Journal of Yeungnam Medical Science

Original article

Cardiology and Cardiovascular Medicine
Association between clopidogrel preloading time and post-procedural troponin elevation in patients with stable angina undergoing elective percutaneous coronary intervention: a retrospective cohort study: Sungho Jo, Jeong Tae Byoun, Donghyeon Joo, Jae Young Cho, Kyeong Ho Yun; J Yeungnam Med Sci. 2026;43:34. Published online May 18, 2026; DOI: https://doi.org/10.12701/jyms.2026.43.34

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Abstract PDF: Background
Clopidogrel requires several hours to achieve adequate platelet inhibition. We investigated the association of clopidogrel preloading time with 30-day clinical outcomes and post-procedural troponin elevation in patients with stable angina undergoing elective percutaneous coronary intervention (PCI).
Methods
This single-center retrospective cohort study included 1,020 patients with stable angina (clopidogrel-naive) who received 300 mg clopidogrel preloading within 24 hours before elective PCI between 2012 and 2020. Patients were categorized according to clopidogrel preloading-to-balloon time ≤6 hours or >6 hours. The primary endpoint was 30-day major adverse cardiovascular events (MACE), defined as a composite of all-cause death, myocardial infarction, stroke, and any revascularization. Secondary endpoints included serial troponin T changes and troponin T elevation ≥5×, ≥25×, and ≥70× the upper reference limit. Stabilized inverse probability of treatment weighting (IPTW) was used.
Results
Thirty-day MACE occurred in five patients (0.49%) and did not differ between the ≤6-hour and >6-hour groups after IPTW (0.5% vs. 0.4%, p=0.754). Post-procedural troponin T levels at 6, 24, and 48 hours were higher in the ≤6-hour group. Patients with shorter preloading-to-balloon times showed higher peak troponin T levels, with the greatest difference at the ≤1-hour cutoff (geometric mean ratio, 2.12; 95% confidence interval, 1.53–2.95; p<0.001) and progressive attenuation at longer cutoffs. Troponin T elevation ≥5× and ≥25× was more frequent in the ≤6-hour group, whereas ≥70× elevation did not differ.
Conclusion
Clopidogrel preloading ≤6 hours before elective PCI was not associated with increased 30-day MACE but was associated with lower-threshold post-procedural troponin T elevation.

Original Article

Cardiology and Cardiovascular Medicine
Change of Serum Levels of C-Reactive Protein After Coronary Angioplasty and Its Effects on Clinical Restenosis.: Jong Seon Park, Gu Ru Hong, Chae Hoon Lee, Dong Gu Shin, Young Jo Kim, Bong Sup Shim; Yeungnam Univ J Med. 2001;18(2):215-225. Published online December 31, 2001; DOI: https://doi.org/10.12701/yujm.2001.18.2.215

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Abstract PDF: BACKGROUND
There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. MATERIALS AND METHODS: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. RESULTS: Baseline CRP level was 0.30+/-0.01 mg/dL in stable and 0.46+/-0.28 mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was 0.32+/-0.31 mg/dL in stable and 0.79+/-0.73 mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). CONCLUSION: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.

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