardial infarction (MI) and hyperhomocysteinemia, low folate or methylenetetrahydrofolate reductase (MTHFR) genotypes. The effect of oral contraceptive (OC) use on plasma homocysteine levels is not clear. We assessed the association between hyperhomocysteinemia, low folate, MTHFR 677TT mutation and risk of MI, and we investigated the effect of OC use on homocysteine levels in controls. In 181 patients with a first MI and 601 controls 18-49 years of age from a population-based case-control study, non-fasting blood samples were available. The homozygote mutant allele (TT) was detected in 12% of the patients and in 10% of controls. The odds ratio (OR) for MI in TT patients compared with the wild-type (CC) controls was 1.3 [95% confidence interval (CI) 0.8, 2.3]. For all MTHFR genotypes combined, the OR for MI in the lowest quartile of folate (<5.4 nmol L-1) compared with the highest quartile (>10.4 nmol L-1) was 3.0 (95% CI 1.7, 5.1). A 2-fold increased risk of MI was found in women with the TT genotype who had folate levels below the median of 7.4 nmol L-1 compared with CC genotype and folate levels above the median (OR = 2.0; 95% CI 1.0, 3.7). Mean homocysteine levels were 12.2 micromol L-1 in OC users and 12.3 micromol L-1 in non-users. Only at the 97.5 percentile (cut-off 21.0 micromol L-1) was the adjusted OR for higher vs. lower homocysteine levels increased by 2.8-fold (95% CI 1.2, 6.8). Low folate is a risk factor for MI, particularly in women with the MTHFR 677TT genotype. Homocysteine levels were not influenced by OC use.

Adolescent↗

PubMed2003

[Surgical decompression in space-occupying cerebral infarct; notification of a randomized trial].

Patients with a hemispheric infarct and massive space-occupying brain oedema have a poor prognosis. Despite intensive conservative treatment, the case fatality rate may be as high as 80%, and most survivors are left severely disabled. Non-randomised studies suggest that decompressive surgery substantially reduces mortality and improves the functional outcome of survivors. The 'Hemicraniectomy after middle cerebral artery infarction with life-threatening edema trial' (HAMLET) is a newly-conceived randomised multi-centre clinical trial that compares the efficacy of decompressive surgery to improve functional outcome with that of conservative treatment in patients with space-occupying supratentorial infarction.

Brain↗

PubMed2003

[Hospital-wide vascular screening program at the University Medical Center, Utrecht: prevalence of risk factors and asymptomatic vascular disease from 1996 to 2002].

OBJECTIVE: Tracing and treating cardiovascular risk factors in patients with arterial vascular disease and in patients with high risk of developing vascular diseases. DESIGN: Descriptive. METHOD: In September 1996 at the University Medical Center Utrecht, the Netherlands, a vascular screening and prevention programme was started for newly referred patients aged between 18 and 79 years presenting with one or more of the following: coronary artery disease, cerebrovascular disease, peripheral arterial disease, hypertension, diabetes mellitus or lipid disorders. In all patients, risk factors for developing (new) vascular diseases were assessed and non-invasive vascular diagnostics aimed at finding asymptomatic vascular disease were done. RESULTS: Between 1 September 1996 and 31 October 2002, 3075 patients took part in the screening programme. Within the various patient groups and often despite treatment, there was a high prevalence of hypertension, smoking, dyslipidaemia, hyperhomocystemia and overweight. In patients with peripheral artery disease, carotid artery stenosis > or = 50% was detected in 17% and an aneurysm of the abdominal aorta in 5%. In patients presenting with diabetes mellitus, hypertension or lipid disorders the prevalence of asymptomatic arterial disease was 1-5%. Asymptomatic vaso-dilatory disease in particular was uncommon. CONCLUSION: A hospital-wide vascular screening and prevention programme for a wide range of high-risk vascular patients was shown to be feasible and resulted in the detection of risk factors and asymptomatic arterial disease. It is a reliable starting point for actual risk intervention. More attention should be paid to treating existing risk factors.

Adolescent↗

PubMed2003

Polymorphisms and Risk of Ischemic Stroke (POLARIS) study: rationale and design.

