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Abstrak :
ABSTRAK
Tujuan : Koreksi transatrial-transpulmonary tanpa transannular patch (TA-TP tanpa TAP) memiliki keuntungan berupa preservasi annulus katup pulmonal dan fungsi ventrikel kanan, Namun sering terjadi gradien RV-PA dan pRV/LV ratio yang masih tinggi sehingga terjadi low cardiac output syndrome (LCOS). Penelitian ini bertujuan untuk mencari batasan gradien RV-PA dan pRV/LV ratio yang merupakan nilai prediktif terbaik terhadap kejadian LCOS pascakoreksi tetralogi Fallot TA-TP tanpa TAP. Metode : Pada bulan Oktober 2012 sampai Maret 2013, sebanyak 30 pasien TF menjalani koreksi TF TA-TP tanpa TAP (mean usia 8,37±7,90 tahun). Dilakukan pengukuran gradien RV-PA dan pRV/LV ratio intraoperatif dan postoperatif di ICU. Evaluasi kejadian LCOS dilakukan selama perawatan di ICU. Sebelum pasien pulang, dilakukan pemeriksaan ekokardiografi untuk menilai gradien RV-PA, fungsi ventrikel kanan, defek septum ventrikel residual, derajat regurgitasi katup pulmonal dan katup trikuspid. Hasil : Sebanyak 30 (100%) subjek penelitian memiliki z-value ≥ -1, menjalani koreksi TF TA-TP tanpa TAP. Mean gradien RV-PA intraoperatif adalah 21,13±10,60 mm Hg dan mean pRV/LV ratio intraoperatif adalah 0,53±0,14. Mean gradien RV-PA di ICU adalah 20,83±7,10 mmHg dan mean pRV/LV ratio di ICU adalah 0,49±0,10. Tidak terjadi LCOS pada 30 (100%) subjek penelitian sehingga tidak dapat dilakukan analisis untuk mencari batasan nilai gradien RV-PA dan pRV/LV ratio sebagai nilai prediktif terbaik terhadap kejadian LCOS pascakoreksi TF TA-TP tanpa TAP. Mean gradien RV-PA sebelum subjek penelitian rawat jalan adalah 23,47±6,95 mmHg. Regurgitasi katup pulmonal ringan pada 15 (50%) subjek penelitian dan regurgitasi katup trikuspid trivialmild pada 16 (53%) subjek penelitian. Disfungsi ventrikel kanan ringan 3 (10%), sedang 20 (67%) dan berat pada 7 (23%) subjek penelitian. Mean TAPSE postoperatif adalah 1,03±0,19. DSV residual tidak dijumpai, aritmia tidak dijumpai, reoperasi dan mortalitas tidak ada. Simpulan : Koreksi TF TA-TP tanpa TAP memberikan hasil operasi dini yang baik pada pasien TF dengan z-value katup pulmonal ≥ -1, pRV/LV ratio < 0,5 dan gradien RV-PA < 25 mmHg pascakoreksi.

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ABSTRACT
Objective : The benefits of the transatrial-transpulmonary (TA-TP) without transannular patch (TAP) correction of tetralogy of Fallot (TOF) are preservation of pulmonary valve annulus and right ventricular function. However, TA-TP without TAP correction of TOF had a higher incidence of low cardiac output syndrome (LCOS) because of the high right ventricle and pulmonary artery (RV-PA) pressure gradient and right ventricle and left ventricle pressure (pRV/LV) ratio. The purpose of this study were to analyze the cut off value of RV-PA pressure gradient dan pRV/LV ratio as the best predictor value for postoperative LCOS in TA-TP without TAP correction of TOF. Methods : Between Oktober 2012 and Maret 2013, 30 patients with TOF underwent TATP without TAP correction (mean age 8,37±7,90 years, range 1-27 years). At the end of correction, all patients underwent intraoperative direct measurement of RV-PA pressure gradient and pRV/LV ratio. The patients were evaluated for postoperative LCOS at the Intensive Care Unit (ICU). All the patients underwent echocardiographic examination before hospital discharge. This included investigation of the presence RV-PA pressure gradien, RV function, residual VSD, pulmonary and tricuspid valve insufficiency. Results : Thirty patients with pulmonary valve annulus z-value ≥ -1, underwent TA-TP without TAP correction of TOF. Mean intraoperative RV-PA pressure gradient was 21,13±10,60 mmHg and mean intraoperative pRV/LV ratio was 0,53±0,14. Mean RV-PA pressure gradient measured 24 hours after correction at the ICU was 20,83±7,10 mmHg and mean pRV/LV ratio measured at 24 hours after correction at the ICU was 0,49±0,10. No patient had LCOS, we could not analyze the cut off value of RV-PA pressure gradient and pRV/LV ratio as the best predictor value for postoperative LCOS in this study. No patient had residual VSD. Mean RV-PA pressure gradient before hospital discharge was 23,47±6,95 mmHg. Fifteen (50%) patients had mild pulmonary valve insufficiency and 16 (53%) patients had trivial-mild tricuspid valve insufficiency. Three (10%) patients had mild RV dysfunction. Postoperative mean TAPSE was 1,03±0,19. No patient had arrhythmia, reoperation and mortality in this study. Conclusions : The TA-TP without TAP correction of TOF was applied successfully in 30 patients with pulmonary valve annulus z-value ≥ -1, post-correction RV-PA pressure gradient < 25 mmHg and pRV/LV ratio < 0,5.

