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All Journal Heart Science Journal Narra J
Satrijo, Budi
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Biochemistry, Genetics & Molecular Biology Health Professions Immunology & microbiology Medicine & Pharmacology Public Health

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Troubleshooting for Kinked Coronary Catheter: How to Manage? ; A Case Series Noverike, Nikhen; Satrijo, Budi; Widito, Sasmojo; Kurnianingsih, Novi; Abusari, Muchamad
Heart Science Journal Vol. 4 No. 3 (2023): The Essensial Role of the Metabolic Syndrome in the Development of Cardiovascul
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2023.004.03.7

Abstract

Background: Catheter entrapment and knotting are two problems that might arise during coronary angiography, regardless of the method used. It is not uncommon for the catheter shaft to become kinked during diagnostic or interventional procedures. Still, if the manipulation fails, an invasive retrieval method is usually necessary for cases with extensive catheter kinking.Case Illustration: We present two cases illustrating how different angiography approaches could lead to severe catheter kinking. Because of the significant tortuosity of the vasculature, even a gentle opposite rotation maneuver and the antegrade advancement of multiple guidewires failed to untwist the guide catheter. Once a twisted catheter has been identified via fluoroscopy, the twist can be eased by gently twisting the catheter in the opposite direction. It is not always easy. It could lead to using other interventional techniques such as snare, balloon, or surgical procedures. In our cases, we used a snare to snag the catheter's tip and untied the loop's knot. This prevented the need for unscheduled surgical intervention. We evaluated from angiography. There were no further complications. The patients were released from the hospital the following day.Conclusion: Although a kinked catheter could become entrapped, various approaches can be taken to deal with this difficulty and prevent the need for surgical intervention.
Benefits of Low Dosage of Colchicine Administration on Decreasing Rehospitalization and Mortality within 30 Days in Post-Acute Coronary Syndrome Patients with ST-Segment Elevation Undergoing Percutaneous Coronary Intervention Satrijo, Budi; Ashari, Yordan Wicaksono; Rohman, Mohammad Saifur; Anjarwani, Setyasih; Tjahjono, Cholid Tri
Heart Science Journal Vol. 4 No. 3 (2023): The Essensial Role of the Metabolic Syndrome in the Development of Cardiovascul
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2023.004.03.6

Abstract

Background: The role of inflammation in myocardial infarction and post-infarction MI remodeling has become a concern for the development of treatment in the last decade. Colchicine can prevent increased inflammation during acute injury.Objective: This study focused on the role of colchicine as an on-top medical treatment, hoping it can reduce mortality and short-term rehospitalization in patients with STEMI.Methods: 347 AMI patients (18-80 year old adults) who visited RSUD dr. Saiful Anwar Malang, between February 2022 and January 2023, participated in this prospective, randomized, double-blinded, placebo-controlledexperiment. Patients were split into two groups and given either a placebo or  colchicine 0.5 mg daily for a month. Standard medical therapy was administered concurrently to both groups as an approachable guideline. The study endpoints were mortality and rehospitalization rates.Result: After one month of follow-up, there was a reduction in rehospitalization due to cardiovascular causes (2 [1.3%] vs. 4 [2.7%], HR 3.42 [1.36-8.56], p<0.05), which was significant in the treatment group compared to the control group. Also, there was a reduction in all-cause mortality, but not statistically significant (2 [1,3% v 3 [2,0%], HR 3,38 [0,53-7,48], p>0,05). In the treated group, there was also a lower non-cardiovascular rehospitalization rate compared to placebo, but not significant (4 [2.6%] vs. 7 [4.7], HR 0.42 [0.15-1.02], p<0.05).Conclusion: The administration of low-dose colchicine for one month has shown benefits in reducing rehospitalization in patients with STEMI who receive PCI therapy.
Colchicine attenuates chemical hypoxia-induced pyroptosis through downregulation of nuclear factor kappa B and caspase-1 in cardiomyocytes Satrijo, Budi; Rohman, Mohammad S.; Aulanni'am, Aulanni'am; Sujuti, Hidayat; Lestari, Bayu
Narra J Vol. 5 No. 2 (2025): August 2025
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v5i2.2245

