Dual antiplatelet therapy does not affect the incidence of low-dose aspirin-induced small intestinal mucosal injury in patients after percutaneous coronary intervention for coronary stenosis: a multicenter cross-sectional study

Abstract

Although low-dose aspirin (LDA) is known to induce small intestinal mucosal injury, the effect of dual antiplatelet therapy (DAPT; LDA + clopidogrel) on small intestinal mucosa in patients after percutaneous coronary intervention (PCI) for coronary stenosis is unknown. Fifty-one patients with a history of PCI and LDA use were enrolled, and 45 eligible patients were analyzed. Patients were grouped based on DAPT (DAPT: n = 10 and non-DAPT: n = 35) and proton pump inhibitor (PPI) use (PPI user: n = 22 and PPI-free patients: n = 23) to compare small intestinal endoscopic findings. The relationship between LDA-use period and small intestinal endoscopic findings was also examined. Multivariate analysis was performed to identify risk factors for LDA-induced mucosal injury using age, sex, DAPT, PPI, gastric mucoprotective drug, and LDA-use period. The rate of small intestinal mucosal injury incidence did not significantly differ between DAPT and non-DAPT patients (50% vs 51.1%, respectively; p = 0.94), or PPI users and PPI-free patients (50% vs 52.2%, respectively; p = 0.88). Additionally, LDA-use period of ≤24 months (n = 15) yielded a significantly higher rate of small intestinal mucosal injury incidence than LDA-use period >24 months (n = 30) (80% vs 36.7%, respectively; p = 0.006). Multivariate analysis revealed that a LDA-use period of ≤24 months was a significant risk factor for small intestinal mucosal injury (odds ratio: 19.5, 95% confidence interval: 2.48–154.00, p = 0.005). Following PCI for coronary stenosis, neither DAPT nor PPI affected LDA-induced small intestinal mucosal injury. Moreover, patients who used LDA within the last 24 months were at a greater risk of small intestinal mucosal injury.

Current knowledge on non-steroidal anti-inflammatory drug-induced small-bowel damage: a comprehensive review

“…Surprisingly, capsule endoscopy identified mucosal breaks in 10 of patients who took enteric-coated LDA for cardiovascular or cerebrovascular diseases with a maximum number of mucosal breaks being 33 [37]. Although prevalence rates of mucosal breaks varied depending on study design, the reported rates are as high as those in nonselective NSAIDs studies (Table 1) [38][39][40][41]. One reason for this very high incidence of injuries caused by entericcoated LDA seems to be the amplified topical effect caused by exposure of the small-bowel mucosa to high concentrations of aspirin dissolved within the small bowel.…”

Preventive effect of ecabet sodium on low-dose aspirin-induced small intestinal mucosal injury: a randomized, double-blind, pilot study

“…Although there was a significant difference in the median number of small intestinal lesions [range] between baseline and two weeks after LDA administration in group A (baseline: 1 [0–5], after LDA administration: 5 [1–11]; p = 0.0059), there was no difference in group B (baseline: 0.5 [0–9], after LDA administration: 3 [0–23]; p = 0.0586). In group A especially, the amount of spotty redness significantly increased (baseline: 0 [0–3]; after LDA administration: 2 [0–8], p = 0.0039).…”

“…Low-dose aspirin (LDA) exerts antiplatelet effects by inhibiting cyclooxygenase-1 activity and suppressing prostaglandin production; however, the reduction in prostaglandins causes whole intestinal mucosal injury [1–3]. It is recommended that LDA users concurrently use a proton pump inhibitor (PPI) to prevent LDA-induced upper gastrointestinal mucosal injury [4, 5].…”

Current states of prevention of drug-induced gastroduodenal ulcer in real clinical practice: a cross-sectional study

“…(7) Recent reports also have indicated that low-dose aspirin cause not only gastroduodenal mucosal injury but also small bowel injury with high frequency. (13,14) We investigated the chronological changes in use of NSAIDs and LDA in patients with gastroduodenal ulcer since 2002. The percentage of these patients taking NSAIDs or LDA initially increased, but has decreased in recent years.…”