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Aspirin Treatment (aspirin + treatment)

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Medical Sciences	100%

Selected Abstracts

Aspirin reduces anticardiolipin antibodies in patients with coronary artery disease

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2006
I. Ikonomidis
Abstract Background, Anticardiolipin antibodies (aCL) have been found to be elevated in patients with coronary artery disease (CAD) and have been associated with an adverse outcome owing to their prothrombotic activity. The aim of this study was to investigate the effect of aspirin treatment on aCL levels in patients with chronic CAD. Materials and methods, Forty patients with chronic CAD scheduled for elective coronary artery bypass graft surgery (CABG) and 40 healthy controls participated in the study. Patients were treated with 300 mg of aspirin once daily (o.d.) for the first 12 days and placebo for the following 12 days before CABG in a double-blind, cross-over trial. Immunoglobulin (Ig) G-, IgM-, IgA-aCL and C-reactive protein (CRP) levels were measured in the controls and at the end of each treatment period in the patients with CAD. Results, The IgA- and IgG-aCL levels were greater in patients with CAD than in the controls. Compared with the placebo, IgA, IgG subtypes and CRP levels were reduced after aspirin treatment (P = 0·001, P = 0·02, P = 0·04, respectively). The percentage reduction of IgA- and IgG-aCL was related to the percentage reduction of CRP after aspirin (P < 0·05). Conclusion, Aspirin treatment with 300 mg o.d. reduced the serum levels of IgA and IgG subtypes in patients with chronic CAD in parallel to a reduction in CRP. These findings offer an additional pathophysiological mechanism of the beneficial effects of aspirin in patients with chronic CAD. [source]

Pulse pressure and mortality in hypertensive type 2 diabetic patients.

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 3 2006
A cohort study
Abstract Hypothesis Hypertension is a well-known cardiovascular risk factor in type 2 diabetic patients. It has been suggested that pulse pressure (PP) could be an independent cardiovascular risk factor in the general population, particularly in the elderly. An association between office PP and cardiovascular mortality has been previously reported in diabetic patients, while the relationship between ambulatory measurements of PP and all-cause mortality has not been assessed so far. Aim To assess the relationship between ambulatory PP and all-cause mortality in diabetic patients with hypertension. Methods A cohort study was performed on a consecutive series of 435 diabetic outpatients. All patients underwent office blood pressure measurement (OBP) and 24-h ambulatory blood pressure monitoring (ABPM). Mortality was assessed through queries at the Registry Offices of the city of residence for each patient. Mean follow-up was 3.8 ± 1.2 years. Results Fifty-eight patients (13.3%) died during the follow-up. Mortality was significantly (p < 0.05) higher in patients in the highest quartile and lower in patients in the lowest quartile, when compared to the intermediate quartiles, both for office and ABPM-PP. In a multivariate analysis, after adjustment for numerous variables (including current hypoglycaemic, antihypertensive statin and aspirin treatment), mortality was increased by 3.1 and 5.3% for each incremental mmHg of office PP (p < 0.05) and ABPM-PP (p < 0.001) respectively. Conclusions High PP, assessed through office measurement or ABPM, was associated with increased mortality in hypertensive type 2 diabetic patients. In our sample, PP assessed with ABPM is a better predictor of mortality than office PP. Copyright © 2005 John Wiley & Sons, Ltd. [source]

Aspirin reduces anticardiolipin antibodies in patients with coronary artery disease

Effect kinetics of desmopressin-induced platelet retention in healthy volunteers treated with aspirin or placebo

HAEMOPHILIA, Issue 1 2000
Lethagen
Desmopressin is often used for haemostatic treatment in platelet dysfunction, but the effect kinetics of platelet responses and the mechanism of action are poorly known. This study aimed to determine the kinetics of platelet function responses induced by desmopressin in healthy volunteers treated with aspirin or placebo. Another aim was to correlate platelet responses to changes of von Willebrand factor (vWF) in plasma. We measured platelet function with a glass bead retention test, Ivy bleeding time, vWF:Ag and multimeric structure in plasma. Median baseline platelet retention was 12% (normal reference range 16,27%) during aspirin treatment and 18% during placebo. Median peak platelet retention after desmopressin was 33% during aspirin treatment and 34% during placebo. After about 3 h platelet function had returned to baseline. A second desmopressin dose after 3 h stimulated platelet retention to a similar extent as the first dose. There was no correlation between platelet responses and quantitative or qualitative changes of vWF in plasma. Platelet count did not change significantly. Thus, desmopressin's effect on platelet function lasts for about 3 h, but may be prolonged by a second dose immediately thereafter. These findings may have important clinical implications for patients with aspirin-induced platelet dysfunction undergoing surgery. [source]

The genetics of aspirin resistance

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 5 2007
Timothy Goodman
Summary Aspirin is widely used for the prophylaxis of cardiovascular events in patients with cardiovascular risk factors or established atherosclerotic disease. However, despite aspirin treatment, a substantial number of patients experience recurrent events. Such ,aspirin resistance' is generally defined as failure of aspirin to produce an expected biological response, for example inhibition of platelet aggregation or of thromboxane A2 synthesis. Whilst its aetiology is multifactorial, genetic factors are also likely to play their part. Here we review the evidence for and against such a genetic contribution, as well as the data suggesting the involvement of specific genes. [source]

A critical review of aspirin in the secondary prevention of noncardioembolic ischaemic stroke

