[ABSTRAK
Latar belakang : Pada masa sekarang, reperfusi miokardium dengan trombolitikatau intervensi koroner perkutan primer ( IKPP) adalah terapi utama pada pasienyang mengalami IMA EST. Tujuan utama IKPP untuk mengembalikan patensiarteri epikardial yang mengalami infark dan mencapai reperfusi mikrovaskularsecepat mungkin. Namun keberhasilan mengembalikan patensi dari arteri koronerepikardial setelah oklusi tidak selalu menjamin cukupnya reperfusi ke levelmikrovaskular, yang disebut sebagai fenomena no reflow atau microvascularobstruction (MVO). Terdapat dua mekanisme yang berperan pada no reflowyaitu disfungsi mikrovaskular dan kerusakan intergritas mikrostruktur endotel.Kerusakan endotel dapat diakibatkan berbagai hal, diantara nya jejas reperfusiyang akan mengaktivasi netrofil. Netrofil teraktivasi akan mengeluarkan radikalbebas oksigen, enzim proteolitik dan mediator proinflamasi yang secara langsungmenyebabkan kerusakan jaringan dan endotel. Trimetazidine adalah obatantiangina yang dapat menurunkan netrofil yang dimediasi oleh trauma jaringansetelah jantung mengalami iskemia. Akan tetapi belum diketahui secara luaspengaruh pemberian trimetazidine terhadap akumulasi netrofil pada kejadian IMAEST yang dilakukan tindakan IKPP.Metode : Sebanyak 68 pasien IMA EST yang menjalani IKPP dipilih secarakonsekutif sejak Januari 2015 sampai Juni 2015 diambil saat masuk UGD,dilakukan pengambilan darah vena perifer untuk menghitung jumlah netrofilsebelum IKPP, kemudian pasien menjalani IKPP. Setelah 6 jam paska IKPPdilakukan pengambilan kembali darah vena perifer untuk menghitung kembalijumlah netrofil paska IKPP. Hitung netrofil diperiksa dengan Sysmex 2000i.Perhitungan statistik dinilai dengan SPSS 17.Hasil : Dari 68 subyek, dibagi menjadi 28 subyek pada kelompok yang diberikantrimetazidine dan 40 subyek yang diberikan plasebo. Tidak didapatkan perbedaanjumlah netrofil pada kelompok perlakuan dan kelompok kontrol baik sebelummaupun sesudah IKPP, netrofil pre IKPP pada trimetazidine vs plasebo 10.71 ±3.263 vs 10.99 ± 3.083,nilai p:0,341. Nilai netrofil post IKPP pada trimetazidinevs plasebo 9.49 ± 3.135 vs 9.92 ± 3.463,nilai p:0,664.Kesimpulan : Tidak terdapat penurunan jumlah netrofil pasca pemberiantrimetazidine pada pasien IMA EST yang menjalani IKPP.

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ABSTRACT
BackgroundNowadays, reperfusion strategy, either with thrombolytic or Primary PercutaneousCoronary Intervention (PPCI), is the core treatment for Acute ST-SegmentElevation Myocardial Infarct (STEMI). The goal of PPCI is to restore the patencyof infarcted epicardial artery and establish microvascular reperfusion as soon aspossible so that necrotic myocardial area can be reduced. However, successfulrestoration of infarcted epicardial artery is not always followed by enoughreperfusion to the microvascular part. Trimetazidine is an antianginal drug, canreduce neutrophil which was mediated by tissue trauma during ischemic heartcondition. Trimetazidine is currently approved and widely known as antianginaldrug which affect metabolism. Unfortunately, its influence over neutrophilaccumulation in acute STEMI patients which undergo PPCI is not wellunderstood.MethodThere were 68 consecutive-selected acute STEMI patients which undergo PPCIsince January 2015 until Juni 2015. They were admitted in emergency department.Peripheral vein blood sampling was taken to measure neutrophil before PPCI wasperformed. Six hour after PPCI was conducted, another peripheral vein bloodsampling was taken for another neutrophil measurement. Neutrophil measurementwas performed with Sysmex 2000i. Statistical analysis was performed by usingSPSS 17.ResultAmong 68 patients, divided in two groups, trimetazidine 28 patients and plasebo40 patients. There were no differences amount of neutrophils in trimetazidine orplasebo group, before or after PPCI. Neutrophil pre PPCI in trimetazidine vsplasebo group 10.71 ± 3.263 vs 10.99 ± 3.083, p:0,341. Neutrophil post PPCI intrimetazidine vs plasebo group 9.49 ± 3.135 vs 9.92 ± 3.463, p:0,664.ConclusionThere were no reducing amount of neutrophils after trimetazidine was given inpatients STEMI which underwent PPCI., BackgroundNowadays, reperfusion strategy, either with thrombolytic or Primary PercutaneousCoronary Intervention (PPCI), is the core treatment for Acute ST-SegmentElevation Myocardial Infarct (STEMI). The goal of PPCI is to restore the patencyof infarcted epicardial artery and establish microvascular reperfusion as soon aspossible so that necrotic myocardial area can be reduced. However, successfulrestoration of infarcted epicardial artery is not always followed by enoughreperfusion to the microvascular part. Trimetazidine is an antianginal drug, canreduce neutrophil which was mediated by tissue trauma during ischemic heartcondition. Trimetazidine is currently approved and widely known as antianginaldrug which affect metabolism. Unfortunately, its influence over neutrophilaccumulation in acute STEMI patients which undergo PPCI is not wellunderstood.MethodThere were 68 consecutive-selected acute STEMI patients which undergo PPCIsince January 2015 until Juni 2015. They were admitted in emergency department.Peripheral vein blood sampling was taken to measure neutrophil before PPCI wasperformed. Six hour after PPCI was conducted, another peripheral vein bloodsampling was taken for another neutrophil measurement. Neutrophil measurementwas performed with Sysmex 2000i. Statistical analysis was performed by usingSPSS 17.ResultAmong 68 patients, divided in two groups, trimetazidine 28 patients and plasebo40 patients. There were no differences amount of neutrophils in trimetazidine orplasebo group, before or after PPCI. Neutrophil pre PPCI in trimetazidine vsplasebo group 10.71 ± 3.263 vs 10.99 ± 3.083, p:0,341. Neutrophil post PPCI intrimetazidine vs plasebo group 9.49 ± 3.135 vs 9.92 ± 3.463, p:0,664.ConclusionThere were no reducing amount of neutrophils after trimetazidine was given inpatients STEMI which underwent PPCI.]