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BACKGROUND
Obesity is a cluster of medical conditions affecting several pathophysiological processes, including platelet (PLT) function.
OBJECTIVE
We evaluated the association between obesity and PLT response to dual antiplatelet therapy over 1 month in patients with stable angina pectoris after
OBJECTIVE
Platelet aggregation responses to acetylsalicylic acid (ASA) show considerable interindividual variation, the causes of which are largely unknown. We determined whether variation in insulin action is associated with that of ASA on platelets.
METHODS
In all, 10 nonobese (age 50+/-3 y, BMI
OBJECTIVE
Acetylsalicylic acid (ASA) treatment in diabetic patients is very important owing to the increasing hyperactivity of thrombocytes and atherosclerosis. In several investigations, it was reported that diabetes caused increased coronary artery disease, cerebrovascular disease, and death. In
UNASSIGNED
Cardiovascular (CV) diseases remain a leading global cause of death. It has been proven that the use of acetylsalicylic acid (ASA) in secondary prevention reduces the CV risk, while the benefits of ASA in primary prevention have recently been debated. The aim of the study was to compare
Data on the absorption of orally administered drugs following Roux-en-Y gastric bypass (RYGB) surgery in obese patients are limited and inconclusive. As it is difficult to predict changes in absorption, studies on frequently used drugs in this population are necessary. Acetylsalicylic acid (ASA) and
The prostaglandin synthesis inhibitor acetylsalicylic acid (ASA) increases acute insulin response to glucose and improves glucose tolerance in man. In an effort to provide further information on the mechanism whereby ASA improves glucose tolerance, we studied the effect of ASA on C-peptide, insulin,
The effect of acetylsalicylic acid (ASA) on tissue sensitivity to insulin was studied in 14 non-obese subjects with impaired glucose tolerance. For the determination of insulin sensitivity a 1 h priming dose-constant insulin infusion technique was used. The percent decrease of plasma glucose and
OBJECTIVE
The first cause of low-dose acetylsalicylic-acid (ASA) inefficacy is poor adherence to treatment. No non-invasive technique is available to assess ASA intake. Current-induced vasodilation (CIV) was found abolished in healthy volunteers after low-dose ASA intake. We tested clinical
The debate over acetylsalicylic acid (ASA) therapy for primary prevention of cardiovascular disease (CVD) has recently resurfaced, but scarce data are available on prophylactic ASA use in Canada for this purpose. This study aimed to evaluate the prevalence and factors associated with BACKGROUND
Chronically elevated interleukin-6 (IL-6) is implicated in obesity-associated pathologies, where a proportion of this cytokine is derived from adipose tissue. Proinflammatory prostaglandins, which regulate this cytokine elsewhere, are also produced by this tissue.
OBJECTIVE
To investigate
The metabolic syndrome (MS), a cluster of risk factors, such as obesity, hyperglycemia, hypertension and dyslipidemia, contributes to the development of cardio-vascular diseases and type 2 diabetes mellitus (DM2). Insulin resistance (IR) plays a key role in MS being strongly linked to abdominal
People with diabetes mellitus have higher risk of cardiovascular morbidity and mortality from thrombo-vascular complications than non-diabetics and it is recommended that they should use acetylsalicylic acid (ASA) as anitiplatelet agent regularly. The aim of this study was to examine current
In this retrospective database study, carried out using The Health Improvement Network, a UK primary care database, we followed up patients who were prescribed low-dose acetylsalicylic acid (ASA) (75-300 mg/day) for the secondary prevention of cardiovascular disease in 2000-2007, and who
Central obesity is a relevant risk factor for major cardiovascular events due to the atherosclerotic involvement of coronary, cerebral and lower limb arterial vessels. A major role in the increased cardiovascular risk is played by platelets, which show an increased activation and a reduced
Serum and urine uric acid were evaluated during prolonged therapeutic fasting in 15 obese patients. With increasing ketonemia the serum uric acid rose from a control value of 5.9 +/- 0.4 to 12.5 +/- 1.0 mg/100 ml at 7 days and then decreased progressively to 7.7 +/- 1.3 mg/100 ml by 28 days despite