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"Penyakit kardiovaskuler merupakan salah satu penyebab kematian global. Tindakan reperfusi dengan Intervensi Koroner Perkutan Primer (IKPP) adalah tatalaksana untuk revaskularisasi, namun tindakan ini memiliki efek paradoks berupa cedera iskemik pasca reperfusi yang meningkatkan morbiditas dan mortalitias. Mekanisme patogenesis cedera reperfusi yaitu respon inflamasi melalui pelepasan sitokin proinflamasi salah satunya IL-1b. Penelitian ini bertujuan mengkaji perubahan IL-1b pada serum pasien infark miokard akut-elevasi segmen- ST (IMA-EST) yang menjalani IKPP sebelum dan pasca 48 jam tindakan reperfusi dengan pemberian kolkisin. Penelitian melibatkan 64 subjek terdiri dari 30 subjek kelompok kolkisin dan 34 subjek kelompok plasebo. Hasil penelitian menunjukkan peningkatan kadar IL-1b pasca 48 jam IKPP pada kedua kelompok  dengan delta perubahan pada kelompok kolkisin 0,4 pg/mL (-0,2 – 11,3 pg/mL) dan kelompok kontrol 0,3 pg/mL (-1,2 – 14,0 pg/mL), namun tidak didapatkan perbedaan bermakna antar kedua kelompok (p=0,136). Penelitian ini merupakan penelitian pertama yang menilai efek kolkisin terhadap perubahan kadar IL-1b pada pasien IMA-EST yang menjalani IKPP, sehingga dapat digunakan sebagai acuan bagi penelitian selanjutnya.

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Cardiovascular disease is one of the leading causes of death globally. Reperfusion with Primary Percutaneous Coronary Intervention (PCI) is a management for revascularisation, but it has a paradoxical effect of post-reperfusion ischaemic injury that increases morbidity and mortality. Pathogenesis of reperfusion injury is an inflammatory response through release of proinflammatory cytokines, including IL-1b. This study aims to assess levels of IL-1b changes in serum of ST-elevation acute myocardial infarction (STEMI) patients who underwent PCI before and after 48 hours of reperfusion action with colchicine administration. The study involved 64 subjects consisting of 30 subjects in colchicine group and 34 subjects in placebo group. Study results showed an increase in IL-1b levels after 48 hours of PCI in both groups with delta changes in colchicine group of 0.4 pg/mL (-0.2 – 11.3 pg/mL) and control group of 0.3 pg/mL (-1.2 – 14.0 pg/mL), but there was no significant difference between the two groups (p=0.136). This is the first study to assess the effect of colchicine on levels of IL-1b changes in STEMI patients undergoing PCI, so it can be used as a reference for future studies."

"Latar Belakang: Iskemia dan cedera reperfusi pada tungkai dapat berdampak sistemik sampai kegagalan fungsi organ. Beberapa penelitian telah dilakukan untuk mencegah komplikasi jauh atau remote dari cedera reperfusi, namun hal ini masih banyak diperdebatkan. Penelitian ini dilakukan untuk melihat perbedaan kerusakan tubulus ginjal pada iskemia tungka bawahi akut yang tanpa perlakuan, perlakuan prekondisi iskemik dan perlakuan hipotermia Penelitian ini merupakan Metode: Penelitian eksperimental yang dilakukan pada 18 ekor kelinci New Zealand White, dengan ligasi arteri iliaka komunis kanan selama 4 jam dan reperfusi selama 8 jam, dibagi menjadi 3 kelompok: kelompok 1, tanpa perlakuan sebagai kontrol; kelompok 2, diberikan perlakuan prekondisi iskemik sebelum tindakan iskemik: dan kelompok 3; diberikan perlakuan hipotermia pada tungkai kanan selama iskemia. Setelah euthanasia, diambil sampel ginjal untuk pemeriksaan histopatologi.Hasil: Perbandingan kerusakan tubulus ginjal antara kelompok iskemia saja dengan kelompok perlakuan prekondisi iskemik tidak menunjukkan perbedaaan yang bermakna (p= 0.092), sedangkan perbandingan antara kelompok iskemia saja dengan kelompok perlakuan hipotermia menunjukkan hasil perbedaan yang bermakna (p = 0.033). Kesimpulan: Perlakuan hipotermia dapat mengurangi kerusakan tubulus ginjal akibat cedera remote reperfusi iskemia tungkai bawah akut.

