Summaries of Must-Read Clinical Literature, Guidelines, and FDA Actions
Aspirin Nonresponsiveness in Patients with T2D
J Am Coll Cardiol; ePub 2017 Jan 9; Bhatt, et al
Complete inhibition of serum thromboxane B2 (TXB2) generation was not achieved in a high proportion of patients with diabetes who were treated with enteric coated (EC) aspirin, a recent study found. The rate and extent of serum thromboxane generation and aspirin pharmacokinetics was measured in 40 patients with diabetes in a randomized, single-blind, triple-crossover study. Patients were exposed to three 325-mg aspirin formulations: plain aspirin, PL2200 (a modified-release lipid-based aspirin), and a delayed release EC aspirin. Researchers found:
- The rate of aspirin nonresponsiveness was 15.8%, 8.1%, and 52.8% for plain aspirin, PL2200, and EC aspirin, respectively.
- 56% of enteric coated aspirin-treated participants had serum TXB2 levels >3.1 ng/ml vs 18% and 11% of those after administration of plain aspirin and PL2200.
- The high rate of nonresponsiveness with EC aspirin was associated with lower exposure to acetylsalicylic acid and 66% and 72% lower maximal decrease of TXB2 with marked interindividual variability, when compared to plain aspirin and PL2200.
Bhatt DL, Grosser T, Dong J, et al. Enteric coating and aspirin nonresponsiveness in patients with type 2 diabetes mellitus. [Published online ahead of print January 9, 2017]. J Am Coll Cardiol. doi:10.1016/j.jacc.2016.11.050.
This Week's Must Reads
Must Reads in Cardiology
Consumption of SSBs & Risk of Mortality, Circulation; ePub 2019 Mar 18; Malik, et al
Dietary Cholesterol or Egg Consumption & CVD, JAMA; 2019 Mar 19; Zhong, Van Horn, et al
Physical Activity & Incidence of CHD & CVD in Women, JAMA Netw Open; ePub 2019 Mar 15; LaCroix, et al
Intensive BP Control in Adults with Hypertension Who Smoke, JAMA Netw Open; ePub 2019 Mar 8; Scarpa, et al
Suppression of the effect of serum thromboxane B2 (TXB2) is believed to lead to the effect of aspirin on decreasing platelet adhesiveness and therefore aspirin’s effect in decreasing heart attack and stroke. It is known that some people do not seem to respond to the effect of aspirin, and this study suggests that a large proportion of non-response may be due to non-absorption of aspirin due to enteric coating. It is important to note that this trial only looked at platelet effect for 3 days in each of the groups, and the effect of enteric coating on aspirin absorption and platelet adhesion may be different long term. Since it is not clear that enteric coating of aspirin substantially decreases gastric ulceration, there may not be a compelling reason to use enteric coated aspirin as this study suggests that enteric coated aspirin may not yield as great an effect in decreasing CV disease as plain aspirin. —Neil Skolnik, MD