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"Latar belakang: Latihan fisik anaerobik yang lama (latihan fisik ketahanan/endurance dengan intensitas berat yang melebihi kapasitas aerobik) mengakibatkan remodeling morfologi dan sistem konduksi listrik jantung. Connexin 43 (Cx43) adalah protein penyusun gap junction pada diskus interkalaris kardiomiosit ventrikel, yang bertanggung jawab atas konduksi listrik jantung. Penelitian ini bertujuan untuk menganalisis pola distribusi dan ekspresi Cx43 kardiomiosit pasca-latihan serta pasca-henti-latih fisik anaerobik.Metode: Identifikasi Cx43 dilakukan dengan cara pulasan imunohistokimia dan analisis kuantitatif luas area ekspresi Cx43 dilakukan pada kelompok kontrol (K4M, K8M, K12M dan K16Minggu) dan perlakuan latihan fisik (AN4M, AN12M) serta henti-latih (AN4MD, AN12MD).Hasil: Analisis data menunjukkan peningkatan luas area ekspresi Cx43 (pixel) pada kelompok pasca-latihan fisik (K4M: 77006±7513 dan AN4M: 116932±5552, p<0,001; K12M: 51727±2209 dan AN12M: 123781±6019, p<0,001), yang disertai oleh peningkatan proporsi lateralisasi ekspresi Cx43 (persentase area lateralisasi: K4M: 11,34±0,8% dan AN4M: 25,11±1%, p<0,001; K12M: 11,32±0,37% dan AN12M: 30,36±2,2%, p<0,001). Kelompok pascahenti-latih menunjukkan regresi luas area ekspresi Cx43 (AN12M: 123781±6019 dan AN12MD: 93908±9348, p<0,005) dan persentase area lateralisasi (AN12M: 30,36±2,2% dan AN12MD: 21,2±1,1%, p<0,001).Kesimpulan: Peningkatan ekspresi Cx43 (yang dipredominansi oleh peningkatan lateralisasi) kardiomiosit ventrikel kiri jantung tikus pasca-latihan fisik anaerobik merupakan suatu proses adaptasi fisiologis dan bersifat sementara.

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Introduction: Long-term non-resistance anaerobic exercise (excessive endurance training that exceed aerobic capacity) causes remodeling of cardiac morphology and conduction system. Major gap junction protein expressed on ventricular cardiomyocyte, connexin 43 (Cx43) is an important determinant of cardiac conduction system. The aims of this study are to analyse Cx43 expression and distribution on cardiomyocyte post-anaerobic exercise and detraining.Methods: Cx43 expression is identified by immunohistochemistry labeling and quantitative analyses on Cx43 areas are conducted on 4 and 12 weeks postanaerobic exercise rats (AN4M, AN12M) along with 4 weeks of detraining groups (AN4MD, AN12MD) and time-matched sedentary control groups (K4M, K8M, K12M dan K16M).Results: Data analyses show an increased Cx43 area expression (pixel) on postanaerobic exercise groups (K4M: 77006±7513 vs. AN4M: 116932±5552, p<0,001 and K12M: 51727±2209 vs. AN12M: 123781±6019, p<0,001), and characterized by marked increased on lateralization (K4M: 11,34±0,8% vs. AN4M: 25,11±1%, p<0,001 and K12M: 11,32±0,37% vs. AN12M: 30,36±2,2%, p<0,001). Detraining groups show regression on Cx43 area expression (AN12M: 123781±6019 vs. AN12MD: 93908±9348, p<0,005) and lateralization (AN12M: 30,36±2,2% vs. AN12MD: 21,2±1,1%, p<0,001).Conclucion: Increased Cx43 expression (predominated by lateralization) of left ventricular cardiomyocyte post-anaerobic exercise is a physiological adaptation and reversible upon detraining."