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Background: Ischemia and reperfusion injury of the lower limb may cause a systemic effect to multi-organ failure. Several studies have been done to prevent distant or remote complication from reperfusion injury, but it is still in debate. This study was conducted to see the differences in renal tubular damage in acute limb ischemia without treatment, treatment of ischemic precondition and treatment of hypothermia.

Methods: An experimental study in 18 New Zealand White rabbits, who performed right common iliac artery ligation for 4 hours and reperfusion during 8 hours, divided into 3 groups: group 1, no treatment as a control; group 2, given the treatment of ischemic precondition before ischemic action: and group 3; given the treatment of hypothermia on the right leg during ischemia. After euthanasia, kidney samples were taken for histopathological examination.

Results: Comparison of renal tubular damage among any group of ischemia with ischemic preconditioning treatment group showed no significant difference (p = 0.092), whereas the comparison between groups ischemia alone with hypothermia treatment group showed a significant difference (p = 0.033).

Conclusion: Treatment of hypothermia may reduce renal tubular damage due to remote reperfusion injury in acute limb ischemia."

"Introduksi: Iskemia yang terjadi di suatu lokasi di tubuh mengakibatkan kerusakan pada lokasi yang berjauhan; kondisi ini dikenal dengan sebutan cedera reperfusi. Vili intestinal merupakan satu target organ terjadinya kerusakan pada cedera reperfusi dan menjadi motor kegagalan multi organ sistemik. Hipotermia yang ditakuti pada syok justru menunjukkan keuntungan karena bersifat proteksi terjadinya kerusakan vili. Penelitian ini bertujuan membandingkan efek protektif hipotermia dan pre-conditioning pada iskemia.Metode. Dilakukan penelitian eksperimental pada kelinci New Zealand White (n=18) dengan satu kelompok kontrol (iskemia) dan dua kelompok perlakuan (hipotermia dan pre-conditioning). Dilakukan ligasi a. iliaca communis selama 4 jam, hipotermia sedang (28°C), dan iskemia pre-conditioning pada masing-masing kelompok. Kemudian kelinci dibiarkan hidup selama 8 jam. Setelah dekapitasi, diambil sampel ileum untuk pemeriksaan histopatologi.Hasil: Dari 18 kelinci eksperimental, 1 mengalami drop out karena infeksi. Dilakukan skoring kerusakan vili intestinal berdasarkan kriteria Pusponegoro yang dimodifikasi dengan nilai minimal 4 dan maksimum 12. Kelompok perlakuan pre-conditioning mengalami kerusakan paling minim (= 6,2 ) diikuti kelompok hipotermia (= 7,1).Konklusi: Pre-conditioning menunjukkan kerusakan paling minim; dengan kata lain memberi efek proteksi lebih baik dibandingkan dengan kelompok lainnya.

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Introduction: Ischemia occurring in a location in the body results in damage to distant locations; this condition is known as reperfusion injury. Intestinal vilia is a target organ of the occurrence of damage to reperfusion injury and a motor failure of multi-organ systemic. The dreaded hypothermia in shock actually shows an advantage because it protects the occurrence of villous damage. This study aimed to compare the protective effect of hypothermia and pre conditioning on ischemia.

Methods: Experimental studies were conducted on New Zealand White rabbit (n = 18) with one control group (ischemia) and two treatment groups (hypothermia and pre-blocking). Conducted ligation a. iliaca communist for 4 hours, moderate hypothermia (28°C), and preconditioning ischemia in each group. Then the rabbit is left alive for 8 hours. After decapitation, ileum samples were taken for histopathologic examination.

