Journal
JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE
Volume 10, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/jcdd10040137
Keywords
aspirin; coronary artery disease; cerebrovascular disease; diabetes mellitus; essential thrombocythemia; platelet function; thromboxane; gastrointestinal bleeding; enteric-coated aspirin; cardiovascular prevention
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Aspirin irreversibly inhibits platelet function by inhibiting the synthesis of TxA2. Although widely used at low doses for cardiovascular prevention, chronic treatment with aspirin can lead to gastrointestinal discomfort, mucosal erosions/ulcerations, and bleeding. Enteric-coated (EC) aspirin, the most commonly used formulation, is less effective than plain aspirin in inhibiting TxA2 production, especially in individuals with high body weight. It causes fewer erosions in the stomach but can still cause mucosal erosions in the small intestine. Several studies have shown that EC aspirin and buffered aspirin do not significantly reduce the incidence of clinically relevant gastrointestinal ulceration and bleeding. Plain aspirin should be the preferred formulation for cardiovascular prevention due to its favorable pharmacological profile.
Aspirin inhibits platelet function by irreversibly inhibiting the synthesis of thromboxane A2 (TxA2). Aspirin, at low doses, is widely used for cardiovascular prevention. Gastrointestinal discomfort, mucosal erosions/ulcerations and bleeding are frequent complications of chronic treatment. To reduce these adverse effects, different formulations of aspirin have been developed, including enteric-coated (EC) aspirin, the most widely used aspirin formulation. However, EC aspirin is less effective than plain aspirin in inhibiting TxA2 production, especially in subjects with high body weight. The inadequate pharmacological efficacy of EC aspirin is mirrored by lower protection from cardiovascular events in subjects weighing >70 kg. Endoscopic studies showed that EC aspirin causes fewer erosions of the gastric mucosa compared to plain aspirin (which is absorbed in the stomach) but causes mucosal erosions in the small intestine, where it is absorbed. Several studies demonstrated that EC aspirin does not reduce the incidence of clinically relevant gastrointestinal ulceration and bleeding. Similar results were found for buffered aspirin. Although interesting, the results of experiments on the phospholipid-aspirin complex PL2200 are still preliminary. Considering its favorable pharmacological profile, plain aspirin should be the preferred formulation to be used for cardiovascular prevention.
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