"Latar belakang: Latihan fisik anaerobik adalah latihan fisik yang dilakukan dalam waktu singkat dengan intensitas tinggi dan dapat merangsang apoptosis pada kardiomiosit ventrikel kiri. Penelitian ini bertujuan untuk menganalisis ekspresi apoptosis kardiomiosit pasca latihan serta pasca henti latih latihan fisik anaerobik. Metode : Identifikasi Caspase-3 dilakukan dengan cara pulasan imunohistokimia dan analisis kuantitatif persentase Caspase-3 yang dilakukan pada kelompok kontrol 4,8,12 dan 16 minggu, kelompok perlakuan latihan fisik anaerobik 4 dan 12 minggu serta henti latih 4 minggu pasca latihan (minggu ke 8 dan 16). Hasil: Analisis data menunjukkan peningkatan persentase caspase-3 pada kelompok latihan fisik anaerobik 4 dan 12 minggu dengan p=0,027. Penurunan persentase capase-3 pasca henti latih yang bermakna juga ditemukan antara kelompok latihan fisik anaerobik 4 minggu dengan kelompok henti latih 4 minggu (p=0,0001) dan antara kelompok latihan anaerobik 12 minggu dengan kelompok henti latih 16 minggu (p=0,0001).

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Introduction : Anaerobic physical exercise is a high intensity physical exercise performed in a short time. This exercise can stimulate apoptosis in left ventricular cardiomyocytes. The aims of this study is to analyze the expression of cardiomyocyte apoptosis after anaerobic exercise and detraining.

Methods : Caspase-3 expression is identified by immunohistochemistry labeling and quantitative analysis of the percentage of Caspase-3 in the control group 4,8,12 and 16 weeks, groups with 4 and 12 weeks of anaerobic physical exercise, and groups after 4 weeks of detraining ( week 8 and 16).

Conclucion: Data analyses showed a significant increase in the percentage of caspase-3 in the 4 and 12 weeks anaerobic physical exercise groups with p = 0.027. The percentage of Capase-3 after detraining showed a significant decline between the groups of 4 weeks of anaerobic physical exercise and detraining with p = 0.0001 and between groups of 12 weeks of anaerobic exercise and detraining with p = 0, 0001."

"Latar Belakang : Beberapa penelitian terbaru memperlihatkan bahwa apoptosis terjadi pada beberapa keadaan jantung patologis seperti pada keadaan kerusakan ?iskemia-reperfusi?, infark miokardium dan gagal jantung. Di sisi lain terdapat penelitian yang memperlihatkan bahwa latihan fisik dapat menurunkan apoptosis kardiomiosit. Dari beberapa jenis latihan fisik, latihan fisik aerobik merupakan latihan yang paling dianjurkan karena diyakini efektif dalam mencegah dan bahkan sebagai terapi rehabilitasi pada penyakit kardiovaskular. Keadaan henti latih pasca latihan fisik ternyata dapat mengembalikan seluruh atau sebagian adaptasi yang sudah terbentuk setelah latihan fisik. Tujuan : Penelitian ini bertujuan ingin melihat bagaimana pengaruh latihan fisik aerobik dan henti-latih terhadap apoptosis kardiomiosit ventrikel kiri dengan menggunakan protein caspase-3 sebagai parameter apoptosis. Desain : Penelitian ini menggunakan studi eksperimental in vivo pada tikus Metode : identifikasi protein caspase-3 pada jaringan ventrikel kiri jantung tikus dengan pemeriksaan pulasan imunohistokimia pada 8 kelompok tikus ( kelompok kontrol 4 minggu (K4M), kontrol 8 minggu (K4MD), kontrol 12 minggu (K12M), kontrol 16 minggu (K12MD) dan kelompok perlakuan latihan aerobik 4 minggu (AR4M), perlakuan latihan aerobik 12 minggu (AR12M), perlakuan latihan aerobik 4 minggu diikuti dengan henti-latih 4 minggu (AR4MD) serta kelompok latihan aerobik 12 minggu diikuti dengan henti-latih 4 minggu(AR12MD)). Hasil : Analisis data menunjukan peningkatan persentase ekspresi caspase-3 kelompok pasca latihan fisik aerobik (K4M 6,40%1,78 dan AR4M 65,38%2,54, p<0,001; K12M 5,72%0,88 dan AR12M 41,81%3,21, p<0,001; K4MD 8,64%±3,59 dan AR4MD 66,55%±1,88; K12MD 7,35%±2,06 dan AR12MD 46,78%±2,45, p<0,001). Kecenderungan Peningkatan persentase ekspresi caspase-3 kelompok pasca henti latih (AR4M 65,38%2,54 dan AR4MD 66,55%1,88%, p=1,000; AR12M 41,81%3,21dan AR12MD 46,78%±2,45, p=0,230). Ekspresi caspase 3 kelompok latihan aerobik 4 minggu lebih tinggi dibanding kelompok latihan aerobik 12 minggu (AR4M 65,38%2,54 dan AR12M 41,81%3,21, p<0,001). Kesimpulan : latihan fisik aerobik tidak menurunkan apoptosis kardiomiosit ventrikel kiri jantung tikus dan program henti latih tidak meningkatkan apoptosis kardiomiosit ventrikel kiri jantung tikus.

