Use of aspirin for primary and secondary prevention of cardiovascular disease in diabetic patients in an ambulatory care setting in Spain

Sicras‐Mainar, Antoni; Navarro‐Artieda, Ruth; Rejas‐Gutiérrez, Javier; Bobadilla, Jaime Fernández de; Frias-Garrido, X; Ruiz-Riera, Rafael

doi:10.1186/1471-2296-8-60

Cited by 6 publications

(2 citation statements)

References 36 publications

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“…The augmented COX-2 expression was explained to contribute to the production of PGH 2 and then TXA 2 in aspirin treated patients [20,23,24]. The aspirin concentrations (4250 mM) used in the present study are higher than blood concentrations shown by those on normal aspirin treatment of 75-325 mg/day for platelet inhibition [25][26][27]. According to the recently published guidelines from the American Heart Association, routine low dose aspirin therapy may be considered in women aged 65 or older regardless of cardiovascular diseases risk status, and the dosages of aspirin for high risk women increases to 325 mg per day rather than 162 mg [28].…”

Section: Discussionmentioning

confidence: 69%

Augmentation of U46619 induced human platelet aggregation by aspirin

et al. 2009

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Aspirin is known to suppress platelet function markedly. However, aspirin at concentrations higher than 1 mM was observed to augment 1.3 microM U46619 (a stable thromboxane receptor (TP receptor) agonist) induced human platelet aggregation in this study. Moreover, at a concentration as low as 250 microM aspirin increased the aggregation induced by U46619 in 13% of normal and healthy individuals. The degree of platelet aggregation and the amount of ATP release were enhanced in U46619 stimulated platelet rich plasma by the addition of aspirin (>250 microM). U46619 was previously reported to inhibit forskolin-stimulated adenyl cyclase and to reduce the cAMP formation. Both of the augmentation effects of aspirin on U46619-induced aggregation and ATP release were blocked by MeSAMP, a P2Y(12) receptor antagonist. U46619 induced aggregation was suppressed by the addition of ADP scavenger (CP/CPK) with no significant change on ATP measured and the effect of CP/CPK could not be reversed by aspirin. In addition, aspirin augmented the inhibitory effect of U46619 on the cAMP production. Our present results suggested that the potentiation effect of aspirin on U46619 induced aggregation was related with the secreted ADP and the subsequent P2Y(12)/Gi related signaling.

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Section: Discussionmentioning

confidence: 69%

Augmentation of U46619 induced human platelet aggregation by aspirin

et al. 2009

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“…Sicras-Mainar et al [ 39 ] conducted a retrospective, observational study assessing the use of aspirin for primary and secondary prevention of CVD in patients 18 years of age or older with diabetes (mean age, 64.1 years). They analyzed 4140 individuals, with 79.1% in the primary prevention group and 20.9% in the secondary prevention group.…”

Section: Management Of Elderly Patients With Diabetes For Risk Factormentioning

confidence: 99%

Diabetes in the elderly

Botts

Munshi²

2008

Curr Cardio Risk Rep

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The association of diabetes and cardiovascular disease is a major health concern in the elderly population. Patients 65 years of age or older with diabetes have a greater risk of ischemic heart disease and cardiovascular mortality than nondiabetic patients of the same age. In addition, although there has been an overall reduction in cardiovascular disease morbidity and mortality in the United States over the past 50 years, the burden of cardiovascular disease attributable to diabetes mellitus has actually increased over this time. In addition to traditional risk factors (eg, hypertension, dyslipidemia), the effect of nonclassical cardiovascular risk factors, such as exogenous and endogenous insulin, metabolic syndrome, impaired fasting glucose, chronic kidney disease, advanced glycation end products, and adipokines, in elder patients with diabetes is currently being evaluated. This article addresses current evidence related to cardiovascular risk in elderly patients with diabetes.

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