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“Background: Dual antiplatelet therapy with aspirin plus clopidogrel is the mainstay of therapy in patients click here undergoing percutaneous coronary intervention (PCI). However, the optimal dose of aspirin following PCI has not been established.
Hypothesis: There is no difference for definite stent thrombosis in patients taking low dose versus standard aspirin.
Methods: Lovi-dose (81 mg) aspirin was used as part of a standard dual antiplatelet
therapy in patients receiving bare-metal stents (BMS) or drug-eluting stents (DES) at a large tertiary medical center. We retrospectively analyzed 5368 consecutive cases treated with stent placement and dual antiplatelet therapy. The incidence of definite stent thrombosis (DST) at our institution was compared to DST as reported in a large, published cohort of 24 trials and 12 973 patients. We stratified DST events into early (<30 days) and late (>30 days) timing and also stratified by stent type. The effect of aspirin dosing was evaluated using X(2), Cochran-Mantel-Haenszel, and homogeneity testing.
Results: A total of 5187 patients underwent
JQ1 ic50 7604 stent implantations during the study period. The cumulative incidence of DST was 0.60% (95% confidence interval [Cl], 0.42%-0.84%) at 30 days and 0.76% (95% Cl, 0.56%-1.03%) at 1 year. The overall incidence of DST during the study period was not different based on type of stent (0.53% for DES and 0.75% for BMS, P = 0.36). Compared to the historic, standard-dose
aspirin (162-325 mg) cohort, DST in our low-dose aspirin (81 mg) cohort was not significantly different at either 30 days (0.72% vs 0.60%, P = 0.39) or at 1 year (1.08% vs 0.76%, P = 0.07). There was no appreciable interaction of aspirin dose on the incidence of DST, controlling for stent type, or timing of the event.
Conclusions: Low-dose aspirin therapy in combination with clopidogrel following implantation of either BMS or DES in our cohort does not learn more appear to increase the risk of DST compared to a higher-dose aspirin regimen.”
“Prazosin is an alpha 1 adrenoceptor antagonist, and it is used as an antihypertensive agent. The effects of prazosin on the activity of hepatic triacylglycerole lipase (HTGL) are not fully understood. In this study, we demonstrated that prazosin stimulates the release of HTGL activity from primary cultures of rat hepatocytes in a time- and dose-dependent manner. U-73122, a phopholipase C (PLC) inhibitor, suppresses prazosin’s stimulation of the release of HTGL activity. Moreover, prazosin stimulated the increase of PLC activity in the hepatocytes in a time- and dose-dependent manner.