Re: Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data
This result should not be at all surprising. Low dose aspirin has a beneficial effect on inhibiting COX-1 which produces prostaglandins, most of which are pro-inflammatory, and thromboxanes, which promote clotting. However in higher doses aspirin loses its anti-clotting activity effect by inhibiting COX-2 in endothelial cells resulting in lower levels of the anti-coagulant, prostacyclin thus increasing the risk of thrombus and associated heart attacks and other circulatory problems. This is why aspirin is given at the low dose of 75mg (or 100mg) as an antiplatelet agent. Aspirin at therapeutic analgesic doses like any other NSAID will have an effect on inhibiting prostacyclin that outweighs any beneficial effect on reducing COX-1. I wonder how many patients continue on 75mg of aspirin while taking therapeutic doses of an NSAID which totally negates its effect?
Rapid Response:
Re: Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data
This result should not be at all surprising. Low dose aspirin has a beneficial effect on inhibiting COX-1 which produces prostaglandins, most of which are pro-inflammatory, and thromboxanes, which promote clotting. However in higher doses aspirin loses its anti-clotting activity effect by inhibiting COX-2 in endothelial cells resulting in lower levels of the anti-coagulant, prostacyclin thus increasing the risk of thrombus and associated heart attacks and other circulatory problems. This is why aspirin is given at the low dose of 75mg (or 100mg) as an antiplatelet agent. Aspirin at therapeutic analgesic doses like any other NSAID will have an effect on inhibiting prostacyclin that outweighs any beneficial effect on reducing COX-1. I wonder how many patients continue on 75mg of aspirin while taking therapeutic doses of an NSAID which totally negates its effect?
Competing interests: No competing interests