Results: Of the 18 experimental rabbits, 1 had dropped out due to infection. Scores of villus intestinal damage were performed based on modified Pusponegoro criteria with a minimum score of 4 and a maximum of 2. The pre-treatment group experienced the least damage (=6.2) followed by the hypothermia group (=7,1).

Conclusion: Pre conditioning shows the least damage; in other words gives a better protective effect compared to other groups."

"Tumor necrosis factor alpha (TNF-alpha) adalah salah satu sitokin proinflamasi yang berperan pada timbulnya cedera iskemia-reperfusi pasien infark miokard akut yang menjalani tindakan intervensi koroner perkutan primer (IKPP). Kolkisin merupakan salah satu obat antiinflamasi yang diduga memiliki pengaruh terhadap TNF-alpha. Penelitian ini bertujuan untuk mengetahui peran kolkisin terhadap kadar TNF-alpha serum pasien infark miokard akut dengan tindakan intervensi koroner perkutan primer. Desain penelitian uji klinis acak tersamar ganda menggunakan sampel sisa serum penelitian dari subjek pasien infark miokard akut Rumah Sakit dr. Cipto Mangunkusumo. Subjek penelitian dibagi menjadi dua kelompok. Kelompok studi diberikan loading dose kolkisin 2 mg, kemudian dilanjutkan 2 x 0,5 mg per hari secara oral selama 48 jam, sementara kelompok kontrol diberikan plasebo. Analisis kadar TNF-alpha menggunakan metode ELISA yang diperiksa sebelum dan 48 jam pasca-IKPP untuk mendapatkan delta perubahan kadar TNF-alpha. Terdapat 64 subjek yang dianalisis terdiri dari 30 kelompok kontrol dan 34 kelompok studi. Delta kadar TNF-alpha pasca-IKPP kelompok kontrol (2,2) terhadap delta kadar TNF-alpha kelompok studi (0,7). Penelitian ini merupakan penelitian pertama tentang pengaruh kolkisin terhadap kadar TNF-alpha pada pasien infark miokard akut dengan tindakan intervensi koroner perkutan primer di Indonesia. Pengukuran TNF-alpha perlu dilakukan lebih dari dua kali untuk melihat dinamika kadar TNF-alpha pada pasien infark miokard akut yang menjalani tindakan intervensi koroner perkutan primer dan penelitian lanjutan diperlukan untuk menilai peran kolkisin sebagai obat antiinflamasi dengan pemeriksaan menggunakan metoda ELISA dengan reagen high-sensitive.

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Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that plays a role in the emergence of ischemia-reperfusion injury in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention (PCI). Colchicine is an anti-inflammatory drug believed to affect TNF-alpha. This study aimed to determine the role of colchicine on serum TNF-alpha levels in acute myocardial infarct patients undergoing primary percutaneous coronary intervention. The research design was a double-blind, randomized clinical trial using residual research serum samples from patients with acute myocardial infarction at Dr. Hospital. Cipto Mangunkusumo. The research subjects were divided into two groups. The study group was given a loading dose of 2 mg colchicine and then continued at 2 x 0.5 mg per day orally for 48 hours, whereas the control group was given a placebo. Analysis of TNF-alpha levels using the ELISA method was performed before and 48 hours after primary percutaneous coronary intervention to obtain the delta of changes in TNF-alpha levels. There were 64 subjects analyzed, comprising 30 control groups and 34 study groups. The delta of TNF-alpha levels post-PCI in the control group (2.2) compared with the delta of TNF-alpha levels in the study group (0.7). This is the first study on the effect of colchicine on TNF-alpha levels in acute myocardial infarction patients with primary percutaneous coronary intervention in Indonesia. TNF-alpha measurements need to be carried out more than twice to determine the dynamics of TNF-alpha levels in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention, and further research is needed to assess the role of colchicine as an anti-inflammatory drug by ELISA with high-sensitive reagents."

