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"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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"Kondisi infark miokard akut (IMA) sering disertai hiperglikemia yang meningkatkan risiko aritmia maligna melalui mekanisme yang diduga berupa kerusakan miokard, perubahan kanal ion dan peningkatan respons inflamasi. Penelitian mengenai hubungan hiperglikemia akut dengan kejadian aritmia maligna pada pasien dengan sindrom koroner akut (SKA) sudah banyak dilakukan, namun pada pasien IMA yang merupakan populasi khusus SKA dan memiliki risiko aritmia maligna lebih tinggi, belum ada penelitian yang menelaah peran kerusakan miokard, perubahan kanal ion dan peningkatan respons inflamasi sebagai patomekanisme terjadinya aritmia maligna pada pasien IMA. Tujuan penelitian ini adalah untuk menentukan pengaruh hiperglikemia akut terhadap kejadian aritmia maligna, troponin I, VLP, strain ekokardiografi, perubahan kanal ion (CaMKII) dan hsCRP. Penelitian ini juga bertujuan menilai pengaruh troponin I, VLP, GLS, CaMKII dan hsCRP terhadap kejadian aritmia maligna pada pasien IMA dengan hiperglikemia akut.Penelitian potong lintang yang dilanjutkan kohort prospektif pada pasien IMA yang dirawat di ICCU RSCM Jakarta, dilakukan November 2018-Mei 2019. Pasien dengan infeksi berat dan sudah mengalami aritmia maligna saat masuk RS dieksklusi. Data karakteristik dasar dan variabel kadar glukosa darah sewaktu, troponin I, VLP, GLS, CaMKII pertama dan hsCRP diambil pada hari pertama perawatan. Kejadian aritmia maligna sebagai luaran utama penelitian dan kadar CaMKII kedua dinilai pada hari ke-5 perawatan. Pasien yang meninggal sebelum hari perawatan ke-5 bukan akibat aritmia maligna dikeluarkan dari penelitian. Hubungan hiperglikemia akut dengan VLP dan kejadian aritmia maligna dianalisis dengan uji chi-square, sedangkan troponin I, GLS, CaMKII dan hsCRP berdasarkan status hiperglikemia diuji dengan uji-t atau Mann-Whitney.Sejumlah 110 pasien diikutkan dalam penelitian, 2 pasien meninggal pada hari ke-3 perawatan akibat aritmia maligna. Tidak ditemukan hubungan bermakna antara hiperglikemia akut pada IMA dengan aritmia maligna. Pada analisis bivariat, CaMKII hari ke-1 dan ke-5 memiliki hubungan bermakna dengan kejadian aritmia maligna (p = 0,03, p = 0,01). Pada kelompok hiperglikemia akut terdapat perbedaan kadar CaMKII di hari ke-5 antara VLP positif dan negatif (p = 0,03).Disimpulkan bahwa IMA pada fase awal akan menimbulkan kerusakan miokard yang lebih dominan dibandingkan peran metabolik. Fase berikutnya terjadi peningkatan katekolamin yang berakibat terjadinya hiperglikemia akut dan akan meningkatkan ROS serta aktivasi perubahan kanal ion yang digambarkan dengan CaMKII. Perubahan ini berakibat remodeling elektrofisiologi jantung yang terlihat dari gambaran VLP pada pemeriksaan SA-ECG.Kata Kunci: Aritmia maligna, CaMKII, Hiperglikemia Akut, hsCRP, IMA, VLP

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Acute Myocardial Infarction (AMI) is often followed by hyperglycemia which will increase the risk of malignant arrhythmias through mechanisms that are thought to be myocardial damage, ion channel changes and increased inflammatory response.There have been many studies on the correlation of acute hyperglycemia with the occurrence of malignant arrhythmias in acute coronary syndromes (ACS), but not much in AMI as a special population of ACS with a higher risk of malignant arrhythmias.There are no studies that examine the role of myocardial damage, ion channel changes and increased inflammatory response as a pathomechanism of malignant arrhythmias in AMI patients.

The purpose of this study was to determine the effect of acute hyperglycemia on the occurence of malignant arrhythmias, troponin I, VLP, echocardiographic strain, ion channel changes (CaMKII) and hsCRP. This study also aims to assess the effect of troponin I, VLP, GLS, CaMKII and hsCRP on the occurence of malignant arrhythmias in AMI patients with acute hyperglycemia.

A cross-sectional study followed by a prospective cohort of AMI patients treated at ICCU Cipto Mangunkusumo Hospital Jakarta was done from November 2018– May 2019. Patients with severe infections and who had experienced malignant arrhythmias at admission were excluded. Data on baseline characteristics and random blood glucose levels, troponin I, VLP, GLS, the first CaMKII and hsCRP were collected on the first day of treatment. The occurence of malignant arrhythmias as the main outcome of this study and the second CaMKII level were assessed on the fifth day of treatment. Patients who died before the fifth day of treatment not due to malignant arrhythmias were excluded. The correlation between acute hyperglycemia with VLP and the occurence of malignant arrhythmias was analyzed by chi-square test, whereas troponin I, GLS, CaMKII and hsCRP based on the hyperglycemia status were tested by t-test of Mann-Whitney test.

A total of 110 patients were included in the study, 2 patients died on the third day due to malignant arrhythmias. No significant relationship was found between acute hyperglycemia in AMI and malignant arrhythmias. On the first day and fifth day CaMKII bivariate analysis had a significant correlation with the occurence of malignant arrhythmias (p = 0.03, p = 0.01, respectively). In the acute hyperglycemia group there were differences in CaMKII levels on the fifth day between positive and negative VLP (p = 0.03).

It was concluded that AMI in the initial phase would cause more dominant myocardial damage compared to the role of metabolic factors. In the next phase there is an acute hyperglycemia and will increase ROS and activation of ion channel changes described by CaMKII. This change results in the electrophysiological remodeling of the heart as seen from the VLP picture on SA-ECG.

Key Words: Acute hyperglycemia, AMI, CaMKII, hsCRP, Malignant arrhythmias, VLP"