Aspirin therapy has come in to the forefront of chest pain, heart disease, and stroke discussion due to its therapeutic antiplatelet capabilities. However, In the recent couple years, it has been found that certain things affect Aspirin’s effectiveness at platelet inhibition to include resistance, medications, and even patient disease. When it is necessary to be given, especially in the inpatient setting, we need to be aware of these factors that affect Aspirin’s ability to do its job so that we can look out for out patient’s best interests.
Aspirin has several indications for use. It has long been used for pain, fever, and even as an anti-inflammatory. It has recently, following studies of platelet inhibition and cox and aracadonic acid, become even more popular for its ability to inhibit platelet aggregation. This action does several things including reducing risk of coronary artery disease, minimizing progression of coronary artery disease, reduce risk of stroke, and heart attack. It is also commonly used in conjunction with other antiplatelets in the prevention of coronary stent occlusion due to thrombosis.
It has long been supported that a daily dose of 81 mg of Aspirin, when person is not resistant to its anti platelet effects, is sufficient for proper platelet aggregation inhibition. However, recently arguments suggesting that a higher dose is necessary have come up. Thus, best evidence as shown here has been developed to investigate this and has again found that 75 mg is sufficient and as effective as 81 mg, 125 mg or even 325 mg at platelet inhibition. It is also interesting to point out that in those patients on daily aspirin therapy (and not those who are not), those suffering an acute AMI actually see a spike in platelet inhibition when another loading dose of Aspirin is given at symptom onset or as soon as possible. This is believed to help reduce severity of AMI and slow progression.
There are several factors that can affect the ability of Aspirin to do its job. Unfortunately, one of this things are other medicines. Studies have consistently demonstrated lowered platelet inhibition with Aspirin therapy in patients taking ranitidine, proton pump inhibitors, as well as those taking enteric coated aspirin.
Studies show a correlation between concomitant use of PPI’s and Aspirin and a decrease in measured antiplatelet effect suggesting that use of a PPI in conjunction with Aspirin may in fact render it ineffective. This is thought to be due to the decreased acid levels resulting in altered absorption. It is recommended that patient’s taking Aspirin, especially for its anti-platelet effects, should avoid PPI’s (such as omperazole-prilosec, and Pepcid). For those who experience upset stomach from the daily use of Aspirin, PPI’s and H2 antagonists (such as ranitidine) are needed but should not be used. This is one the dilemnas surrounding aspirin use.
Enteric coating has shown to actual lower the affects of Aspirin on platelet inhibition as well. This is thought to be a result of the resultant delayed absorption as well as the fact that this requires the aspirin to be absorbed further down the intestinal tract in a less acidic and opportune environment. However, this does significantly help with the upset stomach frequently associated with Aspirin use.
Unfortunately, as with many medications, there are things that prevent certain parts of the population from taking Aspirin. Contraindications are asthma and GI-bleeding (also considered a side effect), especially that which is associated with Aspirin use. Aspirin is known to cause GI-bleeding obviously due to its anti-platelet action (which when directly acting on an area of the GI tract that has an injury, say an ulcer, it would potentially cause some issues! As for asthma patients, Aspirin is know to cause, in certain patients, asthmaticus, which can result in death. Finally, obviously if the person has a sensitivity or allergy to Aspirin, or alternative should be found to which the patient is not allergic.
Safe and effective Aspirin regimen
Indication for Use <ul><li>Anti-platelet </li></ul><ul><li>Pain </li></ul><ul><li>Fever </li></ul><ul><li>Anti-inflammatory </li></ul>
Effective Dose <ul><li>Minimum dose with maximum effect is 75 mg daily </li></ul><ul><li>Randomized Control Trial </li></ul><ul><li>Level of Evidence 2 </li></ul><ul><li>Second loading dose effective in AMI’s </li></ul><ul><ul><li>Gurbel et al., 2007 </li></ul></ul><ul><ul><li>Fuchs et al., 2010 </li></ul></ul>
Things that affect Efficacy <ul><li>Ranitidine </li></ul><ul><ul><li>Effect of ranitidine on the antiplatelet effects of aspirin in healthy human subjects. </li></ul></ul><ul><li>Level 2 </li></ul><ul><li>Randomized control study </li></ul><ul><ul><ul><li>Lev et al., 2007 </li></ul></ul></ul>
Things That affect efficacy <ul><li>Enteric Coating </li></ul><ul><ul><li>Effect of enteric coating on antiplatelet activity of low-dose aspirin in healthy volunteers. </li></ul></ul><ul><ul><li>Level 2 </li></ul></ul><ul><ul><li>Randomized Control Trial </li></ul></ul><ul><ul><li>Cox et al., 2006 </li></ul></ul>
References <ul><li>Cox, D., Maree, A., Dooley, M., Conroy, R., Byrne, M., & Fitzgerald, D. (2006). Effect of enteric coating on antiplatelet activity of low-dose aspirin in healthy volunteers. Stroke (00392499) , 37 (8), 2153-2158. </li></ul><ul><li>Fuchs, I., Spiel, A., Frossard, M., Derhaschnig, U., Riedmüller, E., & Jilma, B. (2010). Platelet hyperfunction is decreased by additional aspirin loading in patients presenting with myocardial infarction on daily aspirin therapy. Critical Care Medicine , 38 (6), 1423-1429. doi:10.1097/CCM.0b013e3181de8b1e </li></ul><ul><li>Gurbel, P., Bliden, K., DiChiara, J., Newcomer, J., Weng, W., Neerchal, N., & ... Tantry, U. (2007). Evaluation of dose-related effects of aspirin on platelet function: results from the Aspirin-Induced Platelet Effect (ASPECT) study. Circulation , 115 (25), 3156-3164. </li></ul><ul><li>Lev, E., Ramabadran, R., Guthikonda, S., Patel, R., Kleiman, A., Granada, J., & ... Kleiman, N. (2007). Effect of ranitidine on the antiplatelet effects of aspirin in healthy human subjects. American Journal Of Cardiology , 99 (1), 124-128. </li></ul><ul><li>Würtz, M., Grove, E., Kristensen, S., & Hvas, A. (2010). The antiplatelet effect of aspirin is reduced by proton pump inhibitors in patients with coronary artery disease. Heart , 96 (5), 368-371. doi:10.1136/hrt.2009.181107 </li></ul>