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Abstrak :
Kejadian infark miokard akut pada pasien diabetes mellitus adalah masalah kesehatan utama yang disebabkan oleh penurunan laju filtrasi glomerulus. Penelitian ini bertujuan untuk mengetahui hubungan laju filtrasi glomerulus dengan kejadian infark miokard akut pada pasien diabetes mellitus. Penelitian ini menggunakan desain analitik korelasi dengan rancangan cross sectional. Jumlah sampel adalah 96 rekam medis pasien diabetes mellitus yang dirawat di RSPAD Gatot Subroto Ditkesad periode 2007-2011. Hasil analisis menggunakan Chi-Square menunjukkan bahwa ada hubungan laju filtrasi glomerulus dengan kejadian infark miokard akut (p= 0,012). Variabel perancu terhadap hubungan laju filtrasi glomerulus dengan kejadian infark miokard akut adalah lama menderita diabetes mellitus (p= 0,065). Berdasarkan hal tersebut, perawat perlu melakukan intervensi yang tepat untuk mencegah komplikasi terjadinya infark miokard akut pada pasien diabetes mellitus.

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Incidence of acute myocardial infarction in diabetes mellitus is a major health problem caused by a decrease in glomerular filtration rate. This study aimed to determine the correlation between glomerular filtration rate with the incidence of acute myocardial infarction in patients with diabetes mellitus. This study used an analytic design of a correlation with cross sectional design. The number of samples was 96 medical records of patients with diabetes mellitus who were treated at RSPAD Gatot Subroto Ditkesad between 2007 and 2011. The analysis using Chi-Square indicated that there is a correlation between glomerular filtration rate with the incidence of acute myocardial infarction (p=0.012). Confounding variable of correlation between glomerular filtration rate with the incidence of acute myocardial infarction is length of illness of diabetes mellitus (p= 0.065). Based on the findings, nurses need to make appropriate interventions to prevent complications of acute myocardial infarction in patients with diabetes mellitus.

Abstrak :
Inflamasi berperan penting dalam proses ateroklerosis mulai sejak awal sampai tahap akhir hingga terjadinya ruptur plak. Berbagai penelitian menunjukkan bahwa LDL teroksidasi memegang peranan kunci terhadap terjadinya inflamasi ini. Terbentuknya LDL teroksidasi dipengaruhi oleh stress oksidatif karena ketidakseimbangan antara oksidan dan antioksidan. Produksi radikal bebas oksigen pada pasien IMA lebih tinggi dibanding orang normal. Sementara itu, latihan fisik pada pasien IMA kini dianjurkan untuk dilakukan lebih dini. Walaupun aktifitas fisik akut dapat meningkatkan produksi radikal bebas oksigen, tetapi exercise training justru dapat menyebabkan produksi radikal bebas oksigen lebih rendah yang selanjutnya akan menurunkan proses oksidasi lipid. Namun hingga kini belum ada penelitian yang melihat efek latihan fisik yang teratur dan terukur terhadap proses oksidasi lipid pada pasien IMA. Tujuan penelitian ini adalah untuk mengetahui efek latihan fisik secara teratur dan terukur terhadap proses oksidasi lipid (LDL teroksidasi) pada pasien IM.