Twin and family-based studies indicate that genetic factors might be involved in the risk of transient ischemic attack (TIA) and ischemic stroke (IS). Identification of genetic risk factors for new vascular events after cerebral ischemia may target secondary prevention. The overall aim of POLARIS is to study which polymorphisms predispose to new vascular events after TIA/IS and to assess their predictive value. Patients who have had a TIA or IS of presumed arterial origin are included. The study design is twofold. In part one the prevalences of polymorphisms will be compared between 300 long-term survivors of the Dutch TIA Trial (average follow-up 10 years) and 820 patients with recent TIA/IS. In part two a cohort of 820 patients with recent TIA/IS will be followed for the occurrence of vascular events for an average of 3.5 years. Several polymorphisms of interest will be genotyped, including factor V Leiden, prothrombin 20210A, 5,10-methylenetetrahydrofolate reductase, HR2 haplotype factor V and factor XIII Val34Leu.

Brain Ischemia↗

PubMed2003

Glucose levels and outcome after subarachnoid hemorrhage.

In a cohort of 337 patients with subarachnoid hemorrhage (SAH), we investigated the relationship between blood glucose levels, baseline characteristics, and outcome by means of Student's t-test and multivariate logistic regression. The mean glucose levels on admission and from day 1 to 10 were significantly higher in patients with poor condition on admission and in patients with poor outcome. In a multivariate analysis, glucose level on admission was not an independent predictor of outcome. Hyperglycemia may be a link in the association between poor condition on admission and poor outcome.

Blood Glucose↗

PubMed2003

Timing of the effect of acetaminophen on body temperature in patients with acute ischemic stroke.

The authors assessed the time of onset of the hypothermic effect of acetaminophen in 102 patients with acute ischemic stroke. These patients were randomized to treatment with either 1000 mg of acetaminophen (n = 52) or placebo (n = 50), given six times daily. Treatment with high-dose acetaminophen resulted in a 0.26 degrees C (95% CI 0.07 to 0.46 degrees C) lower mean body temperature than placebo treatment within 4 hours. This effect remained present throughout the next 20 hours. A large phase III trial seems warranted.

Acetaminophen↗

PubMed2003

Cochrane review: dipyridamole for preventing major vascular events in patients with vascular disease.

BACKGROUND: Patients enrolled in clinical trials after nondisabling cerebral ischemia have an annual risk of vascular events (death from all vascular causes, nonfatal stroke, or nonfatal myocardial infarction) of 4% to 11%. Aspirin reduces the incidence by 13%. Many trials in patients presenting with vascular disease investigated the efficacy of (addition of) dipyridamole in secondary prevention. We systematically compared the efficacy and safety of dipyridamole versus control in the presence and absence of other antiplatelet drugs in clinical trials on the secondary prevention of vascular events in patients with vascular disease. SUMMARY OF REVIEW: Randomized trials with concealed treatment allocation in patients with a nonembolic arterial vascular disease were selected. Therapy consisted of dipyridamole in the presence or absence of other antiplatelet drugs compared with no drug or an antiplatelet drug(s) other than dipyridamole. Twenty-six trials were included, with a total of 19 842 patients. Dipyridamole was not more efficacious in the prevention of vascular death (relative risk [RR], 1.02; 95% CI, 0.90 to 1.17). It appeared more efficacious in the prevention of vascular events (RR, 0.90; 95% CI, 0.83 to 0.98), but this result only reached statistical significance because of 1 large trial in patients presenting with cerebral ischemia. Combination treatment of dipyridamole and aspirin compared with aspirin had an RR of 1.03 (95% CI, 0.87 to 1.22) for vascular death and an RR of 0.90 (95% CI, 0.80 to 1.00) for vascular events. CONCLUSIONS: For patients who presented with arterial vascular disease, there was no evidence that dipyridamole, in the presence or absence of another antiplatelet drug (chiefly aspirin), reduced the risk of vascular death, although it may reduce the risk of further vascular events. However, this benefit was found only in a single large trial and only in patients presenting after cerebral ischemia. There was no evidence that dipyridamole alone was more efficacious than aspirin. Further trials comparing the effects of the combination of dipyridamole plus aspirin with aspirin alone are justified.

Death, Sudden, Cardiac↗

PubMed2003

Risk factors for intracerebral hemorrhage in the general population: a systematic review.