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Background: Recent studies showed that apoptosis occurs in several pathological heart condition as in myocardial ischemia-reperfusion injury, myocardial infarction and heart failure. It has been also research showing that physical exercise can reduce apoptosis on cardiomyocyte. Of some kind of physical exercise, aerobic exercise is an exercise that is most recommended because it is believed to be effective in preventing and even as a rehabilitation therapy on cardiovascular disease. Detraining was able to restore all or part of adaptation that has been formed after the exercise.

Objective: This study aimed to see the effect of aerobic exercise and detraining on left ventricular cardiomyocyte apoptosis using caspase-3 protein as a parameter of apoptosis. Design: This study used an experimental in vivo study on rats.

Methods: Caspase-3 protein in rat cardiac left ventricular tissue is identified by immunohistochemistry staining conducted on 4 sedentary control group ( 4 weeks control group (K4M), 8 weeks control group (K4MD), 12 weeks control group (K12M), 16 weeks control (K12MD)) and 4 treatment groups ( 4 & 12 weeks post aerobic exercise group (AR4M, AR12M) and 4&12 weeks post aerobic exercise followed by 4 weeks detraining (AR4MD,AR12MD)).

Results: Analysis of the data shows an increase percentage of caspase-3 expression on post-aerobic exercise group (K4M 6,40%1,78 and AR4M 65,38%2,54, p<0,001; K12M 5,72%0,88 and AR12M 41,81%3,21, p<0,001; K4MD 8,64%±3,59 and AR4MD 66,55%±1,88; K12MD 7,35%±2,06 and AR12MD 46,78%±2,45, p<0,001) The data also shows tendency an increase percentage of caspase-3 expression on detraining group (AR4M 65,38%2,54 and AR4MD 66,55%1,88%, p=1,000; AR12M 41,81%3,21 and AR12MD 46,78%±2,45, p=0,230). Percentage of caspase-3 expression on post-4 weeks aerobic exercise group is higher than post-12 weeks aerobic exercise (AR4M 65,38%2,54 and AR12M 41,81%3,21, p<0,001).

Conclusion: Aerobic physical exercise does not decrease left ventricular cardiomyocyte apoptosis and does not improve left ventricular cardiomyocyte apoptosis."

"Lima puluh persen penderita gagal jantung merupakan gagal jantung dengan fraksi ejeksi yang normal (HFPEF). Morbiditas dan mortalitas HFPEF belumlah jelas. Latihan olahraga telah menjadi rekomendasi pertama dalam beberapa panduan klinis, namun belum pada HFPEF. Strain longitudinal apikal 4 ruangan dapat digunakan sebagai nilai prognostik. Perbaikan fungsi longitudinal intrinsik ventrikel kiri menggunakan strain longitudinal apikal empat ruangan akibat latihan olahraga belumlah diketahui. Kuasi eksperimental menggunakan 30 sampel konsekutif HFPEF, dilakukan program latihan olahraga tersupervisi. Program latihan olahraga dilakukan selama satu bulan. Dilakukan pemeriksaan ekokardiografi, 6MWT, kuesioner MLWHF dan WHO. Terdapat perbedaan yang signifikan dalam 6MWT, nilai skoring MLWHF dan WHO5 sebelum dan sesudah latihan olahraga. Didapatkan nilai strain longitudinal sebesar -16,20% (-10,7% sampai dengan -17,81%). Strain longitudinal apikal 4 ruangan mengalami perbaikan pada minggu ke 2 dan ke 4 latihan olahraga (sebelum latihan olahraga LS = -16,20 [-10,70 to -17,81]; minggu ke dua latihan olah raga LS = -18,00±2,69 dan minggu ke 4 latihan olahraga LS = -21,86±1,79) dan terdapat perbedaan yang signifikan (p < 0,001). Terdapat perbaikan fungsi intrinsik longitudinal ventrikel kiri sebelum dengan sesudah diberikan program latihan olahraga pada penderita gagal jantung dengan fraksi ejeksi yang normal.

