Although there is a low prevalence of MPH use in France, this survey revealed a wide profile of users and heterogeneous use patterns.
Background: By inhibiting prostaglandin synthesis, aspirin can interfere with both arterial functional and angiotensin-converting enzyme inhibitor (ACEI) properties and be deleterious in chronic heart failure (CHF). Aim: Our aim was to prospectively evaluate the effect of aspirin on arterial functional properties in CHF patients treated with ACEIs. Methods and results: Over three consecutive treatment periods of 7 days, 18 patients received placebo, followed by aspirin 100 mgyday, and then aspirin 325 mgy day. Single blind prospective assessment of reflected wave and time reflection by radial applanation tonometry; pulse wave velocity; blood pressure; thromboxane B2 (TxB2) and prostaglandins in plasma and urine was performed. Aspirin 325 mgyday induced a significant increase in augmentation index of reflected wave (P-0.0001 and Ps0.0013 vs. placebo and aspirin 100 mg, respectively) and a significant decrease in reflected wave traveling times (Ps0.0007 vs. placebo). Aspirin 100 mgyday produced a similar, though non-significant, trend in these parameters compared with placebo. Both aspirin treatments produced a statistically significant decrease in serum TxB2 (P-0.0001) but did not have an effect on the metabolite of prostaglandin I2 (Ps0.136). Conclusion: This study demonstrates the existence of a dose-mediated deleterious effect of aspirin upon arterial functional properties in CHF patients treated with ACEI.
Aspirin and angiotensin-converting enzyme inhibitors (ACEIs) are often associated for the treatment of coronary disease and/or chronic heart failure, but conclusions of some prospective and retrospective studies show a possible negative interaction between aspirin and ACEIs. ACEIs inhibit the conversion of angiotensin I to angiotensin II and also the catabolism of bradykinin, which results in increased synthesis of vasodilatory agents [prostaglandins and nitric oxide (NO)], whereas aspirin inhibits prostaglandin synthesis. Thus, a potential interaction from the opposing effects of aspirin and ACEIs could affect the metabolism of bradykinin. We conducted an extensive Medline search, as well as a manual search, of published literature including pharmacodynamic studies and clinical trials concerning the impact of aspirin on the effect of ACEIs in hypertension, coronary disease and chronic heart failure. A review of this literature shows five studies in hypertension (all prospective and using blood pressure as the main criterion of assessment), five in coronary disease (three retrospective and two prospective trials, four of which use mortality as the criterion of assessment) and 13 in chronic heart failure (eight using haemodynamic measurements of which seven are prospective--one prospective study using pulmonary tests, four using clinical events including mortality as criterion of assessment of which two are prospective). The counteraction of ACEI efficacy by aspirin is demonstrated in one out of five studies in hypertension, one out of four of studies in coronary disease and nine out of thirteen in chronic heart failure. This counteraction is more often observed with high dosages of aspirin (greater than 250 mg/day, four out of six studies) and less often with lower dosages (less than or equal to 250 mg/day, three out of 11 studies). These studies are retrospective analyses or use haemodynamic end-points, so there is as yet no methodological argument strong enough to contraindicate the aspirin-ACEI association or to prove the clinical relevance of this interaction. In conclusion, prospective studies using mortality as a criterion of assessment are needed to offer the practitioner the answer to the question of ACEI-aspirin association.
ObjectivesTo assess HIV/AIDS research productivity in the 27 countries of the European Union (EU), and the structural level factors associated with levels of HIV/AIDS research productivity.MethodsA bibliometric analysis was conducted with systematic search methods used to locate HIV/AIDS research publications (period of 1 January 2002 to 31 December 2011; search databases: MEDLINE (Ovid, PubMed), EMBASE, ISI-Thomson Web of Science; no language restrictions).The publication rate (number of HIV/AIDS research publications per million population in 10 years) and the rate of articles published in HIV/AIDS journals and selected journals with moderate to very high (IF ≥3) 5-year impact factors were used as markers for HIV research productivity. A negative binomial regression model was fitted to assess the impact of structural level factors (sociodemographic, health, HIV prevalence and research/development indicators) associated with the variation in HIV research productivity.ResultsThe total numbers of HIV/AIDS research publications in 2002–2011 by country ranged from 7 to 9128 (median 319). The median publication rate (per million population in 10 years) was 45 (range 5–150) for all publications. Across all countries, 16% of the HIV/AIDS research was published in HIV/AIDS journals and 7% in selected journals with IF ≥3. Indicators describing economic (gross domestic product), demographic (size of the population) and epidemiological (HIV prevalence) conditions as well as overall scientific activity (total research output) in a country were positively associated with HIV research productivity.ConclusionsHIV research productivity varies noticeably across EU countries, and this variation is associated with recognisable structural factors.
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