BACKGROUND AND PURPOSE: Although data on some risk factors for intracerebral hemorrhage (ICH) already are beyond doubt, for other factors, the evidence is less clear. We performed a systematic overview of case-control and cohort studies on risk factors for ICH. METHODS: We searched MEDLINE, LILACS, EXTRAMED, and Pascal from 1966 to 2001 to identify studies. Studies were included if they met predefined methodological criteria. When possible, 2x2 tables were extracted and combined with the Mantel-Haenszel method. Summary odds ratios (ORs) were calculated for case-control studies, and summary relative risks (RRs) were found for cohort studies and for case-control and cohort studies combined. RESULTS: Fourteen case-control and 11 cohort studies were identified. We could not always combine the results of case-control and cohort studies. In cohort studies, the crude RR for age (every 10-year increase) was 1.97 (95% confidence interval [CI], 1.79 to 2.16). In case-control studies, the crude OR for high alcohol intake was 3.36 (95% CI, 2.21 to 5.12) and for hypertension was 3.68 (95% CI, 2.52 to 5.38). Two cohort studies showed an increasing risk of ICH with increasing degree of hypertension. In cohort and case-control studies combined, the crude RR for sex (male versus female) was 3.73 (95% CI, 3.28 to 4.25); for current smoking, 1.31 (95% CI, 1.09 to 1.58); and for diabetes, 1.30 (95% CI, 1.02 to 1.67). CONCLUSIONS: Risk factors for ICH appeared to be age, male sex, hypertension, and high alcohol intake. High cholesterol tends to be associated with a lower risk of ICH. We could not assess whether these risk factors are independent.

Age Factors↗

PubMed2003

Aspirin and stroke prevention.

According to meta-analyses aspirin provides a relative reduction in the rate of major vascular events of 19% in patients with arterial disease in general, whereas for patients with ischaemic cerebrovascular disease this reduction is only 13%. The discrepancy may well result from pathophysiological differences and not from a play of chance. There is no proven difference in efficacy according to dose. The evidence for this equivalence is most compelling in the range between 75 and 1300 mg daily, but still fairly convincing for doses between 30 and 50 mg. In contrast, side effects are clearly more frequent as the dose is higher. Other antiplatelet agents (sulfinpyrazone, ticlopidine, clopidogrel, dipyridamole, orally administered IIb/IIIa inhibitors) have no clear advantages over aspirin and in some cases definite disadvantages; the combination of aspirin and dipyridamole may be more efficacious than aspirin alone, but the evidence hinges on a single trial. If recurrent TIAs occur under treatment with aspirin, the rational response is not to change to a different antiplatelet agent, but to review the diagnosis and consider causes other than artery-to-artery embolism. Platelet aggregation can probably still occur despite complete acetylation of platelets, via pathways other than COX-1 inhibition, but in vitro aggregation tests are an unreliable measure.

Aspirin↗

PubMed2003

Dipyridamole for preventing stroke and other vascular events in patients with vascular disease.