"Much has been written about reperfusion injury in the past decade but unfortunately the information has been generally presented in the form of original specialist papers and little if any integral publication exists on the topic, summarising and analysing the clinical impact of the condition and its management. The pathophysiology and molecular mechanisms of reperfusion injury are complex and, regarding diagnosis, individual diagnostic techniques have been proposed but without a proper assessment of the relative values of these methods. A publication dealing with integral diagnostic strategies would be welcome by the managing physician. Management of the condition is also problematic, as strategies that appear to work in the experimental models do not translate into beneficial interventions in patients. There is a need for these issues to be addressed and discussed in a monographic fashion. Management of myocardial reperfusion injury will tackle these issues in a modern and systematic way and the information will be delivered in a fashion that will be appealing to the reader."

"Pendahuluan: Cedera iskemia reperfusi CI/R merupakan masalah serius yang dihadapi pascahipoksia menyebabkan kerusakan sel yang letaknya berjauhan remote organ injury. Strategi yang digunakan untuk mengurangi kerusakan hepar pascaiskemia adalah melalui penerapan ischemic pre conditioning PI/R dan hiportemia. PI/R telah terbukti mengurangi kerusakan jaringan melalui mekanisme resistensi terhadap iskemia dan kebutuhan energi lebih rendah. Sedangkan hipotermia menghambat laju kematian sel sehingga dapat diterapkan sebagai terapi awal pada tatalaksana trauma dengan tujuan mencegah kerusakan bertambah berat. Penelitian ini bertujuan untuk diketahuinya efek protektif PI/R dan hipotermia terhadap perubahan morfologi jaringan hepar dan peningkatan kadar malondialdehyde MDA sebagai respon stress oksidatif. Metode: Studi eksperimental pada 24 ekor Oryctolagus cuniculus. Kelompok iskemia dilakukan ligasi arteri femoralis komunis dalam pembiusan selama empat jam untuk menginduksi iskemia, kemudian ligasi dibuka dan kelinci dibiarkan beraktivitas selama delapan jam. Pada kelompok PI/R dilakukan ligasi berulang arteri femoralis komunis kanan selama dua menit, dilepaskan tiga menit sebanyak dua siklus, kemudian diligasi selama empat jam. Kelompok hipotermia, dilakukan iskemia disertai membungkus ekstremitas bawah kanan dengan es, suhu antara 31-33oC Kemudian dilakukan laparotomi, dan diambil organ hepar. Pemeriksaan histopatologi hepar dilihat dari 3 zona, sentral, midzonal, perifer. Untuk menilai stress oksidatif jaringan dilakukan pemeriksaan biokimia dengan malondialdehyde MDA. Dilakukan uji statistik terhadap variabel tersebut dengan kemaknaan. Hasil: Pada pemeriksaan histomorfologi terdapat perbedaan perubahan histomorfologi pada sampel kontrol PI/R, dan Hipotermia terhadap iskemia (p<0,05). Derajat kerusakan histomorfologi pada kelompok PI/R lebih rendah dibandingkan kelompok iskemia reperfusi pada semua zona (p sentral = 0,015, p medial = 0,019, p perifer = 0,026). Analisis kadar MDA memperlihatkan terjadi peningkatan pada kelompok iskemia reperfusi menujukkan adanya stress oksidatif. Kadar MDA pada kelompok PI/R dan hipotermia lebih rendah dibandingkan kelompok iskemia.(p = 0,002). Konklusi: Keadaan iskemia reperfusi menyebabkan perubahan histomorfologi dan stres oksidatif sel–sel hepar. PI/R dan hipotermia mempunyai efek protektif pada cedera iskemia reperfusi. Efek protektif PI/R lebih baik dari hipotermia.

