Main Article Content
Abstract
Coronary heart disease is often found in workers, including hospital health workers. The purpose of the study was to determine the relationship between the type of work, working period and work pattern on the risk of coronary heart disease in health workers at the Jakarta Islamic Hospital Pondok Kopi. This study is an analytical research with a cross sectional method. Samples were obtained by taking primary data from questionnaires and secondary data from medical check-up results. A total of 70 people met the inclusion criteria as a sample. The risk of cardiovascular disease is calculated using the Framingham score online. Based on the results of the analysis using SPSS 21.0, the relationship between the working period and the risk of CHD was obtained with a value of p=0.029 (p<0.05). Meanwhile, the type of work and work pattern were not found to be associated with the risk of Coronary Heart Disease (p=0.361 and p=0.735).
Penyakit jantung koroner sering dijumpai pada pekerja antara lain tenaga kesehatan rumah sakit. Tujuan penelitian untuk mengetahui hubungan antara jenis pekerjaan, masa kerja dan pola kerja terhadap risiko penyakit jantung koroner pada tenaga kesehatan Rumah Sakit Islam Jakarta Pondok Kopi. Penelitian ini merupakan penelitian analitik dengan metode cross sectional. Sampel diperoleh dengan pengambilan data primer kuesioner dan data sekunder dari dokumen hasil medical check up. Sebanyak 70 orang memenuhi kriteria inklusi sebagai sampel. Risiko penyakit cardiovaskuler dihitung menggunakan skor Framingham secara online. Berdasarkan hasil analisis menggunakan SPSS 21.0 didapatkan hubungan antara masa kerja dengan risiko PJK dengan nilai p=0,029 (p<0,05). Sedangkan jenis pekerjaan dan pola kerja tidak didapatkan hubungan dengan risiko Penyakit Jantung Koroner (nilai p=0,361 dan p=0,735).
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References
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References
Baines CP, Kaiser RA, Purcell NH, et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death. Nature. 2005;434(7033):658-662.
https://doi.org/10.1038/nature03434
Basso E, Fante L, Fowlkes J, et al. Properties of the permeability transition pore in mitochondria devoid of cyclophilin D. J Biol Chem. 2005;280(19):18558-18561.
https://doi.org/10.1074/jbc.C500089200
Baughman JM, Perocchi F, Girgis HS, et al. Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter. Nature. 2011;476(7360):341-345.
https://doi.org/10.1038/nature10234
Bell DSH, Goncalves E. Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose‐lowering medications. Diabetes Obes Metab. 2019;21:1277-1290.
https://doi.org/10.1111/dom.13652
Cadrin-Tourigny J, Shohoudi A, Roy D, et al. Decreased mortality with beta-blockers in patients with heart failure and coexisting atrial fibrillation: an AF-CHF substudy. JACC Heart Fail. 2017;5:99-106.
https://doi.org/10.1016/j.jchf.2016.10.015
Clarke SJ, McStay GP, Halestrap AP. Sanglifehrin A acts as a potent inhibitor of the mitochondrial permeability transition and reperfusion injury of the heart by binding to cyclophilin-D at a different site from cyclosporin A. J Biol Chem. 2002;277(38):34793-34799.
https://doi.org/10.1074/jbc.M202191200
Crompton M, Costi A, Hayat L. Evidence for the presence of a reversible Ca2+-dependent pore activated by oxidative stress in heart mitochondria. Biochem J. 1987;245(3):915-918.
https://doi.org/10.1042/bj2450915
Csordas G, Golenar T, Seifert EL, et al. MICU1 controls both the threshold and cooperative activation of the mitochondrial Ca(2)(+) uniporter. Cell Metab. 2013;17(6):976-987.
https://doi.org/10.1016/j.cmet.2013.04.020
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https://doi.org/10.1038/nature10230
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https://doi.org/10.35508/tjph.v1i4.2143
Disrinama AM, Rachman F. Analisis Pengaruh Tingkat Risiko PJK dengan Framingharm. Politeknik Perkapalan Negeri Surabaya. 2016;1:23-28.
