A Phase 2 interventional study of Antipac in STEMI - ST Elevation Myocardial Infarction (MI) and Primary PCI - STEMI, sponsored by dr. Ahmad Yasa, Sp.JP, Subsp.K.I.(K), M.Kes, FIHA, FasCC, FA. Completed at 1 site in Indonesia. Open to participants aged 18 Years to 65 Years. Per ClinicalTrials.gov, last updated 2026-10-02.
Sponsored by dr. Ahmad Yasa, Sp.JP, Subsp.K.I.(K), M.Kes, FIHA, FasCC, FA · Phase 2, Interventional, and Treatment
Myocardial ischemia-reperfusion injury still poses a major therapeutic challenge in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). N-acetylcysteine (NAC) is a thiol-containing antioxidant and precursor to glutathione, and may attenuate oxidative stress, inflammatory activation, apoptosis-related signaling and myocardial damage during early reperfusion. However, evidence from clinical trials exploring early intracoronary NAC delivery during PPCI is still limited.
We performed a pilot randomised, double-blind, placebo-controlled trial to determine whether early intracoronary N-acetylcysteine (NAC) administration during primary percutaneous coronary intervention (PPCI) reduces biomarker responses to reperfusion injury and is associated with functional recovery in patients with ST elevation myocardial infarction (STEMI). Participants will be randomized to intracoronary NAC or intracoronary placebo in addition to standard PPCI and guideline based STEMI therapy. The main outcome is the change in malondialdehyde (MDA) from baseline to 24 hours after PPCI. Secondary outcomes include changes in high-sensitivity troponin I, interleukin-6 and caspase-3 and global longitudinal strain and metabolic equivalents derived from the six-minute walk test during follow-up.
The standard reperfusion strategy for patients with ST-segment elevation myocardial infarction is primary percutaneous coronary intervention. While PPCI restores epicardial coronary blood flow and limits ischemic myocardial injury, the process of reperfusion itself may contribute to additional myocardial damage through myocardial ischemia-reperfusion injury. It is mediated through several interacting mechanisms including generation of reactive oxygen species, lipid peroxidation, inflammatory activation, endothelial dysfunction, mitochondrial injury, calcium overload, and programmed cell death.
N-acetylcysteine is an antioxidant with a thiol group and a glutathione precursor which may have cardioprotective effects in ischemia-reperfusion. NAC may reduce oxidative stress by donating thiols, by repleting intracellular glutathione, and by modulating reactive oxygen species . It may also modulate pathways involved in inflammation and apoptosis that are activated during early myocardial reperfusion. Prior studies in the clinical setting of NAC in acute myocardial infarction have largely been administered orally or intravenously. Evidence is limited for direct intracoronary delivery of NAC during PPCI.
This is a pilot, randomized, double-blind, placebo-controlled trial of early intracoronary NAC administration in STEMI patients undergoing PPCI. Eligible patients are adults undergoing PPCI for STEMI who give written informed consent. Participants will be randomized 1:1 to intracoronary NAC or intracoronary placebo in addition to standard PPCI and guideline-directed medical therapy.
In the intervention arm intracoronary NAC is given at a dose of 480 mg diluted in 10 mL normal saline. NAC is administered as early as possible during reperfusion after guidewire crossing when any antegrade coronary flow has been established. If crossing the guidewire alone does not restore flow, NAC is given after initial balloon dilatation when minimal flow is obtained. Solution is delivered through a microcatheter positioned proximal to the culprit lesion over 10 minutes. In the control arm, participants receive an intracoronary placebo of 10 mL normal saline by the same method and duration. The placebo solution appears and has the same volume as the NAC solution to maintain the blinding.
The primary end point was change in serum malondialdehyde from baseline to 24 h after PPCI. Circulating marker of oxidative stress and lipid peroxidation in early reperfusion. MDA . Secondary mechanistic end points are change from baseline to 24 hours after PPCI in high-sensitivity troponin I, interleukin-6, and caspase-3. High-sensitivity troponin I is used as a marker for release of the biomarker of myocardial injury, interleukin-6 as a marker for inflammatory response, and caspase-3 as a marker related to apoptosis.
Secondary functional end points are global longitudinal strain and metabolic equivalents from the six-minute walk test. Two-dimensional speckle-tracking echocardiography is used to measure global longitudinal strain at admission, discharge and 6 months after admission. Functional capacity was measured by the six-minute walk test at discharge and at 6 months, and the walking distance was expressed in metabolic equivalents.
This trial is intended to provide mechanistic and hypothesis-generating evidence regarding whether early intracoronary NAC during PPCI can attenuate reperfusion injury biomarker responses and support functional recovery signals in STEMI patients.
668 studies on the registry are indexed under ST Elevation Myocardial Infarction; 180 are open to participants now.
This study's enrollment of 110 is below the median of 194 across 427 interventional studies indexed under ST Elevation Myocardial Infarction.
Browse ST Elevation Myocardial Infarction studies →This is the only study on the registry with dr. Ahmad Yasa, Sp.JP, Subsp.K.I.(K), M.Kes, FIHA, FasCC, FA as lead sponsor.
Counted across the registry records on this site, refreshed daily.
Exclusion Criteria:
The intervention group will have intracoronary NAC 480 mg immediately after the lesion is opened during primary PCI is performed besides standard treatment of STEMI before further evaluation.
Drug: Antipac
The intervention group will have intracoronary N-AC 480 mg immediately after the lesion is opened during primary PCI besides standard treatment of STEMI before further evaluation.
Drug: Antipac
The first group is the NAC group, which will get intracoronary NAC 480 mg immediately after the lesion is opened during primary PCI. And the second group will have placebo immediately after the lesion is opened during primary PCI.
Malondialdehyde (ng/ml)
Improvements in Biomolecular Parameters (Oxidative Stress)
Time frame: Baseline and 24 hours after intervention
hs-Troponin I (ng/L)
Myocardial necrosis parameter
Time frame: Baseline and 24 hours after intervention
Caspase-3 (pg/dl)
Apoptosis parameter
Time frame: Baseline and 24 hours after intervention
IL-6 (pg/dl)
Inflammation parameter
Time frame: Baseline and 24 hours after intervention
Global Longitudinal Strain (%)
Improvements in Echocardiographic Parameters
Time frame: Baseline, discharge at day-5, and 1 weeks after discharge
Improvements in Physical Parameters
6 Minutes Walking Test (METs)
Time frame: Day-5 after intervention (at discharge) and 6-month after discharge
Plan to share: No — This study was conducted as part of the final project for doctoral program, there was no sponsorship during this study therefore the IPD cannot be shared
From the registry record's own update history. This site started tracking changes on Sep 25, 2026; for anything earlier, see the record history on ClinicalTrials.gov ↗
This study is completed, as verified in Sep 2026. You cannot join it, but the record below documents what was studied.
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