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Introduction: Ischemia-reperfusion injury IRI is a serious problem occuring after hypoxia it causes injuries to cells located remotely from one another remote organ injury. Strategies used to decrease hepatic injuries post ischemic condition are composed as ischemic pre-conditioning IPC and hypothermia management procedures. IPC has been proven to decrease tissue injuries through resistance mechanisms towards ischemia and lower energy requirements. Meanwhile, hypothermia detained the rate of cell deaths, therefore, it can be used as initial therapy on trauma management in order to prevent worsening of the injuries. This research aims to evaluate the protective effects of IPC and hypothermia towards morphological changes of hepatic tissues and the increase of malondialdehyde MDA level as a response to oxidative stress.Methods.

Methods: This research is an experimental, descriptive-analytical study on 24 Oryctolagus cuniculus. The specimens were divided into four groups, with one group as control. The ischemia group underwent femoral artery ligations under anesthesia for four hours to induce ischemia. Afterwards, the ligations were released and the rabbits were free to roam for eight hours. The IPC group underwent repeated ligations of right communal femoral artery for two minutes and three minutes of release in two cycles. Afterwards, the arteries were ligated for four hours. The hypothermia group underwent ischemia and wrapping of right lower extremities using ice, with temperature around 31-33oC. Afterwards, laparotomies were conducted on all groups to obtain and evaluate the liver. Hepatic histopathology assessment were conducted from 3 zones, the central, midzone, and peripheral zone. To evaluate the effects of oxidative stress on the tissue, a biochemical assessment with malondialdehyde MDA was conducted. Statistical tests were then conducted to assess the relationship between the variables with significance level p < 0.05.

Results: On histomorphological assessment, there were histomorphologic changes on control samples for IPC and hypothermia compared to ischemia p < 0.05. On MDA level analysis, there were increases in all four groups p < 0.05. However, there were no significant differences for the histomorphological changes when compared between central, medial, and peripheral zones.

Conclusion: Ischemic reperfusion condition causes histomorphological changes and oxidative stress on hepatic cells. IPC and hypothermia have protective effects from ischemia-reperfusion injuries. The protective effects of IPC was better than hypothermia."

"Latar Belakang. Cedera Reperfusi Iskemia merupakan eksaserbasi paradoks mengakibatkan disfungsi dan kematian sel setelah aliran darah direstorasi ke jaringan yang sebelumnya iskemia. Pada iskemia tungkai akut, reperfusi menimbulkan reaksi kompleks melibatkan inflamasi lokal maupun sistemik dengan dampak lokal sindroma kompartemen dan dampak sistemik berupa disfungsi hingga kegagalan multi organ. Platelets activating factors (PAF) sebagai mediator inflamasi pospholipid mempunyai efek fisiologis yang poten dan beragam, sehingga meningkatkan respon inflamasi pada cedera reperfusi iskemik.Berbagai upaya untuk mencegah dan memperingan cedera reperfusi iskemik, antara lain penggunaan prosedur ischemic preconditioning, antioksidan dan terapi anti-sitokin telah diteliti namun hasil dan manfaat klinisnya belum memuaskan. PTX, phosphodiesterase nonspesifik derivat xanthine, memperlihatkan efek penekanan inflamasi dan menghambat interaksi lekositendotel yang menjanjikan dalam mencegah cedera reperfusi. Namun hasil penelitian mengenai peran pentoxifylinne dalam menekan reaksi inflamasi melalui penekanan PAF pada iskemia tungkai akut tidak konsisten. Sehingga penelitian ini bertujuan untuk menilai peran PTX dalam mengurangi cedera reperfusi melalui penekanan mediator inflamasi PAF pada hewan coba kelinci dengan Reperfusi Iskemia tungkai akut.Metodologi. Dilakukan tindakan iskemik tungkai kiri selama 3 jam yang diikuti 2 jam periode reperfusi pada 10 ekor kelinci New Zealand White jantan yang dibagi menjadi 2 kelompok (kelompok pentoksifin dan kelompok kontrol) secara acak. Pada kelompok perlakuan diberikan PTX 30 menit sebelum reperfusi dengan dosis initial bolus 40 mg/kgBB diikuti dengan dosis rumatan 1 mg/kg BB/jam hingga 3 jam periode reperfusi. Pada kelompok kontrol diberikan cairan garam fisiologis dengan kecepatan dan volume yang sebanding. Tindakan Iskemik dilakukan dengan oklusi arteri iliaka komunis sinistra mengunakan klem selama 3 jam kemudian dilanjutkan dengan restorasi aliran darah. Pengambialn sampel untuk pemeriksaan kadar PAF dilakukan pada 2,5 jam iskemik dan pada 2 jam reperfusi.Hasil. Pada periode Iskemik dua jam tiga puluh menit tidak mengakibatkan perbedaan bermakna (p=0,754), kadar rerata PAF pada kelompok PTX 13,09 ± 0,41 pg/mL dan kelompok kontrol I3,38 ± 0,28 pg/mL. Pada jam ke dua tindakan reperfusi ditemukan perbedaan bermakna (p=0,009) kadar rerata PAF dari kelompok PTX menurun menjadi 11,36±0,78 pg/mL dan kelompok kontrol meningkat menjadi 25,5±0,78 pg/dL.Kesimpulan. PTX menurunkan kadar PAF plasma kelinci dengan cedera reperfusi iskemikia tungkai akut.

