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dc.contributor.advisorLubis, Abdrurrahim Rasyid
dc.contributor.authorLuman, Andy
dc.date.accessioned2021-07-14T04:02:30Z
dc.date.available2021-07-14T04:02:30Z
dc.date.issued2014
dc.identifier.urihttp://repositori.usu.ac.id/handle/123456789/35937
dc.description.abstractBackground: A substantial proportion of uncomplicated, treated primary hypertensive patients have failure of hypertension treatment. The enzyme creatine kinase (CK) regenerates adenosine triphosphate in striated muscle, myocardium and blood vessels. Several studies showed serum CK was found to be a predictor of blood pressure in the general population. High tissue CK precedes hypertension and is high in population with high hypertension risk. Objective: To evaluate the association between creatine kinase with control of blood pressure in hypertension. Methods: A cross sectional study from November until December 2013 had been done in 82 hypertensive patients and had been conducted anamneses, measured for blood pressure and body mass index. Serum was obtained and analyzed for serum CK, random blood glucose and lipid profile. Independent t test and Mann Whitney was used to assess the difference in mean CK and others variable between hypertension categories. Spearman correlation test was used to assess the association between systolic and diastolic blood pressure with CK and multivariat logistic regression model analyzed related factors with control of blood pressure in hypertension. Results: There was significance difference of mean CK (p=0,0001) in controlled hypertension group (81,83+29,70) compared with uncontrolled hypertension (132,17+55,91). There was significant correlation (p=0,0001) between CK with systolic (r=0,483) and diastolic blood pressure (r=0,278). CK was associated with control of blood pressure (p=0,0001) along with the history of diabetes (p=0,015), male sex (p=0,009) and drug classes (p=0,030). Conclusion: There was higher CK level in uncontrolled hypertensive patients and CK level can be used to assessing control of blood pressure in hypertension.en_US
dc.description.abstractLatar Belakang: Dijumpai proporsi besar pasien hipertensi primer yang berobat dan tanpa komplikasi mengalami kegagalan pengobatan hipertensi. Enzim kreatin kinase (CK) membentuk adenosine trifosfat pada otot rangka, jantung dan pembuluh darah. Beberapa penelitian menunjukkan CK serum merupakan prediktor tekanan darah pada populasi umum. CK jaringan yang tinggi mencetuskan hipertensi dan dijumpai pada populasi resiko tinggi hipertensi. Tujuan: Untuk mengetahui hubungan kreatin kinase dengan kontrol tekanan darah pada hipertensi. Metode: Penelitian potong lintang dari bulan November hingga Desember 2013 terhadap 82 pasien hipertensi dan dilakukan anamnesis, pengukuran tekanan darah dan indeks massa tubuh. Serum diambil dan dilakukan pemeriksaan CK, kadar gula darah sewaktu dan profil lipid. Uji t-independen dan Mann-Whitney menilai perbedaan rerata kadar CK dan variabel lainnya terhadap kategori hipertensi. Uji korelasi Spearman menilai hubungan tekanan darah sistolik dan diastolik dengan CK dan model regresi logistik multivariat menganalisis faktorfaktor yang berhubungan dengan kontrol tekanan darah pada hipertensi. Hasil: Dijumpai perbedaan rerata CK yang signifikan (p=0,0001) antara kelompok hipertensi terkontrol (81,83+29,70) dan hipertensi tidak terkontrol (132,17+55,91). Dijumpai hubungan yang signifikan (p=0,0001) antara CK dengan tekanan darah sistolik (r=0,483) dan diastolik (r=0,278). CK berhubungan dengan kontrol tekanan darah (p=0,0001) bersama dengan faktor riwayat DM (p=0,015), jenis kelamin laki-laki (p=0,009) dan golongan obat (p=0,030). Kesimpulan: Dijumpai kadar CK lebih tinggi pada pasien hipertensi tidak terkontrol dan kadar CK dapat digunakan untuk menilai kontrol tekanan darah pada hipertensi.en_US
dc.language.isoiden_US
dc.publisherUniversitas Sumatera Utaraen_US
dc.subjectkontrol tekanan darahen_US
dc.subjecthipertensien_US
dc.subjectCKen_US
dc.titleHubungan Kreatin Kinase dengan Kontrol Tekanan Darah pada Hipertensien_US
dc.identifier.nimNIM117101007
dc.description.pages118 Halamanen_US


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