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Abstrak :
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.

Abstrak :
Level rekomendasi penggunaan rutin intra-arotic balloon pump (IABP) pada pasien dengan renjatan kardiogenik diturunkan menjadi level III. Manfaat penggunaan IABP sebelum revaskularisasi belum diinvestigasi secara uji klinis acak. Tujuan studi ini untuk menilai pengaruh penggunaan IABP sebelum revaskularisasi pada pasien infark miokard akut dengan komplikasi renjatan kardiogenik. Uji klinis acak pembanding terbuka dilakukan di Pusat Jantung Nasional Harapan Kita periode januari 2018 hingga Mei 2020. Randomisasi dilakukan pada 69 subjek infark miokard dengan renjatan kardiogenik. Alokasi kelompok kontrol 34 subjek dan perlakuan (IABP sebelum revaskularisasi) 35 subjek. Luaran primer adalah mortalitas rumah sakit dan pasca revaskularisasi hari ke_30. Luaran sekunder perfusi global (bersihan asam laktat jam ke_12), perfusi regional (kreatinin), performa jantung yang dinilai secara ekokardiografi (Global longitudinal strain) dan penanda biologis untuk regangan miokard (NT-proBNP dan ST2). Variabel hemodinamik ekokardiografi dan komplikasi tindakan juga dilaporkan. Setelah drop out, Analisis perprotokol dilakukan pada 18 subjek kelompok kontrol dan 16 subjek kelompok perlakuan. Mortalitas rumah sakit dan 30 hari pasca revaskularisasi, 12 (66,7%) subjek pada kelompok kontrol dan 9 (56,3%) subjek pada kelompok perlakuan, p 0,533. Pada luaran sekunder tidak ditemukan perbedaan bermakna pada kedua kelompok untuk bersihan laktat efektif jam ke-12; pemeriksaan kreatinin, global longitudinal strain, hemodinamik ekokardiografi dan nilai NT-proBNP dan ST2. Pada hari ke_3, kurva kaplan meier berpisah dan mortalitas RS dini pada kelompok kontrol 9 (50%) subjek dan pada kelompok perlakuan 1 (6,25%) subjek, hasil uji fisher p 0,013. Mortalitas RS lanjut berhubungan dengan IABP dan sepsis. Dua patomekanisme diusulkan untuk menerangkan patomekanisme kematian pada kelompok kontrol dan kelompok perlakuan Simpulan: Penggunaan IABP sebelum revaskularisasi pada subjek infark miokard akut dengan komplikasi renjatan kardiogenik tidak memperbaiki mortalitas rumah sakit dan pasca perawatan hari ke-30. Pada kelompok kontrol diusulkan patomekanime mortalitas serangan fisiologis kali satu. Kelompok perlakuan, patomekanime mortalitas diusulkan serangan fisiologis kali dua. ......The guideline recommendation on routine use of Intra Aortic balloon pump (IABP) in cardiogenic shock had been downgraded to level recommendation III. The role of IABP insertion before revascularization has never been investigated in randomized control trial. The aim of this study is to investigate the role of IABP insertion before revascularization in acute myocardial infarction complicated by cardiogenic shock. Randomized control trial was performed in National Cardiac Center Harapan Kita at the period January 2018–April 2020. We randomly assigned 69 patients cardiogenic shock due to acute myocardial infarction. There are 34 patients assigned to control group (no IABP) and 35 patients assigned to intervention group (IABP before revascularization). Percutaneous Coronary Intervention and medical care were performed according to local protocol. The primary end points were in-hospital mortality and mortality at 30 days post revascularization. The secondary end points were perfusion (lactate clearance, creatinine), cardiac performance (global longitudinal strain), Biomarker for myocardial stretch (NT-proBNP & ST2). Echo hemodynamic and complication variables were also reported. After drop out, a total of 18 patients in the control group and 16 patients in intervention group (IABP before revascularization were included in per protocol analysis for the primary and secondary end points. The primary end result of in hospital mortality and 30 days post revascularization mortality were identical in 12 patients in the control group (66.7%) and 9 patients in the intervention group (56.3%), p 0,533. There were no significant differences in secondary end points, effective lactate clearance at 12 hour, creatinine, Global Longitudinal Strain, NT-proBNP, ST2 including echo hemodynamic, dose of catecholamine therapy and sepsis. At the third day, Kaplan Meier curve demonstrated early separation with significant difference in mortality 9 patients in the control group (50%) and 1 patients in the intervention group (6,25%), p 0,013. Late in hospital was associated with IABP and sepsis. There was also a trend of greater elevation of NT-proBNP on day 3 in the intervention group. Therefore, pathomechanisms of death for control group and intervention group were proposed. Conclusion: The use IABP before percutaneous intervention in patient shock cardiogenic due to acute myocardial infarction did not improve clinical outcome in hospital mortality or 30 days post Revascularization. One hit of physiological deterioration model for cardiogenic cardiogenic shock patient and two hit of physiological deterioration model for cardiogenic shock patient treated with IABP before revascularization were proposed.