INTERNATIONAL JOURNAL OF STROKE, Issue 4 2010
Domenico Inzitari
Both secondary prevention (such as lifestyle modifications, pharmacotherapy or surgery) and an understanding of the influence of risk factors (including the different aetiologic mechanisms of cerebral ischaemia) play a pivotal role in reducing the burden of recurrent stroke. Regarding the types of preventative treatments available, variations exist across all clinical studies, including differences in target populations (including the type of cerebral ischaemia), risk factors, length of follow-up, drop-out rates and outcomes, which makes translating the results of clinical trials to individual patients difficult. However, with such limitations in mind, this critical albeit nonsystematic review, which compared aspirin with other antiplatelets and in combination with other drugs, showed that the benefit from aspirin treatment is consistently shown in ischaemic stroke, while harms are limited. Furthermore, no definite superiority is apparent across different antiplatelet therapies. Dual antiplatelet regimens may expose to a slight but measurable higher risk of haemorrhagic complications, perhaps in selective groups of patients (i.e. those with severe small-vessel disease or in selective racial groups). Based on our analysis, the indication of aspirin as the first-line choice, also recommended by several acknowledged international or national guidelines, may be confirmed. However, the complex nature of patients at risk of recurrent ischaemic stroke necessitates a comprehensive approach, which should be driven by the primary care physician, whose role is central to successful actions for secondary stroke prevention. [source]

Antiplatelet therapy and spontaneous perirenal hematoma

INTERNATIONAL JOURNAL OF UROLOGY, Issue 4 2005
KEISUKE YAMAMOTO
Abstract This case report clarifies an adverse reaction of antiplatelet therapy which has been a standard prophylactic method for patients harboring significant risks of thromboembolic events. A 71-year-old Japanese man who had been taking aspirin tablets (81 mg) for a year presented with sudden colic pain in the left flank region. An abdominal computed tomography scan revealed a significant perirenal hematoma of the left kidney. There were no pathological kidney conditions, such as renal tumors, calculi or vascular diseases, found by magnetic resonance imaging examination. After cessation of aspirin administration followed by conservative management, the hematoma completely disappeared 6 months later. This is the first documented case of spontaneous perirenal hematoma secondary to low-dose aspirin treatment. While such unpleasant events occur extraordinarily, this should be noted as a severe risk of antiplatelet therapy. [source]

Thromboxane and prostacyclin biosynthesis in heart failure of ischemic origin: effects of disease severity and aspirin treatment

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2010
F. SANTILLI
Summary.,Background: Thromboembolism is a relatively common complication of chronic heart failure (HF) and the place of antiplatelet therapy is uncertain. Objectives: We characterized the rate of thromboxane and prostacyclin biosynthesis in chronic HF of ischemic origin, with the aim of separating the influence of HF on platelet activation from that of the underlying ischemic heart disease (IHD). Patients and Methods: We compared urinary 11-dehydro-thromboxane (TX)B2, 2,3 dinor 6-keto-PGF1,, 8-iso-prostaglandin (PG)F2,, and plasma N-terminal pro-brain natriuretic peptide (NT-pro-BNP), asymmetric dimethylarginine (ADMA), and soluble CD40 ligand (sCD40L), in 84 patients with HF secondary to IHD, 61 patients with IHD without HF and 42 healthy subjects. Results: HF patients not on aspirin had significantly higher urinary 11-dehydro-TXB2 as compared with healthy subjects (P < 0.0001) and IHD patients not on aspirin (P = 0.028). They also showed significantly higher 8-iso-PGF2, (P =,0.018), NT-pro-BNP (P = 0.021) and ADMA (P < 0.0001) than IHD patients not on aspirin. HF patients on low-dose aspirin had significantly lower 11-dehydro-TXB2 (P < 0.0001), sCD40L (P = 0.007) and 2,3-dinor-6-keto-PGF1, (P = 0.005) than HF patients not treated with aspirin. HF patients in NYHA classes III and IV had significantly higher urinary 11-dehydro-TXB2 than patients in classes I and II, independently of aspirin treatment (P < 0.05). On multiple linear regression analysis, higher NT-pro-BNP levels, lack of aspirin therapy and sCD40L, predicted 11-dehydro-TXB2 excretion rate in HF patients (R2 = 0.771). Conclusions: Persistent platelet activation characterizes HF patients. This phenomenon is related to disease severity and is largely suppressable by low-dose aspirin. The homeostatic increase in prostacyclin biosynthesis is impaired, possibly contributing to enhanced thrombotic risk in this setting. [source]

Platelet activation in type 2 diabetes mellitus

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2004
P. Ferroni
Summary., The abnormal metabolic state that accompanies diabetes renders arteries susceptible to atherosclerosis, being capable of altering the functional properties of multiple cell types, including endothelium and platelets. In particular, an altered platelet metabolism and changes in intraplatelet signaling pathways may contribute to the pathogenesis of atherothrombotic complications of diabetes. A variety of mechanisms may be responsible for enhanced platelet aggregation. Among them, hyperglycemia may represent a causal factor for in vivo platelet activation, and may be responsible for nonenzymatic glycation of platelet glycoproteins, causing changes in their structure and conformation, as well as alterations of membrane lipid dynamics. Furthermore, hyperglycemia-induced oxidative stress is responsible for enhanced peroxidation of arachidonic acid to form biologically active isoprostanes, which represents an important biochemical link between impaired glycemic control and persistent platelet activation. Finally, increased oxidative stress is responsible for activation of transcription factors and expression of redox-sensitive genes leading to a phenotypic switch of endothelium toward an adhesive, pro-thrombotic condition, initial platelet activation, adhesion and subsequent platelet aggregate formation. All this evidence is strengthened by the results of clinical trials documenting the beneficial effects of metabolic control on platelet function, and by the finding that aspirin treatment may even be more beneficial in diabetic than in high-risk non-diabetic patients. Attention to appropriate medical management of diabetic patients will have great impact on long-term outcome in this high-risk population. [source]