BACKGROUND: Patients with transient ischaemic attacks (TIA) and minor ischaemic strokes are at risk of serious vascular events (death from all vascular causes, non-fatal stroke, or non-fatal myocardial infarction). Their risk of vascular events lies between 4 and 11 percent per year. Aspirin only, in a daily dose of 30 mg or more, offers only modest protection in such patients: it reduces the incidence of major vascular events by 13 percent. In a single trial, adding dipyridamole (an alternative antiplatelet agent) to aspirin was associated with a 22 percent reduction in the risk of major vascular events compared with aspirin alone. However, a systematic review of all trials of antiplatelet agents by the Antithrombotic Trialists' Collaboration showed that, in high risk patients, there was virtually no difference between the aspirin-dipyridamole combination and aspirin alone. We therefore sought to assess the effects of dipyridamole in more detail. OBJECTIVES: 1) To assess the efficacy of dipyridamole versus control in the secondary prevention of vascular events in patients with vascular disease in the presence and absence of other antiplatelet drugs. 2) To assess the safety of dipyridamole versus control in the secondary prevention of vascular events in patients with vascular disease in the presence and absence of other antiplatelet drugs. SEARCH STRATEGY: The Cochrane Stroke Group Trials Register was searched and other relevant Cochrane Groups were contacted to search their specialised registers (last search 29 April 2002). In addition the Cochrane Controlled Trials Register, MEDLINE and EMBASE were searched and Dutch manufacturers of dipyridamole were contacted to identify further published and unpublished studies. SELECTION CRITERIA: Randomised long term secondary prevention trials with concealed treatment allocation, treatment for > 1 month, starting within 6 months after presentation of a arterial vascular disease were selected (coronary artery disease, myocardial infarction, angina pectoris, retinopathy, nephropathy, peripheral arterial disease, stroke, TIA, amaurosis fugax). Therapy consisted of dipyridamole in any dose in the presence or absence of other antiplatelet drugs compared with no drug or an antiplatelet drug(s) other than dipyridamole (control group). DATA COLLECTION AND ANALYSIS: Two reviewers selected trials which met the inclusion criteria and extracted details of randomisation methods, blinding of treatments and assessments, whether intention-to-treat analysis was possible from the published data, whether treatment groups were comparable with regard to major prognostic factors, the number of patients who were excluded or lost to follow-up, definition of outcome events, and entry and exclusion criteria. The methodological quality of each trial was assessed by the two reviewers on the basis of these extracted data. In addition, dose and type of antiplatelet treatments, duration of follow-up and the numbers of defined outcome events were recorded. Data published by the Antithrombotic Trialists' Collaboration were used. The remaining data were independently extracted by the same two reviewers and cross checked. Data were analysed according to the intention-to-treat principle. Relative and absolute risk reductions were calculated by means of the statistical software provided by the Cochrane Collaboration (RevMan). MAIN RESULTS: Twenty-six trials were included, with a total of 19842 patients, among whom 1399 vascular deaths and 3085 fatal and non-fatal vascular events occurred during follow-up. Compared with control, dipyridamole had no clear effect on vascular death (RR 1.02, 95% CI 0.90 to 1.17). This result was not influenced by the dose of dipyridamole or type of presenting vascular disease. Compared with control, dipyridamole appeared to reduce the risk of vascular events (RR 0.90, 95% CI 0.83 to 0.98), but this effect was only statistically significant due to a single large trial in patients presenting with cerebral ischaemia (6602 patients). Comparing dipyridamole plus aspirin with aspirin alone: there was no clear difference in vascular death, the RR was 1.03 (95% CI 0.87 to 1.22); the combination was associated with fewer vascular events with an RR of 0.90 (95% CI 0.80 to 1.00). Combination treatment of dipyridamole and aspirin compared with placebo had an RR of 0.89 (95% CI 0.79 to 1.01) for vascular death and an RR of 0.74 (95% CI 0.68 to 0.80) for vascular events. REVIEWER'S CONCLUSIONS: This review found that, for patients who presented with arterial vascular disease, there was no evidence that dipyridamole, in the presence or absence of an other antiplatelet drug (chiefly aspirin) reduced the risk of vascular death, though it may reduce the risk of further vascular events. However, this benefit was found in only a single large trial and only in patients presenting after cerebral ischaemia. There was no evidence that dipyridamole alone was more efficacious than aspirin. Further trials comparing the effects of the combination of dipyridamole with aspirin with aspirin alone are justified.

Anticoagulants↗

PubMed2003

Influence of atherosclerosis on age-related changes in renal size and function.

BACKGROUND: Renal size and function reflect the health of the kidney. These parameters are associated with age, gender and body weight. The kidneys are also influenced by micro- and macrovascular diseases. Atherosclerotic markers and risk factors may influence the age-related changes of renal size and function. METHODS: Data of 1056 patients who entered the SMART-study (Second Manifestations of ARTerial disease) were used to assess the effect of atherosclerosis on the relationship between age and renal size and function and to study the effect of atherosclerosis on renal size and function. Patients who were newly referred to the hospital with manifestations of vascular disease were screened for asymptomatic atherosclerosis with noninvasive tests. The carotid intima-media thickness (IMT) and albuminuria were used as estimates for the atherosclerotic burden. Renal size was defined as the mean pole-to-pole length of both kidneys measured by ultrasonography. Renal function was represented by serum creatinine. RESULTS: Intima-media thickness was a significant effect modifier of the age-renal size relationship (P = 0.041). The increase of serum creatinine with age was more pronounced in the highest tertile of IMT (P = 0.048). Renal size decreased equally with age in patients with and without hypertension or diabetes mellitus (DM). The same held true for the age-renal function relationship. Albuminuria and DM were independent predictors of renal size and function. CONCLUSION: Atherosclerosis accelerates the decrease of renal size and the increase of serum creatinine with age. Renal size and function are determined by albuminuria and DM.

Aged↗