# Aspirin Responsiveness and Early Saphenous Vein Graft Occlusion After Coronary Artery Bypass Grafting: A CT Coronary Angiography Study

**Authors:** Petar Milacic, Zoran Tabakovic, Milica Ivanovic, Ivana Petrovic, Milan Milojevic, Jelena Rakocevic, Ivan Stojanovic, Slobodan Micovic, Igor Zivkovic

PMC · DOI: 10.3390/medicina62020367 · 2026-02-12

## TL;DR

This study found that aspirin non-responsiveness before heart surgery does not increase the risk of early vein graft failure, as seen through CT scans.

## Contribution

The study provides new evidence that preoperative aspirin non-responsiveness is not linked to early saphenous vein graft occlusion after CABG.

## Key findings

- Aspirin non-responders did not have a higher rate of early graft occlusion compared to responders.
- Female patients had a significantly higher early graft occlusion rate than males.
- Rehospitalization was more common among aspirin non-responders due to wound infections.

## Abstract

Background and Objectives: Early saphenous vein graft (SVG) failure remains a clinically significant limitation of contemporary coronary artery bypass grafting (CABG). Platelet function testing has been proposed to identify patients with an attenuated aspirin effect who may be at higher thrombotic risk. Therefore, this study aimed to determine whether preoperative aspirin non-responsiveness, assessed by the platelet function assay, is associated with early graft failure after CABG, as evaluated by CT coronary angiography. Materials and Methods: In this prospective observational study, consecutive patients undergoing elective, first-time isolated on-pump CABG with ≥1 SVG and preoperative aspirin therapy were enrolled. Platelet function was measured preoperatively using a point-of-care assay (ASPI, aspirin reaction units [ARU]), and patients were stratified as responders (<550 ARU) or non-responders (≥550 ARU). The primary endpoint was early SVG occlusion, detected by CT angiography performed before discharge after CABG. Secondary endpoints included postoperative cardiac and renal biomarkers, myocardial infarction, stroke, rehospitalization, and 30-day mortality. Results: Early CT-confirmed SVG occlusion occurred in 22/170 patients (12.9%) and did not differ between responders and non-responders (20/136 [14.7%] vs. 2/34 [5.9%]; p = 0.21). Cardiac biomarkers were similar between the groups for 4–24 h. Thirty-day mortality (1.5%), myocardial infarction (5.9% in each group), and stroke (2.2% vs. 5.9%) were infrequent and similar between groups. Rehospitalization was more common among non-responders, driven by deep wound infection (5.9% vs. 0%; p = 0.040). In exploratory analysis, females had a significantly higher early graft occlusion rate than males (27.3% vs. 8.6%; p = 0.004). Conclusions: Aspirin non-responsiveness, as assessed by ASPI testing, was not associated with early CT-confirmed SVG occlusion, and these data do not support intensifying antiplatelet therapy based solely on a single preoperative platelet-function measurement. Given the absence of serial postoperative platelet function measurements, future studies should prioritize postoperative platelet reactivity and different treatment strategies during the early window of graft vulnerability.

## Linked entities

- **Chemicals:** aspirin (PubChem CID 2244)
- **Diseases:** coronary artery disease (MONDO:0005010), myocardial infarction (MONDO:0005068), stroke (MONDO:0005098)

## Full-text entities

- **Genes:** TNNT2 (troponin T2, cardiac type) [NCBI Gene 7139] {aka CMD1D, CMH2, CMPD2, LVNC6, RCM3, TnTC}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}, PTGS1 (prostaglandin-endoperoxide synthase 1) [NCBI Gene 5742] {aka COX1, COX3, PCOX1, PES-1, PGG/HS, PGHS-1}, P2RY12 (purinergic receptor P2Y12) [NCBI Gene 64805] {aka ADPG-R, BDPLT8, HORK3, P2T(AC), P2Y(12)R, P2Y(AC)}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, COX1 (cytochrome c oxidase subunit I) [NCBI Gene 4512] {aka COI, MTCO1}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}
- **Diseases:** vessel disease (MESH:C536223), ischemic (MESH:D002545), SVG failure (MESH:D051437), NSTEMI (MESH:D000072658), angina pectoris (MESH:D000787), hyperglycemia (MESH:D006943), platelet aggregation (MESH:D001791), injury to (MESH:D014947), disease (MESH:D004194), coronary disease (MESH:D003327), acute coronary syndromes (MESH:D054058), bleeding (MESH:D006470), STEMI (MESH:D000072657), sternal (MESH:C537489), Stroke (MESH:D020521), myocardial injury (MESH:D009202), ischemic complications (MESH:D017202), infection (MESH:D007239), myocardial infarction (MESH:D009203), SVG occlusion (MESH:D006083), wound infection (MESH:D014946), SVG thrombosis (MESH:D012170), thrombosis (MESH:D013927), anemia (MESH:D000740), death (MESH:D003643), Occlusion (MESH:D001157), pulmonary hypertension (MESH:D006976), peripheral arterial disease (MESH:D058729), saphenous vein (MESH:D000071078), coronary artery disease (MESH:D003324), postoperative bleeding (MESH:D019106)
- **Chemicals:** ADP (MESH:D000244), Aspirin (MESH:D001241), thromboxane A2 (MESH:D013928), ARNI (-), clopidogrel (MESH:D000077144), ticagrelor (MESH:D000077486), hs (MESH:D006859), Ca (MESH:D002118), creatinine (MESH:D003404), lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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Source: https://tomesphere.com/paper/PMC12943505