Abstrak :
ABSTRAK
Diagnosis infark miokard akut ditegakkan apabila memenuhi 2 dari 3 kriteria, yaitu klinis, perubahan EKG, dan peningkatan kadar penanda biokimia jantung. Troponin merupakan penanda biokimia jantung yang spesifik untuk infark miokard, akan tetapi memiliki keterbatasan yaitu kurang sensitif apabila dilakukan pada fase awal karena troponin akan meningkat dalam darah setelah 4 -10 jam setelah infark miokard. Copeptin merupakan penanda stres endogen, yang dapat meningkat pada awal onset infark miokard akut, namun kurang spesifik. Penelitian tentang copeptin-us sebagai penanda biokimia jantung masih sedikit dan di Indonesia penelitian tentang copeptin-us sebagai penanda biokimia jantung belum pernah dilakukan. Penelitian ini mengikutsertakan 91 pasien tersangka sindrom koroner akut yang terbagi atas 15 (16,5%) NSTEMI, 43 (47,3%) UA, dan 33 (36,3%) non SKA. Diagnosis ditegakkan oleh dokter di IGD RS Jantung dan Pembuluh Darah Harapan Kita. Karakteristik pasien yang memenuhi kriteria inklusi dan eksklusi dicatat dan kemudian dilakukan pemeriksaan copeptin-us. Nilai rerata copeptin-us pada NSTEMI adalah 151,80 ± 130,03 pmol/L, median copeptin-us pada UA adalah 7,12(1,145 ? 62,23) pmol/L, dan rerata copeptin-us pada non SKA adalah 7,36 ± 4,17 pmol/L. Nilai cut off copeptin-us untuk membedakan NSTEMI dengan UA/non SKA adalah 13,97 pmol/L. Area under curve (AUC) kombinasi hs-cTnT saat masuk rumah sakit dengan copeptin-us adalah 0,941 (0,882 ? 1,00), hs-cTnT saat masuk rumah sakit 0,885 (0,790 ? 0,98), dan AUC hs-cTnT 3 jam kemudian adalah 0,925 (0,824 ? 1,00). Nilai median hs-cTnT saat masuk RS pada NSTEMI adalah 114(29-1102) pg/mL, pada UA adalah 16 (3-3352) pg/mL, dan pada non SKA adalah 6(3-366) pg/mL. Nilai median hs-cTnT 3 jam pada NSTEMI adalah 488 (81-18437) pg/mL, pada UA 14(3-2224) pg/mL, dan pada non SKA adalah 3(3-679) pg/mL. Kombinasi copeptin-us ≥ 13,97 pmol/L dan hs-cTnT ≥ 14 pg/mL dan untuk membedakan NSTEMI dengan UA/non SKA memberikan sensitivitas 100%, spesifisitas 90,78%, NPP 68,18%, dan NPN 100%. Uji diagnostik kombinasi copeptin-us dan hs-cTnT saat masuk RS lebih baik dibandingkan hs-cTnT saat masuk RS saja dan dapat digunakan untuk rule out NSTEMI.ABSTRACT
Diagnosis of acute myocardial infarction is made when two of the followed criterias are met; clinical, ECG changes, and increased levels of cardiac biochemical markers. Troponin is a specific cardiac biochemical marker for myocardial infarction but has limitation. It is less sensitive when measured in the early phase, because troponin will increase in blood after 4 -10 hours post myocardial infarction. Copeptin is an endogenous stress marker, it level increases in the early onset of acute myocardial infarction but study on copeptin-us as cardiac biochemical marker are limited and in Indonesia there is no study on copeptin-us has been done. In this study 91 consecutive patients fulfilled the inclusion and exclusion criteria, consist of 15 (16,5%) NSTEMI, 43 (47,3%) unstable angina, and 33 (36,3%) non acute coronary syndrome. Diagnosis was made by the emergency physician at Harapan Kita cardiovascular centre. Characteristics of these subject were recorded and then the copeptin-us levels were measured. The mean value of copeptin-us in NSTEMI is 151,80 ± 130,03 pmol/L, median copeptin-us in UA is 7,12(1,145 ? 62,23) pmol/L, and the mean copeptin-us in non ACS is 7,36 ± 4,17 pmol/L. Cut off value of copeptin-us to distinguish NSTEMI from UA/non ACS is 13,97 pmol/L. Area under curve of the combination hs-cTnT on admission and copeptin-us is 0,941 (0,882 ? 1,00), hs-cTnT on admission is 0,885 (0,790 ? 0,98), and hs-cTnT 3 hours laters is 0,925 (0,824 ? 