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Fifty percent of patients with heart failure are heart failure with preserved ejection fraction (HFPEF). Morbidity and mortality of HFPEF is unclear. Exercise has become the first recommendation in several clinical guidelines, but not yet in HFPEF. Apical 4 chamber longitudinal strain can be used as a prognostic value. But the improvement of longitudinal intrinsic left ventricular function using apical 4 chamber longitudinal strain due to exercise training is not yet known. Quasi- experimental study using thirty consecutive sample of HFPEF. Exercise training program was conducted for a month. Echocardiography, 6MWT, MLWHF and WHO questionnaire was performed before and after exercise. There was significant differences in the 6MWT, the value of MLWHF and WHO5 score before and after exercise. Longitudinal strain values obtained by -16.20 % (-10.7% to -17.81%). Four chamber longitudinal strain was improved at weeks 2 and 4 of exercise (before exercise LS = -16.20[-10.70 to -17.81]; the second week of exercise training LS = -18.00±2,69 and week 4 exercise LS = -21.86 ± 1.79) and there were significant differences (p < 0.001). There was an improvement in the longitudinal intrinsic left ventricular function before and after exercise training in patients with heart failure with preserved ejection fraction."

"Latar belakang : Overtraining berdampak buruk terhadap kesehatan karena dapat menyebabkan kematian mendadak pada atlet muda. Berdasarkan data epidemiologi ditemukan bahwa kejadian kematian mendadak (suddent cardiac death) pada atlet muda, penyebab paling banyak adalah gangguan kardiovaskular. Tubuh melakukan adaptasi terhadap beban berlebih, berupa remodelling (morfologi dan elektrofisiologi). Remodeling elektrofisiologis yaitu perubahan pada gap junction, berupa perubahan ekspresi Cx43 yang yang mengakibatkan gangguan penghantaran konduksi listrik. Selama latihan fisik dapat terbentuk ROS yang akan menginduksi permeabilitas mitokondria sehingga terjadi kebocoran sitokrom c, selanjutnya akan mengaktifkan kaskade apoptosis.Metode : Penelitian ini dilakukan pada 6 jaringan kardiomiosit tikus Wistar kelompok kontrol dan overtraining. Ekspresi Cx43 dan caspase-3 diamati melalui pulasan imunohistokimia dan diukur dengan image J.Hasil : Hasil penelitian ini menunjukkan peningkatan bermakna pada ekspresi Cx43 total overtraining (43644.57±27711.03) dibandingkan kelompok kontrol (13002.37±3705.41). Tidak ditemukan perbedaan bermakna ekspresi caspase-3 pada kedua kelompok meskipun diperoleh hasil lebih tinggi pada kelompok overtraining (14.15%±10.54%) dibandingkan kelompok kontrol (2,63%±3.56%).Kesimpulan : Overtraining meningkatkan ekspresi Cx43 total tetapi tidak terbukti meningkatkan caspase-3 pada kardiomiosit ventrikel kiri tikus.

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Background: overtraining has bad effect for health, overtraining can cause sudden death in young athlete, reports of sudden death incidences in young athlete claim that cardiovascular disease is the cause. The heart can face the excess load by remodeling as it?s adaptation mechanism. There is 2 type remodeling, morphology and electrophysiology. Remodeling electrophysiology is a change on Cx43 expression which can interfere the heart?s electrical conduction. Free radical which formed from physical exercise can induce mitochondrial permeability that lead leakage of cytochrome c, so that so that activate the apoptosis cascade.

