High on-treatment platelet reactivity to aspirin in patients after myocardial infarction.

Aspirin (ASA) is widely used as an antiplatelet therapeutic drug in secondary prevention. Last years brought many reports on ASA resistance or high on-treatment platelet reactivity (HTPR) to aspirin.This study is a post-hoc prospective analysis with 30 patients evaluated during follow up on average of 6.3 years after hospitalization from myocardial infarction. The examined population was divided into two subgroups according to the response to ASA. In order to estimate the function of blood platelets and their responsiveness to acetylsalicylic acid therapy, ASPI-test was used. The measurements were performed by the method of whole blood impedance aggregometry. During long-term follow up significantly higher percentage of high platelet reactivity was observed, compared with previous visits (p = 0.00001). Considering clinical endpoints of the research that were connected with coronary disease, no differences were obtained.The frequency of HTPR to aspirin in this study was higher than data reported in literature among subjects with CV diseases. In long-term observation the highest percentage of ASA non-responders was reported (58.6%). HTPR to aspirin did not affect the presence of the clinical endpoints for the study.

The differential role of uric acid - The purpose or cause of cardiovascular diseases?

For 40 years many studies have been conducted to verify the connection between serum uric acid concentration and cardiovascular diseases, such as myocardial infarction. Unfortunately, it remains unclear which form of uric acid - prooxidant or antioxidant - could be a predictive marker of cardiovascular disease, especially in patients after myocardial infarction. It is well-known that uric acid is an organic compound and the water-soluble final product of purine catabolism, which is catalysed by xanthine oxidoreductase and excreted by kidneys. An increased concentration of UA in human plasma leads to diseases like tumours, renal disorders, atherosclerosis, hypertension, diabetes, metabolic syndrome, polycythaemia vera, haemolytic anaemias, ischemia, oxidative stress, and rare genetic disorders connected with UA degradation. Epidemiological studies have shown that UA might be a marker of oxidative stress, progression of inflammation, or renal disease. A fortiori, it is possible that could also be a predictor for short/long-term survival of patients with CVD. Evidence provided by multiple studies is controversial and mutually exclusive. Among 71 studies the most of them found an independent association between SUA and CVD risk. Some of those studies confirm that CVD risk is higher in women who had elevated SUA levels. On the other hand, many studies reached the opposite conclusion and did not find any relationship between SUA and CVD mortality and morbidity.

Crushed sublingual versus oral ticagrelor administration strategies in patients with unstable angina. A pharmacokinetic/pharmacodynamic study.

Oral administration of crushed ticagrelor tablets turned out to be an efficacious method that improves its pharmacokinetics and pharmacodynamics. This strategy, however, is unlikely to eliminate the drug-drug interaction in patients receiving intravenous morphine, as the impairment of the P2Y12 inhibitor absorption related to decreased propulsive motility of the gastro-intestinal tract is the most likely mechanism of interaction. Thus, we designed a pharmacokinetic and pharmacodynamic study setting the feasibility of platelet inhibition with a loading dose of ticagrelor given as crushed tablets sublingually compared with two other ticagrelor loading dose administration strategies: integral tablet given orally and crushed tablet given orally in patients with unstable angina. Ticagrelor and its metabolite AR-C124900XX plasma concentration was evaluated in nine time points (time frame of 6 hours) using liquid chromatography coupled with mass spectrometry; platelet reactivity was evaluated using multiple electrode aggregometry. The area under the plasma concentration-time curve for ticagrelor and AR-C124900XX was significantly higher in patients treated with crushed tablets given orally compared with crushed tablets given sublingually only within the first hour after loading dose (936.9 ± 898.0 vs 368.0 ± 422.4, p=0.042 and 103.4 ± 120.8 vs 31.3 ± 43.9, p=0.031, respectively). Moreover, we showed significantly stronger platelet inhibition in patients receiving crushed ticagrelor orally vs. sublingually at 30 and 45 min after the loading dose (p=0.024 and p=0.016, respectively). Therefore, the administration strategy of ticagrelor determines the pharmacokinetic and pharmacodynamic profile of both ticagrelor and its active metabolite AR-C124900XX.