Journal of Yeungnam Medical Science

Original article

Cardiology and Cardiovascular Medicine
The performance of ASpirin-FREE therapy after successful percutaneous coronary intervention for acute coronary syndrome: the ASFREE prospective pilot study: Donghyeon Joo, Sungho Jo, Jeong Tae Byoun, Jae Young Cho, Kyeong Ho Yun; J Yeungnam Med Sci. 2026;43:25. Published online March 19, 2026; DOI: https://doi.org/10.12701/jyms.2026.43.25

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Abstract PDF: Background
Dual antiplatelet therapy with aspirin and a P2Y12 inhibitor is standard after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS); however, bleeding risk remains a major concern. Early discontinuation of aspirin due to potent P2Y12 inhibition may mitigate bleeding without increasing thrombotic events.
Methods
The ASpirin-FREE therapy after successful percutaneous coronary intervention for acute coronary syndrome (ASFREE) study was an investigator-initiated, single-center, prospective, open-label, single-arm pilot study enrolling patients with ACS who underwent PCI with drug-eluting stents. All patients received a single loading dose of aspirin on the day of the PCI, followed by ticagrelor or prasugrel monotherapy. The primary efficacy endpoint was target vessel failure (TVF) at 12 months. The primary safety endpoint was definite stent thrombosis. Event rates are reported with 95% confidence intervals (CIs).
Results
In total, 228 patients were enrolled. TVF occurred in 10 patients (4.4%; 95% CI, 2.1%–7.9%). Definite stent thrombosis was observed in one patient (0.4%; 95% CI, 0.01%–2.4%), with no acute or subacute events. Major bleeding (Bleeding Academic Research Consortium type 3 or 5) occurred in two patients (0.9%; 95% CI, 0.1%–3.1%).
Conclusion
An aspirin-free strategy following a single loading dose with continuation of potent P2Y12 inhibitor monotherapy was feasible in patients with ACS undergoing PCI and was associated with low rates of thrombotic and major bleeding events. These findings should be regarded as hypothesis-generating and supporting further evaluations in adequately powered randomized controlled trials (CRIS registration: KCT0008182).

Review Article

Pharmacology, Drug Therapy, and Toxicology
Effects of AMP-activated Protein Kinase Activating Compounds and Its Mechanism.: Hyoung Chul Choi; Yeungnam Univ J Med. 2012;29(2):77-82. Published online December 31, 2012; DOI: https://doi.org/10.12701/yujm.2012.29.2.77

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AMP-activated protein kinase (AMPK) is an important cellular fuel sensor. Its activation requires phosphorylation at Thr-172, which resides in the activation loop of the alpha1 and alpha2 subunits. Several AMPK upstream kinases are capable of phosphorylating AMPK at Thr-172, including LKB1 and CaMKKbeta (Ca2+/calmodulin-dependent protein kinase kinasebeta). AMPK has been implicated in the regulation of physiological signals, such as in the inhibition of cholesterol fatty acid, and protein synthesis, and enhancement of glucose uptake and blood flow. AMPK activation also exhibits several salutary effects on the vascular function and improves vascular abnormalities. AMPK is modulated by numerous hormones and cytokines that regulate the energy balance in the whole body. These hormone and cytokines include leptin, adiponectin, ghrelin, and even thyroid hormones. Moreover, AMPK is activated by several drugs and xenobiotics. Some of these are in being clinically used to treat type 2 diabetes (e.g., metformin and thiazolidinediones), hypertension (e.g., nifedipine and losartan), and impaired blood flow (e.g., aspirin, statins, and cilostazol). I reviewed the precise mechanisms of the AMPK activation pathway and AMPK-modulating drugs.

Citations

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Original Article

Pharmacology, Drug Therapy, and Toxicology
Effects of Cyclooxygenase Inhibitors on Vascular Reactivity and Alterations of Cyclooxygenase Expression.: Ki Young Lee, Jin Woo Park, Eun A Eum, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi; Yeungnam Univ J Med. 2006;23(1):36-44. Published online June 30, 2006; DOI: https://doi.org/10.12701/yujm.2006.23.1.36

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Abstract PDF: BACKGROUND
There is controversy regarding whether COX-2 specific inhibitors are associated with elevation of blood pressure. We compared the effects of aspirin, indomethacin, and celecoxib for vascular reactivity induced by phenylephrine. We also tested the effects of indomethacin and NO donor on COX-1 and COX-2 protein expression, as well as nitrite production in culture medium of vascular smooth muscle cells. MATERILAS AND METHODS: In this experiment, we used the isometric tension study for vascular reactivity. After 45 minutes of pretreatment with aspirin, indomethacin, celecoxib, and phenylephrine induced contractions were tested. COX-1 and COX-2 protein expressions were analyzed by Western blot and nitrite production by the Griess reaction. RESULTS: Although celecoxib pretreatment caused enhanced arterial contraction, aspirin pretreatment induced more potent arterial contraction than celecoxib in the isometric tension study of rabbit femoral artery. COX-1 protein expression was unchanged by indomethacin, SNP and NOR-3; COX-2 protein expression was increased by the addition of indomethacin, SNP, and NOR-3. Especially, NOR-3, a NO donor, significantly increased COX-2 protein expression with unstimulated conditions as well as LPS stimulation. Induction of nitrite production was higher with NOR-3 treatment than SNP treatment with LPS stimulation. CONCLUSION: These results suggest that aspirin caused more potent vascular contraction than celecoxib and indomethacin. COX-2 expression in VSMC depended on the types of NO donor and LPS stimulation.

Review Article

Neurology
Antithrombotic Therapy for Ischemic Stroke.: Jung Sang Hah, Jun Lee; Yeungnam Univ J Med. 2003;20(1):1-12. Published online June 30, 2003; DOI: https://doi.org/10.12701/yujm.2003.20.1.1

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Abstract PDF: Ischemic stroke is among the principal causes of death and disability in the elderly. Although control of blood pressure, decreased cigarette smoking, and modified dietary habits are among important reasons for stroke decline, the use of antithrombotic therapy, rigorously prescribed. Several antiplatelet agents are approved to reduce the risk of recurrent stroke. Aspirin is the best-studied and most widely used antiplatelet agent for stroke prevention; it provides approximately 15% to 25% relatively risk reduction for secondary prevention of stroke or the major vascular death. Combining 2 antiplatelet agents with different mechanism of action was demonstrated to provide a substantial increase in efficacy in several studies. Anticoagulation should be considered first with potential cardiac sources of embolism. Heparin reduces development of erythrocyte-fibrin thrombi that form in regions of vascular stasis especially within the heart, in severely stenosed arteries sometimes engrafted on white thrombi, in acute arterial occlusion. Heparin should not be indiscriminately given to all acute brain ischemia patients, but may contribute to treatment of large artery occlusion and severe stenosis, cardiogenic embolism with a high acute recurrence risk, and dural sinus and cerebral venous thromobosis.

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