Abstract

Myocardial infarction (MI) is the leading cause of mortality worldwide. During MI, cardiomyocyte necrosis and inflammation are crucial in the post-MI cardiac remodeling process, including pyroptosis. Although colchicine is a well-known anti-inflammatory drug that has been clinically studied in the context of MI, its role in cardiac pyroptosis remains unclear. The aim of this study was to investigate the role of colchicine in pyroptosis in vitro, using CoCl2-induced H9c2 cells. Prior to the primary experiment, the hypoxic model in H9c2 cells was optimized by evaluating hypoxia-inducible factor-1 alpha (HIF-1α) expression and viability in cells exposed to various concentrations of CoCl2 at different time intervals. Subsequently, an in vitro hypoxia model was established by treating H9c2 cells with CoCl2 (600 µM), with or without colchicine (1 µM), for 3 hours. Flow cytometry was used to measure the expression of nuclear factor-kappa beta (NF-κB), interleukin 18 (IL-18), caspase-1, and HIF-1α in pyroptotic cells. Immunofluorescence was used to assess caspase-1 localization and its colocalization with propidium iodide during late-stage pyroptosis. Our data indicated that CoCl2-induced hypoxia significantly upregulated NF-κB, caspase-1, and IL-18 expression, and increased pyroptotic cell death in H9c2 cells. Colchicine treatment attenuated these effects, leading to a marked reduction in NF-κB, caspase-1, and IL-18 expression in hypoxic cells. Colchicine treatment significantly decreased the number of late pyroptotic cells. The protective effect of colchicine was more pronounced in late hypoxia (24-hour) setting compared to early hypoxia (3-hour). These findings suggest that colchicine attenuates cardiac pyroptosis in hypoxic H9c2 cells, as evidenced by the significant downregulation of key proteins involved in this pathway, including NF-κB, caspase-1, and IL-18. This protective effect appeared to be more effective in late hypoxia.
Cardioprotective effects of colchicine: Targeting pyroptosis and inflammation in myocardial infarction Satrijo, Budi; Mohammad Saifur Rohman; Aulanni'am Aulanni'am; Hidayat Sujuti; Bayu Lestari; Rislan Faiz Muhammad
Heart Science Journal Vol. 6 No. 2 (2025): The Complexity in the Management of Heart Rhythm Disorder
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2025.006.02.8

Abstract

Myocardial infarction (MI) is a significant contributor to global morbidity and mortality. The outcome of MI is associated with the inflammatory response triggered by ischemic or necrotic cells. Pyroptosis is a type of programmed cell death that can exacerbate cardiac injury following MI. This study reviewed the potential therapeutic effects of colchicine in regulating cardiac pyroptosis in response to MI. Primarily, colchicine inhibits tubulin polymerization and microtubule formation, disrupting inflammasome advancement and the subsequent secretion of various pro-inflammatory mediators. In particular, colchicine disrupts the NLRP3 inflammasome assembly process by blocking ASC recruitment into the complex, suggesting its potential to mitigate the inflammatory response related to cardiac pyroptosis. Additionally, colchicine binds to P2X7 receptors, reducing ATP-induced microtubule and pore formation, which attenuates reactive oxygen species and IL-1β production. A clinical trial involving colchicine showed positive outcomes in lowering the occurrence of major cardiovascular events in individuals with coronary artery disease (CAD). Nonetheless, additional studies are required to ascertain the ideal dosage, timing, and long-term effects of colchicine in the infarcted myocardium before it can be routinely recommended for post-MI treatment. In conclusion, colchicine's modulation of the inflammatory response and inhibition of pyroptosis highlight its potential as a cardioprotective agent for MI management.
Co-Authors Abusari, Muchamad Afifah, Yuri Anjarwani, Setyasih Aryanugraha, Teguh Ashari, Yordan Wicaksono Aulanni'am Aulanni'am Aulanni'am, Aulanni'am Bayu Lestari Caesario, Fahreza Cholid Tri Tjahjono Djanggan Sargowo Emil Fathoni, Emil Galuh, Lukitasari Ayu Hidayat Sujuti Hidayat Sujuti Indra Prasetya Indrihapsari, Pratiwi Kurnianingsih, Novi Lestari, Bayu Martini, Heny Mayangsari, Veny Millisani, Hayla Iqda Mohammad S. Rohman Mohammad Saifur Rohman Noverike, Nikhen Nugraha, Yudha Tria Putri, Valerinna Yogibuana Swastika Rahimah, Anna Fuji Rislan Faiz Muhammad Rosandy, Kharima Ogit Saskia Dyah Handari Suprayoga, Imam Mi'raj Widito, Sasmojo zunardi, Lutfi hafiz