1,00). Median value hs-cTnT on admission in NSTEMI is 114(29-1102) pg/mL, in UA is 16 (3-3352) pg/mL, and in non ACS is 6(3-366) pg/mL. Median hs-cTnT 3 hours in NSTEMI is 488(81-18437) pg/mL, in UA is 14(3-2224) pg/mL, and in non ACS is 3(3-679) pg/mL. Combination of copeptin-us ≥ 13,97 pmol/L and hs-cTnT ≥14 pg/mL to distinguish NSTEMI from UA/non ACS has sensitivity 100%, specificity 90,78%, PPV 68,18%, and NPV 100%. The diagnostic value of combination on copeptin-us and hs-cTnT is better than only hs-cTnT on admission so that it can be used to rule out NSTEMI.;Diagnosis of acute myocardial infarction is made when two of the followed criterias are met; clinical, ECG changes, and increased levels of cardiac biochemical markers. Troponin is a specific cardiac biochemical marker for myocardial infarction but has limitation. It is less sensitive when measured in the early phase, because troponin will increase in blood after 4 -10 hours post myocardial infarction. Copeptin is an endogenous stress marker, it level increases in the early onset of acute myocardial infarction but study on copeptin-us as cardiac biochemical marker are limited and in Indonesia there is no study on copeptin-us has been done. In this study 91 consecutive patients fulfilled the inclusion and exclusion criteria, consist of 15 (16,5%) NSTEMI, 43 (47,3%) unstable angina, and 33 (36,3%) non acute coronary syndrome. Diagnosis was made by the emergency physician at Harapan Kita cardiovascular centre. Characteristics of these subject were recorded and then the copeptin-us levels were measured. The mean value of copeptin-us in NSTEMI is 151,80 ± 130,03 pmol/L, median copeptin-us in UA is 7,12(1,145 ? 62,23) pmol/L, and the mean copeptin-us in non ACS is 7,36 ± 4,17 pmol/L. Cut off value of copeptin-us to distinguish NSTEMI from UA/non ACS is 13,97 pmol/L. Area under curve of the combination hs-cTnT on admission and copeptin-us is 0,941 (0,882 ? 1,00), hs-cTnT on admission is 0,885 (0,790 ? 0,98), and hs-cTnT 3 hours laters is 0,925 (0,824 ? 1,00). Median value hs-cTnT on admission in NSTEMI is 114(29-1102) pg/mL, in UA is 16 (3-3352) pg/mL, and in non ACS is 6(3-366) pg/mL. Median hs-cTnT 3 hours in NSTEMI is 488(81-18437) pg/mL, in UA is 14(3-2224) pg/mL, and in non ACS is 3(3-679) pg/mL. Combination of copeptin-us ≥ 13,97 pmol/L and hs-cTnT ≥14 pg/mL to distinguish NSTEMI from UA/non ACS has sensitivity 100%, specificity 90,78%, PPV 68,18%, and NPV 100%. The diagnostic value of combination on copeptin-us and hs-cTnT is better than only hs-cTnT on admission so that it can be used to rule out NSTEMI.;Diagnosis of acute myocardial infarction is made when two of the followed criterias are met; clinical, ECG changes, and increased levels of cardiac biochemical markers. Troponin is a specific cardiac biochemical marker for myocardial infarction but has limitation. It is less sensitive when measured in the early phase, because troponin will increase in blood after 4 -10 hours post myocardial infarction. Copeptin is an endogenous stress marker, it level increases in the early onset of acute myocardial infarction but study on copeptin-us as cardiac biochemical marker are limited and in Indonesia there is no study on copeptin-us has been done. In this study 91 consecutive patients fulfilled the inclusion and exclusion criteria, consist of 15 (16,5%) NSTEMI, 43 (47,3%) unstable angina, and 33 (36,3%) non acute coronary syndrome. Diagnosis was made by the emergency physician at Harapan Kita cardiovascular centre. Characteristics of these subject were recorded and then the copeptin-us levels were measured. The mean value of copeptin-us in NSTEMI is 151,80 ± 130,03 pmol/L, median copeptin-us in UA is 7,12(1,145 ? 62,23) pmol/L, and the mean copeptin-us in non ACS is 7,36 ± 4,17 pmol/L. Cut off value of copeptin-us to distinguish NSTEMI from UA/non ACS is 13,97 pmol/L. Area under curve of the combination hs-cTnT on admission and copeptin-us is 0,941 (0,882 ? 1,00), hs-cTnT on admission is 0,885 (0,790 ? 0,98), and hs-cTnT 3 hours laters is 0,925 (0,824 ? 1,00). Median value hs-cTnT on admission in NSTEMI is 114(29-1102) pg/mL, in UA is 16 (3-3352) pg/mL, and in non ACS is 6(3-366) pg/mL. Median hs-cTnT 3 hours in NSTEMI is 488(81-18437) pg/mL, in UA is 14(3-2224) pg/mL, and in non ACS is 3(3-679) pg/mL. Combination of copeptin-us ≥ 13,97 pmol/L and hs-cTnT ≥14 pg/mL to distinguish NSTEMI from UA/non ACS has sensitivity 100%, specificity 90,78%, PPV 68,18%, and NPV 100%. The diagnostic value of combination on copeptin-us and hs-cTnT is better than only hs-cTnT on admission so that it can be used to rule out NSTEMI.