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Background. Ischemic reperfusion injury is a paradoxical exacerbation of cell dysfunction and death following the restoration of blood flow to previously ischemic tissue. Restoration of blood flow is essential to salvage ischemic tissue, however reperfusion itself paradoxically causes further damage to the ischemic tissue, threatening function and viability both organ local and distal through the inflammation response.

In Acute limb ischemia, there are essentially two components: a local component that can result in increasing the regional damage from ischemia inflammatory responses which may result in local syndrome, compartment syndrome, and systemic syndrome, multi organ dysfunction and failure.

Several method and attempt had been studied and performed to prevent and attenuate reperfusion injury such as, ischemic preconditioning, antioxidant, and anti-cytokine therapy, but their clinical benefit were not satisfactory. Pentoxifylline has emerged as an agent that may attenuate inflammation response through several mechanisms. However, studies on PTX and its function to prevent and attenuate inflammation response through attenuating PAF in acute limb ischemic were not consistent. In this study the role of PTX and its function to prevent and attenuate inflammation response through attenuating PAF in acute limb ischemic was investigated.

Methods. Acute limb ischemia in the left lower limbs of 10 New Zealand White male rabbit were performed for 3 hour followed by 2 hours period of ischemia. The rabbits were randomly separated into 2 groups of five (group pentoxifylinne and group control). The Pentoxifylline group was given PTX 40 mg/kg bolus half an hour prior to reperfusion followed by maintenance dose 1 mg/kg/hour until 2 hour post reperfusion, while the control group was given normal saline solution with comparable volume and rate administration. Acute limb Ischemic procedure was performed by direct occlusion of the left femoral artery using non traumatic clamp and followed by releasing the clamp after 3 hours of occlusion. Level of PAF were measured after 2.5 hour of ischemic period and after 2 hours of reperfusion period.

Results. After 2.5 hours of ischemic period, the mean PAF levels did not show any significant difference (p=0.754). The mean PAF level of pentoxifylline group 13.09f0.41 pg/mL, while the mean PAF level of control group 13.38±0.28 pg/mL, After 2 hours period of reperfusion, there were significant differences of mean PAF level between the two groups (p=0.009). The mean PAF level in the control group increase by 12.1 110.79 to became 25.5±0.78 pg/dL, while the mean PAF level of the PTX group decrease by 1.73f1.1 pg/mL and became 11.36±0.78 pg/m L.

Conclusion. PTX decreased the PAF level in rabbits with acute limb ischemic reperfusion injury."

