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Effect of Intracoronary N-Acetylcysteine in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Effect of Intracoronary N-Acetylcysteine on Malondialdehyde, Interleukin-6, High Sensitivity Troponin I, Caspase-3, Global Longitudinal Strain, and 6-Minutes Walking Test in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Status
Completed
Phases
Phase 2
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT06850831
Enrollment
70
Registered
2025-02-27
Start date
2025-04-01
Completion date
2025-12-07
Last updated
2026-02-05

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Primary PCI - STEMI, STEMI - ST Elevation Myocardial Infarction (MI)

Keywords

STEMI, Primary PCI, Intracoronary NAC, Reperfusion Injury, Apoptosis, Necrosis, Oxidative Stress, Remodelling, Left ventricular dysfunction, Physical Recovery

Brief summary

Primary percutaneous coronary intervention (PCI) is the gold standard for reperfusion therapy in patients with ST-elevation myocardial infarction (STEMI), as it restores blood flow by clearing the blocked coronary artery. This process helps reoxygenate the previously hypoxic myocardium, potentially preventing further myocardial cell death. However, despite its benefits, reperfusion therapy, including primary PCI, can also lead to reperfusion injury, which may worsen myocardial damage, increase infarct size, and negatively impact patient outcomes. One of the key contributors to reperfusion injury is reactive oxygen species (ROS), which can induce oncosis, necrosis, and apoptosis, ultimately promoting cell death, myocardial remodeling, left ventricular systolic dysfunction and poorer clinical outcomes. N-Acetylcysteine (NAC), widely known for its mucolytic properties, has also been recognized for its antioxidant and cardioprotective effects. By reducing oxidative stress, NAC has been shown to decrease oncosis, necrosis, and apoptosis, as evidenced by lower levels of malondialdehyde, IL-6, troponin, caspase-3, and major adverse cardiac events in STEMI patients. However, existing research on NAC has only explored oral and intravenous administration. Given that reperfusion injury occurs rapidly, an optimal approach would involve delivering cardioprotective agents directly to the target site, specifically coronary artery endothelial cells. To date, no studies have directly investigated the effects of intracoronary NAC administration in STEMI patients undergoing primary PCI.

Detailed description

This study is a double-blind, randomized controlled trial, single-center study in STEMI patients undergoing primary PCI patients held in Moewardi General Hospital, Central Java, Indonesia. The investigator divided 70 patients with STEMI into two groups, the first is the NAC group, which will get 480 mg of intracoronary NAC immediately after the lesion is opened during primary PCI is performed and the second group will have a normal saline bolus. Each patient will be checked for malondialdehyde, IL-6, hs-troponin I, and caspase-3 just before the primary PCI is performed and 24 hours after intervention. GLS examinations were carried out at admission, discharge, and 6 months after the intervention. The 6MWT examinations were conducted at 1 week and 6 months after the intervention. Furthermore, researchers recorded data on all-cause mortality, rehospitalization, and ACS recurrence at day 30 and 6 months. The study was approved by the hospital ethics committee. The clinical parameters above will then be analyzed. To determine the mean difference between each group (intervention and control) before and after treatment a paired T-test is used if the data distribution is normal (if not, the Wilcoxon test is used). To determine the mean difference between unpaired groups (treatment and control), an independent T-test is used if the distribution is normal (if not, the Mann-Whitney test is used). Normality testing is performed using the Shapiro-Wilk test, considering the sample size is less than 50 per group.

Interventions

DRUGAntipac

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.

Sponsors

dr. Ahmad Yasa, Sp.JP, Subsp.K.I.(K), M.Kes, FIHA, FasCC, FA
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
DOUBLE (Subject, Investigator)

Intervention model description

Randomized Controlled Trial and Double Blind (Researcher & Patients)

Eligibility

Sex/Gender
ALL
Age
30 Years to 60 Years
Healthy volunteers
No

Inclusion criteria

1. STEMI patients according to The Fourth Universal Definition of Myocardial Infarction from the European Society of Cardiology, American College of Cardiology, American Heart Association, and World Heart Federation Treated by Primary PCI. 2. Aged 30-60 years 3. Willing to participate in the study and sign informed consent.

Exclusion criteria

1. Patients with cardiogenic shock (SBP ≤ 80 mmHg, cold extremities, urine output \<0.5 ml/kg/hour) \<24 hours before randomization 2. Patients with a history of myocardial infarction 3. Patients with a history of chronic heart failure before the onset of AMI 4. Patients scheduled for coronary artery bypass surgery 5. Patients with chronic renal failure or requiring dialysis 6. Patients with chronic inflammation 7. Patients with malignancy 8. Patients with a history of hyper/hypothyroidism 9. Patients with acute infection 10. Patients with sepsis 11. Patients with acute stroke 12. Patients with pulmonary fibrosis 13. Patients with a history of autoimmune disease 14. Patients with a history of anti-inflammatory / antioxidant supplementation 15. Patients with allergy to N-acetylcysteine 16. Pregnant and lactating patients

Design outcomes

Primary

MeasureTime frameDescription
Improvements in Biomolecular Parameters (Oxidative Stress)24 hoursMalondialdehyde (ng/L)
Improvements in Biomolecular Parameters (Inflammation)24 hoursInterleukin-6 (ng/L)
Improvements in Biomolecular Parameters (Necrosis)24 hourshigh sensitivity troponin I (ng/L)
Improvements in Biomolecular Parameters (Apoptosis)24 hoursCaspase-3 (ng/L)

Secondary

MeasureTime frameDescription
Improvements in Echocardiographic Parameters1 weeksGlobal Longitudinal Strain (%)
Improvements in Physical Parameters1 week6 Minutes Walking Test (METs)
All-cause mortality30-days and 6 months
Rehospitalization30-days and 6 months
Recurrent ACS events30-days and 6 months

Countries

Indonesia

Contacts

PRINCIPAL_INVESTIGATORAhmad Yasa, MD

Universitas Sebelas Maret

PRINCIPAL_INVESTIGATORTrisulo Wasyanto, Prof. DR.dr.

Universitas Sebelas Maret

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 6, 2026