Abstrak :
Latar Belakang: Hiperhidrasi menyebabkan peningkatan beban volume jantung, tekanan darah, hipertrofi ventrikel kiri, edema paru, gagal jantung kongestif. Hemodialisis yang tidak adekuat menyebabkan hiperhidrasi, peningkatan morbiditas dan mortalitas penyakit kardiovaskular. Hiperhidrasi lama menyebabkan iskemia koroner karena dilatasi jantung, hipertrofi ventrikel kiri, hipertensi, penurunan cadangan koroner. Hiperhidrasi menyebabkan vasokonstriksi sistemik berlebihan, penurunan perfusi jaringan perifer. Disfungsi endotel berperan pada vasokonstriksi yang berlebihan pada hiperhidrasi. Brain-type natriuretic peptide (BNP) merupakan parameter untuk mengukur hiperhidrasi. Asymmetrical dimethyl arginine (ADMA) merupakan inhibitor endogen, bersifat kompetitif terhadap nitric oxide synthase endotel dan digunakan sebagai parameter disfungsi endotel. Tujuan: Mengetahui hubungan hiperhidrasi dengan disfungsi endotel. Metode: Penelitian ini merupakan penelitian potong lintang pada pasien hemodialisis dua kali seminggu. Dengan menggunakan BNP dan ADMA sebagai parameter. Hasil: Dari 126 subjek, proporsi hiperhidrasi (BNP>356 pg/ml) sebesar 64,3%. Median usia 52 (47-62) dengan presumtif penyebab GGK utama adalah hipertensi (38,9%), DM (28,6%), Glomerulonefritis (21,4%). Tidak terdapat hubungan signifikan antara hiperhidrasi dengan disfungsi endotel (PR=1,042, p=0,832 IK 95%=0,714-1,521). HsCRP merupakan faktor perancu utama terhadap hubungan antara hiperhidrasi dan disfungsi endotel (OR (IK95%) 1,604 (0,551-4,666), p=0,386, ΔOR 53,37%) Simpulan: Tidak ada hubungan antara hiperhidrasi dengan disfungsi endotel (PR=1,042, p=0,832 IK95%=0,714-1,521). ...... Background: Hyperhydration leads to increased cardiac volume load, blood pressure, left ventricular hypertrophy, pulmonary edema, congestive heart failure. Hemodialysis that is not adequately causes hyperhydration, increased morbidity and mortality of cardiovascular disease. Prolonged hyperhydration causes coronary ischemia due to heart dilation, left ventricular hypertrophy, hypertension, decrease in coronary reserves. Hyperhydration causes excessive systemic vasoconstriction, decreased perfusion of peripheral tissues. Endothelial dysfunction plays a role in excessive vasoconstriction pada hyperhydration. Brain-type natriuretic peptide (BNP) is a parameter for measuring hyperhydration. Asymmetrical dimethyl arginine (ADMA) is an endogenous inhibitor, competitive against endothelial nitric oxide synthase and used as a parameter of endothelial dysfunction. Purpose: Knowing the relationship of hyperhydration with endothelial dysfunction. Method: This study is a cross-sectional study in hemodialysis patients twice a week. By using BNP and ADMA as parameters Result: Of the 126 subjects, hyperhydration proportion (BNP>356 pg/ml) of 64.3%. Median age 52 (47-62) with presumptive causes of primary GGK is hypertension (38.9%), DM (28.6%), Glomerulonephritis (21.4%). There is no significant association between hyperhydration and endothelial dysfunction (PR=1,042, p=0.832 CI 95%=0.714-1.521). Conclusion: There is no relationship between hyperhydration and endothelial dysfunction (PR=1,042, p=0.832 CI 95%=0.714-1.521).

Abstrak :
Lead editor of Braunwald's Heart Disease, Dr. Douglas L. Mann, and nationally and internationally recognized heart failure expert Dr. G. Michael Felker, bring you the latest, definitive state-of-the art information on heart failure in this outstanding Braunwald's companion volume. Heart Failure, 3rd Edition, keeps you current with recent developments in the field, improved patient management strategies, and new drug therapies and implantable devices that will make a difference in your patients' lives and in your practice. Braunwald's Heart Failure Companion also has an on-line version that is.