"Infark miokard akut (IMA) telah menjadi sebab utama kematian di negara Barat maupun di Indonesia. Keterlambatan diagonis dan tatalaksana dini yang salah seringkali mengakibatkan kegagalan reperfusi dengan trombolitik. Dokter umum sebagai lini kesehatan pertama harus dibekali dengan ketrampilan mendiagnosis dan juga menangani IMA. Dalam tulisan ini dilaporkan kasus gagal terapi trombolitik pada pria usia 47 tahun setelah tujuh jam mengalami nyeri dada angina, yang telah sebelumnya ditangani oleh dokter umum. (Med J Indones 2005; 14:249-52)

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Acute myocardial infarction (AMI) has been the leading cause of death in Western countries, as well as in Indonesia. Delay in diagnosis and incorrect early management often result in failure of thrombolytic reperfusion. General practitioner (GP) as the primary care, needs to be equipped with the ability to diagnose and moreover to manage AMI. A case of fail thrombolytic management in a 47 years old man after seven hours of angina typical chest pain, after previously managed by GP, is being reported. (Med J Indones 2005; 14:249-52)"

"Latar belakang: Inflamasi memegang peranan penting dalam IMA-EST, terutama kejadia cedera reperfusi. Kolkisin merupakan sediaan obat anti inflamasi, yang dapat menekan inflamasi saat terjadi cedera reperfusi. Kami menilai keefektivan dari pemberian kolkisin pada pasien IMA-EST yang menjalani IKPP dalam menekan cedera reperfusi. Metode: Penelitian ini merupakan uji klinis, tersamar ganda, dengan plasebo, yang dilakukan multisenter di dua rumah sakit di Jakarta dengan fasilitas IKPP dari Desember 2022 hingga April 2023. Pasien IMA-EST yan menjalani IKPP diberikan dosis muat kolkisin 2 mg, kemudian dosis pemeliharaan 2x0,5 mg selama 2 hari, dan amilum pada kelompok plasebo. Pasien diamati kejadian cedera reperfusi berupa TIMI flow, kejadian aritmai, syok dan aritmia akibat reperfusi.Hasil: Sebanyak 77 subyek IMA-EST dengan rerata usia 55.2 ± 9.9 tahun menjalani IKPP. 37 subyek mendapat kolkisin, 40 subyek mendapat placebo. Kebanyakan subjek ialah laki-laki (77.5%), menderita 3 vessel disease (44,1%), oklusi di LAD ( 53,2%). Pemberian kolkisin tidak berhasil menurunkan kejadia cedera iskemia reperfusi (51.5% vs. 42.4%; p = 0.437). Analisi komorbiditas ( hipertensi, gagal ginjal, diabetes mellitus, dan obesitas) dan hasil angiografi ( jumlah pembuluh darah coroner yang sakit, diameter pembuluh darah, dan lokasi penyumbatan yang menyebabkan IMA-EST) tidak berhasil menunjukkan kemaknaan secara statistic. Kejadian efek samping sama pada kedua kelompok (21.6% vs. 15%). Kesimpulan: Pemberian kolkisin pada pasien IMA-EST yang menjalani IKPP tidak berhasil menurunkan kejadian cedera reperfusi.

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Background: Inflammation plays a role in ST-segment elevation myocardial infarction (STEMI), especially in reperfusion injury (RI). Colchicine, an anti-inflammatory drug, can suppress inflammation during RI. We assessed the effectiveness of administering colchicine to STEMI patients undergoing primary percutaneous coronary intervention (PPCI) in suppressing RI events.

Methods: This study was a randomized, double-blind, placebo-controlled clinical trial conducted in a multicenter manner at two hospitals in Jakarta with IKPP facilities from December 2022 to April 2023. STEMI patients that underwent PPCI received 2 g of colchicine as a loading dose and a maintenance dose of 0.5 g every 12 hours for two days or amylum at a similar dose. Patients were observed for RI events (low-flow thrombolysis in myocardial infarction (0–2) during angiography procedure, reperfusion arrhythmia, cardiogenic shock, or persistent chest pain).