Dorn GW 2nd, Maack C. SR and mitochondria: calcium cross-talk between kissing cousins. J Mol Cell Cardiol. 2013;55:42-49.
https://doi.org/10.1016/j.yjmcc.2012.07.015
Drago I, Pizzo P, Pozzan T. After half a century mitochondrial calcium in- and efflux machineries reveal themselves. EMBO J. 2011;30(20):4119-4125.
https://doi.org/10.1038/emboj.2011.337
Eisner V, Csordas G, Hajnoczky G. Interactions between sarco-endoplasmic reticulum and mitochondria in cardiac and skeletal muscle - pivotal roles in Ca(2)(+) and reactive oxygen species signaling. J Cell Sci. 2013;126 Pt 14:2965-2978.
https://doi.org/10.1242/jcs.093609
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Ghani L, Susilawati MD, Novriani H. Faktor Risiko Dominan Penyakit Jantung Koroner di Indonesia. Buletin Penilitian Kesehatan. 2016;44(3):153-164.
https://doi.org/10.22435/bpk.v44i3.5436.153-164
Giorgio V, Soriano ME, Basso E, et al. Cyclophilin D in mitochondrial pathophysiology. Biochim Biophys Acta. 2010;1797(6-7):1113-1118.
https://doi.org/10.1016/j.bbabio.2009.12.006
Giorgio V, von Stockum S, Antoniel M, et al. Dimers of mitochondrial ATP synthase form the permeability transition pore. Proc Natl Acad Sci U S A. 2013;110(15):5887-5892.
https://doi.org/10.1073/pnas.1217823110
Griffiths EJ, Halestrap AP. Protection by cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts. J Mol Cell Cardiol. 1993;25(12):1461-1469.
https://doi.org/10.1006/jmcc.1993.1162
Hajnoczky G, Csordas G, Das S, et al. Mitochondrial calcium signalling and cell death: approaches for assessing the role of mitochondrial Ca2+ uptake in apoptosis. Cell Calcium. 2006;40(5-6):553-560.
https://doi.org/10.1016/j.ceca.2006.08.016
Hafliah F, Syafriati A. Pengaruh Pemberian Pendidikan Kesehatan Pra Kateterisasi Jantung Terhadap Peningkatan Pengetahuan Pasien. Jurnal Ilmiah Multi Science Kesehatan. 2023;15(1):49-50.
https://doi.org/10.36729/bi.v15i1.1062
Hayashi T, Martone ME, Yu Z, et al. Three-dimensional electron microscopy reveals new details of membrane systems for Ca2+ signaling in the heart. J Cell Sci. 2009;122 Pt 7:1005-1013.
https://doi.org/10.1242/jcs.028175
Hegg DS. Prevalence of Risk Factors for Cardiovascular disease in Paramedics. International Archives of Occupational and Enviroment Health. 2015;88(7):973-980.
https://doi.org/10.1007/s00420-015-1028-z
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https://doi.org/10.3390/ijerph16060961
Hunter DR, Haworth RA. The Ca2+-induced membrane transition in mitochondria. I. The protective mechanisms. Arch Biochem Biophys. 1979;195(2):453-459.
https://doi.org/10.1016/0003-9861(79)90371-0
Hunter DR, Haworth RA. The Ca2+-induced membrane transition in mitochondria. III. Transitional Ca2+ release. Arch Biochem Biophys. 1979;195(2):468-477.
https://doi.org/10.1016/0003-9861(79)90373-4
Iskandar, Hadi, A., Alfridsyah. Faktor Risiko Terjadinya Penyakit Jantung Koroner pada Pasien Rumah Sakit Umum Meuraxa Banda Aceh. Jurnal Action. 2017;2(1):32-42.
https://doi.org/10.30867/action.v2i1.34
Johanis IJ, Tedju Hinga IA, Sir AB. Faktor Risiko Hipetensi, Merokok dan Usia Terhadap Kejadian Penyakit Jantung Koroner pada Pasien di RSUD Prof. DR. W. Z. Johanes Kupang. Media Kesehatan Masyarakat. 2020;2(1):33-40.
https://doi.org/10.35508/mkm.v2i1.1954
Juliana M, Camelia A, Rahmiwati A. Analisis Faktor Risiko Kelelahan Kerja Pada Karyawan Bagian Produksi PT. Arwana Anugrah Keramik, Tbk. Jurnal Ilmu Kesehatan Masyarakat. 2019;9(1):53-63.
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https://doi.org/10.14740/cr1034
Kotecha D, Manzano L, Krum H, et al. Effect of age and sex on efficacy and tolerability of β blockers in patients with heart failure with reduced ejection fraction: individual patient data meta-analysis. Bmj. 2016;353.
https://doi.org/10.1136/bmj.i1855
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https://doi.org/10.22270/jddt.v12i3-S.5508
Leung AW, Halestrap AP. Recent progress in elucidating the molecular mechanism of the mitochondrial permeability transition pore. Biochim Biophys Acta. 2008;1777(7-8):946-952.
https://doi.org/10.1016/j.bbabio.2008.03.009
Lina N, Saraswati D. Deteksi Dini Penyakit Jantung Koroner di Pos Pembinaan Terpadu Penyakit Tidak Menular (POSBINDU PTM). Jurnal Kesehatan Komunitas Indonesia. 2019;15(2):94-95.
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