"Booster" Doses of Aspirin for Patients Taking Low-Dose Aspirin Every Day
ABSTRACT & COMMENTARY
Source: Balles J, et al. Erythrocyte promotion of platelet reactivity decreases the effectiveness of aspirin as an antithrombotic therapeutic modality. The effect of low-dose aspirin is less than optimal in patients with vascular disease due to prothrombotic effects of erythrocytes on platelet reactivity. Circulation 1998;97:350-355.
Many physicians prescribe 81 or 325 mg of aspirin (ASA) daily to prevent primary and secondary vascular ischemic events. The clinical advantage of low maintenance doses of ASA is that they inhibit platelet synthesis of thromboxane A2 (TXA2) but not the vascular production of prostaglandin I2. Low-dose ASA, however, is not effective antithrombotic therapy in all patients because, among other reasons, erythrocytes enhance platelet reactivity via cell-to-cell interactions.1
In a recent study, the effects of platelet erythrocyte interactions were evaluated in 82 patients with ischemic heart disease or cerebrovascular ischemia. There were 64 men and 18 women, the mean age was 66 ± 11 years, and the daily dosage of ASA was 200 or 300 mg. Patients were classified into three groups according to the capacity of their collagen-stimulated platelets to recruit additional platelets into a developing thrombus.
In group A (n = 32; 39%) platelet recruitment was blocked by ASA in both the presence and absence of red blood cells (RBCs). Only in this group was the dosage of ASA adequate to inhibit the phase of platelet reactivity that leads to thrombus formation.
In group B (n = 37; 45%), recruitment was abolished when platelets were evaluated alone but not when RBCs were present, indicating a suboptimal effect of ASA in this group. In group C (n = 13; 16%), detectable recruitment in stimulated platelets persisted and was enhanced markedly by the presence of RBCs. In all patients, platelet TXA2 synthesis was inhibited more than 94% by ASA administration. Therefore, in two-thirds of a group of patients with vascular disease chronically taking 200-300 mg ASA daily, platelet reactivity and recruitment persisted in the presence of RBCs despite inhibition of TXA2 synthesis.
COMMENTARY
The three different patterns of platelet responses in patients with vascular disease indicate that there is a marked intersubject variation in response to even 300 mg ASA daily. Therefore, in a significant number of patients, even an adult ASA tablet daily may be insufficient to block platelet reactivity promoted by RBCs. So, what is the optimal daily dose of ASA to inhibit platelet reactivity under all circumstances in all patients? The answer may still be a baby ASA every day.
In previous studies, the authors demonstrated that erythrocyte prothrombotic activity is sensitive to ASA in a dose-dependent manner and is blocked after a single dose of 500 mg ASA in normal subjects.2,3 With the passage of time, however, RBCs "escape" from this initial inhibition. To maintain inhibition, normal subjects required a daily ASA maintenance dose of only 50 mg, as long as it was supplemented by an intermittent dose of 500 mg ASA every two weeks. Therefore, there is no need to abandon low-dose aspirin for the prevention of cardiac and cerebrovascular ischemia. Physicians can still recommend that their patients take a baby ASA every day but may wish to also advise them to take two adult ASA every two weeks as a booster, just to be on the safe side. -jjc
References
1. Santos MT, et al. J Clin Invest 1991;87:571-580.
2. Valles J, et al. Blood 1991;78:154-162.
3. Santos MT, et al. Circulation 1997;95:63-68.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content. TESTING
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content