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Abstrak :
ABSTRAK Latar Belakang: Perubahan hemodinamik selama hemodialisis (HD) kronik dapat menimbulkan hipoperfusi dan iskemia koroner yang dapat menyebabkan cedera miokard yang ditandai dengan peningkatan kadar troponin I (cTnI) sehingga dapat menjadi penanda yang potensial untuk kejadian tersebut. Hemodialisis 2 kali seminggu berisiko membuat laju ultrafiltrasi (UFR) dan volume ultrafiltrasi (UFV) yang lebih tinggi sehingga menimbulkan kejadian hipovolemia yang lebih besar. Tujuan: Penelitian ini bertujuan untuk mengetahui proporsi pasien yang mengalami peningkatan cTnI intradialisis dan satu bulan setelah HD serta mengetahui hubungan antara faktor-faktor lama HD, UFR, UFV, hipotensi intradialisis (IDH), dan diabetes melitus (DM) dengan peningkatan kadar cTnI tersebut. Metode: Penelitian ini merupakan studi kohort prospektif untuk menilai kadar cTnI sebelum dan sesudah HD. Sebanyak 138 subyek yang menjalani HD 2 kali seminggu memenuhi kriteria inklusi. Pemeriksaan kadar cTnI menggunakan reagen ARCHITECH STAT. Nilai cut off cTnI untuk laki-laki adalah 34,0 pg/mL dan untuk perempuan 15,6 pg/mL. Analisis bivariat dan multivariat dilakukan untuk mengetahui hubungan antara lama HD, UFR, UFV, IDH dan DM dengan peningkatan cTnI intradialisis dan satu bulan setelah HD. Hasil: Dari 138 subyek, sebanyak 57 subyek (41,3%) mengalami peningkatan kadar cTnI. Kadar cTnI meningkat secara signifikan selama HD (p<0,001) . Faktor DM berhubungan dengan peningkatan kadar cTnI (OR 2,207 (IK 95% 1,056-4,616), p=0,033), yang mempunyai risiko 2,2 kali dalam peningkatan kadar cTnI. Setelah satu bulan, sebanyak 53 dari 132 subyek (40,2%) mengalami peningkatan kadar cTnI yang signifikan. Sebanyak 31 pasien (23,4%) mengalami peningkatan kadar cTnI 50% di atas cut off. Analisis multivariat menunjukan tidak terdapat hubungan antara lama HD, UFR, UFV, IDH, dan DM dengan peningkatan kadar cTnI satu bulan setelah HD. Simpulan: Proporsi pasien yang mengalami peningkatan cTnI intradialisis sebesar 41,3% dan satu bulan setelah HD sebesar 40,2%. Diabetes melitus berhubungan dengan peningkatan cTnI intradialisis, sedangkan lama HD, UFV, UFR, dan IDH tidak berhubungan dengan peningkatan cTnI. Lama HD, UFV, UFR, IDH, dan DM tidak berhubungan dengan peningkatan kadar cTnI satu bulan setelah HD.

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ABSTRACT Background: Hemodynamic changes during chronic hemodialysis (HD) may induce coronary hypoperfusion and coronary ischemia which lead to asymptomatic myocardial injury marked by the increase in cardiac troponin I (cTnI) levels which make this cTnI a potential marker for these events. Two time a week HD increase the risk of higher ultrafiltration rate (UFR) and ultrafiltration volume (UFV) contributing to higher hipovolemia events. Objective: The aims of this study is to identify the proportion of patients experiencing elevated intradialytic and 1-month after HD cTnI, and determine association between HD vintage, UFR, UFV, intradialitic hypotention (IDH) and diabetes mellitus (DM) factors and the elevated of cTnI. Method: This study is a prospective cohort study examining cTnI levels before and after single HD session. A total 138 patient underwent twice-weekly regimens of HD. Levels of cTnI levels was tested using ARCHITECH STAT reagents. The cut-off points of cTnI were 34.0 pg/mL and 15.6 pg/mL for men and women, respectively. Bivariate and multivariate analysis were used to determine the association between HD vintage, UFR, UFV, IDH, and DM and the increased of intradialytic and 1-month after HD cTnI. Results: Out of 138 patients, 57 (41,3%) subjects had elevated intradialytic cTnI level. The cTnI levels increased significantly during HD (p <0.001). Diabetes has association with the increased levels of cTnI during intradialytic (OR 2,207 (CI 95% 1,056-4,616), p=0,033), which has a 2,2 times increased risk of cTnI levels. After 1 month, 53 of 132 subjects (40.2%) experienced significant increases in cTnI levels. A total of 31 patients (23.4%) had an increase of cTnI levels 50% above cut off. Multivariate analysis showed no association between HD vintage, UFR, UFV, IDH, DM and the elevated levels of 1-month after HD cTnI. Conclusion: The proportion of patients with elevated intradialytic cTnI is 41.3%. and 1-month after HD cTnI is 40.2%. Diabetes mellitus has association with the increased levels of cTnI during intradialytic while HD vintage, UFV, UFR and IDH have no association with the increased levels of cTnI. Hemodialysis vintage, UFR, UFV, IDH, and DM have no association with the increased levels of 1- month after HD cTnI.