Results: Seventy-seven STEMI patients with a mean age of 55.2 ± 9.9 years underwent PPCI. Of these patients, 37 received colchicine, and 40 received a placebo. Most subjects were male (77.5%), suffered three-vessel disease (44.15%), and occlusion in left anterior descending coronary artery (53.24%). Colchicine was found to fail to reduce the incidence of ischemia-RI (51.5% vs. 42.4%; p = 0.437). Analysis of comorbidities (hypertension, chronic kidney disease, diabetes mellitus, and obesity) and angiography results (vessel disease, lesion diameter, and culprit artery) failed to demonstrate a statistical difference in RI. Side effects were similar in the colchicine and placebo groups (21.6% vs. 15%).

Conclusion: Colchicine administration in STEMI patients undergoing PPCI failed to reduce RI.

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"Penyakit jantung koroner (PJK) atau infark miokard (IMA) adalah salah satu penyebab utama kematian di seluruh dunia. Tindakan reperfusi miokardial merupakan pendekatan utama dalam penanganan PJK. Cedera iskemia-reperfusi (IRI) mewakili cedera tambahan pada otot jantung yang terjadi akibat disfungsi seluler setelah proses reperfusi. Vascular endothelial growth factor (VEGF) merupakan protein yang berperan dalam induksi angiogenesis dan meningkatkan permeabilitas vaskuler. VEGF penting dalam pembentukan pembuluh darah kolateral pasca IMA, namun kadar VEGF yang terlalu tinggi diketahui mengakibatkan restenosis pasca tindakan intervensi koroner perkutan primer (IKPP). Kolkisin dosis rendah diketahui menurunkan kadar VEGF. Penelitian ini bertujuan menilai pengaruh pemberian kolkisin terhadap penurunan kadar VEGF pada serum pasien infark miokard akut-elevasi segmen ST (IMA-EST) sebelum dan pada 48 jam pasca tindakan reperfusi. Penelitian dilakukan menggunakan desain uji klinik tersamar ganda (double blinded randomized clinical trial) yang melibatkan 63 subjek. Pada hasil penelitian didapatkan penurunan kadar VEGF pada 48 jam pasca reperfusi namun tidak didapatkan perbedaan bermakna pada analisis perubahan (delta) kadar VEGF sebelum dan pada 48 jam pasca tindakan reperfusi antara kedua kelompok. Penelitian ini merupakan penelitian pertama yang menilai pengaruh pemberian kolkisin terhadap kadar VEGF pada pasien IMA-EST pasca reperfusi. Penelitian ini dapat dijadikan dasar penelitian lanjutan untuk menilai penurunan kadar VEGF dengan pemberian kolkisin dalam jangka panjang.

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Coronary heart disease (CHD) or acute myocardial infarction (AMI) is one of the major causes of death throughout the world. Myocardial reperfusion is the main approach in treating CHD. Ischemia-reperfusion injury (IRI) represents additional injury to the heart muscle that occurs due to cellular dysfunction following the reperfusion process. Vascular endothelial growth factor (VEGF) is a protein that plays a role in inducing angiogenesis and increasing vascular permeability. VEGF is important in the formation of collateral blood vessels after MI, but higher levels of VEGF are known to result in restenosis after primary percutaneous coronary intervention (IKPP). Low-dose colchicine is known to reduce VEGF levels. This study aims to assess the effect of colchicine administration on reducing VEGF levels in the serum of patients with acute ST-segment elevation myocardial infarction (IMA-EST) before and 48 hours after reperfusion. The research was conducted using a double-blinded randomized clinical trial design involving 63 subjects. The study result showed the decrease in VEGF levels at 48 hours after reperfusion, but there was no significant difference in the analysis of changes (delta) in VEGF levels before and at 48 hours after reperfusion between the two groups. This study is the first study to assess the effect of colchicine administration on VEGF levels in post-reperfusion IMA-EST patients. This research can be used as a basis for further research to assess the reduction in VEGF levels with long-term administration of colchicine."