Abstrak :
Latar belakang: Penyakit jantung bawaan (PJB) adalah kelainan kongenital dengan insidens tertinggi dan memerlukan pemantauan berkala. Pemeriksaan ekokardiografi memerlukan fasilitas dan tenaga ahli yang belum tersedia secara luas di Indonesia. Troponin I merupakan biomarker spesifik jantung yang terdeteksi pada awal terjadinya kerusakan miokardium. Data mengenai penggunaan biomarker jantung pada pasien anak dengan PJB masih terbatas. Tujuan: Mengetahui korelasi antara kadar troponin I dengan parameter hemodinamik pasien PJB asianotik dengan pirau kiri ke kanan. Metode: Penelitian ini merupakan studi potong lintang terhadap 53 subyek dengan PJB asianotik pirau kiri ke kanan yang berobat di Rumah Sakit dr. Cipto Mangunkusumo (RSCM). Pemeriksaan ekokardiografi dilakukan untuk menilai jenis PJB, ukuran defek, dan parameter hemodinamik yaitu Qp/Qs, tekanan sistolik arteri pulmoner, fraksi ejeksi ventrikel kiri, dan tricuspid annular plane systolic excursion (TAPSE). Kadar troponin I dinilai melalui enzyme linked fluorescent assay (ELISA) dengan sampel darah diambil pada hari yang sama dengan ekokardiografi.. Hasil: Median usia subyek adalah 16 (3-135) bulan dengan jenis kelamin perempuan 54,7% (n=53). Diagnosis PJB terbanyak adalah ASD (45,3%), dengan proporsi terbanyak defek berukuran sedang (43,4%). Peningkatan kadar troponin I didapatkan pada 7 (13,2%) subyek. Tidak ada perbedaan bermakna kadar troponin I pada berbagai jenis PJB. Ada korelasi negatif lemah antara kadar troponin I dengan fraksi ejeksi ventrikel kiri (r=-0,391, p=0,002). Kesimpulan: Terdapat korelasi negatif lemah antara kadar troponin I dengan fraksi ejeksi ventrikel kiri, sementara tidak ada korelasi bermakna dengan parameter hemodinamik lainnya ......Background: Congenital heart disease (CHD) is the most frequent congenital abnormality and requires regular monitoring. Echocardiographic examination requires facilities and experts which are not widely available in Indonesia. Troponin I is a heart-specific biomarker that is detected early in myocardial damage. Data regarding the use of cardiac biomarker in pediatric CHD patients are still limited. Objective: To determine the correlation between troponin I level and hemodynamic parameters in acyanotic CHD patients with left-to-right shunts. Methods: A cross-sectional study of 53 subjects with left-to-right shunt acyanotic CHD as inpatient or outpatient at dr. Cipto Mangunkusumo (RSCM) Hospital. Echocardiography was performed to assess the type and size of CHD, as weel as hemodynanic parameters (Qp/Qs, pulmonary artery systolic pressure, left ventricular ejection fraction/EF, and tricuspid annular plane systolic excursion/TAPSE). Troponin I level was determined by enzyme linked fluorescent assay (ELISA) with blood samples taken on the same day as echocardiography. Results: The median age of the subjects was 16 (3-135) months, with 54.7% female (n=53). Most prevalent of the CHD type was ASD (45.3%), most of the defect were medium-sized (43.4%). Increased troponin I levels were found in 7 (13.2%) subjects. There was no significant difference in troponin I level in various CHD types. There was a weak negative correlation between troponin I level and EF (r=-0.391, p=0.002). Conclusion: There was a weak negatif correlation between troponin I level and EF, while there was no significant correlation with other hemodynamic parameters.

Abstrak :
Nearly 80 short papers originating from the 14th International Symposium on Intracranial Pressure and Brain Monitoring held in Tuebingen, Germany, in September 2010 present experimental as well as clinical research data related to the naming topics of the conference. The papers have undergone a peer-reviewing and are organized in the following sections: methods of brain monitoring and data analysis, methods of invasive and non-invasive ICP assessment, the role of autoregulation, the role of tissue oxygenation and near-infrared spectroscopy, hydrocephalus/IIH imaging and diagnosis, management and therapy of hydrocephalus, management and therapy of traumatic brain injury, management and therapy of subarachnoid and intracranial hemorrhage, experimental approaches to acute brain disease. The book gives a good overview on the latest research developments in the field of ICP and related brain monitoring and on management and therapy of relevant acute brain diseases.