Methods: This study conducted on 12 Wistar rat?s cardiomyocytes tissue that divided into control and overtraining group. Cx43 expression and caspase-3 was observed through immunohistochemical staining and measured by image J.

Results: There was significant increase in the expression of Cx43 total overtraining (43644.57 ± 27711.03) compared to the control group (13002.37 ± 3705.41). Found no significant differences in the expression of caspase-3 in both groups although the result was higher in the group of overtraining (14,15% ± 10,54%) compared to the control group (2,63% ± 3,56%).

Conclusion: Overtraining increase total Cx43 expression but not proven to increase caspase-3 in the rat left ventricular cardiomyocytes."

"ABSTRAKLatar Belakang: Perkembangan ilmu pengetahuan berhasil meningkatkan harapan hiduppasien yang mengalami infark miokardium. Namun pengobatan yang ada saat ini hanyamemperbaiki kondisi klinis pasien, tanpa adanya perbaikan otot jantung yang telah rusak.Hal inilah yang mendasari berkembangnya penelitian yang mempelajari tentang upayaregenerasi sel otot jantung dengan pemanfaatan sel punca yang salah satunya adalahMesenchymal Stem Cell MSC . Namun hasil yang didapatkan dari beberapa penelitianmenunjukkan hasil yang belum optimal. Hal ini disebabkan oleh beberapa faktordiantaranya adalah kadar dan fungsi dari sel punca yang tidak adekuat. Hingga saat inibelum ada penelitian yang mengevaluasi faktor-faktor yang mempengaruhi kadar MSCdalam Bone Marrow Mononuclear Cell BMMC pada pasien penyakit jantung iskemikkhususnya pengaruh fungsi sistolik ventrikel kiri.Tujuan: Menilai hubungan fungsi sistolik ventrikel kiri dengan kadar MSC dalam BMMCpada pasien penyakit jantung iskemik yang menjalani terapi sel punca Metode: Penelitian ini merupakan studi potong lintang dengan menggunakan datasekunder. Subjek penelitian adalah pasien penyakit jantung koroner dengan fungsi sistolikventrikel kiri

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ABSTRACTBackground The development of science succeeded in increasing the life expectancy of patients with myocardial infarction. However, existing treatments only improve the clinical condition of the patient, without any improvement of the damaged heart muscle. Thus supposrt the development of research that studies to regenerate heart muscle cells with stem cells, for example Mesenchymal Stem Cell MSC . However, the results from several studies have shown modest results. It is caused by several factors including the levels and function of stem cells is inadequate. Until now, no study has evaluated the factors affecting the levels of MSC in Bone Marrow mononuclear cell BMMC in patients with ischemic heart disease in particular the influence of left ventricular systolic function.Objective To assess the association of left ventricular systolic function with MSC levels in BMMC in patients with ischemic heart disease who underwent stem cell therapyMethods This was a cross sectional study using secondary data. Subjects were patients with coronary heart disease with left ventricular systolic function "

"Latar Belakang: Reperfusi koroner sangat penting untuk menyelamatkan miokardium yang mengalami iskemia namun tindakan ini ternyata juga dapat mengakibatkan cedera miokardium yang dikenal sebagai jejas reperfusi Manifestasi klinisnya berupa komplikasi pasca BPAK diantaranya aritmia penurunan curah jantung dan perioperatif infark miokard Stres oksidatif merupakan salah satu inisiator utama kejadian jejas reperfusi Allopurinol sebagai inhibitor efektif enzim xantin oksidase dapat menurunkan stres oksidatif dengan menghambat pembentukan reactive oxygen species Sehingga diharapkan pemberian allopurinol pada pasien PJK dengan disfungsi ventrikel kiri yang akan menjalani BPAK dapat menurunkan kejadian komplikasi pasca operasiTujuan: Mengetahui efek allopurinol terhadap komplikasi pasca operasi BPAK low cardiac output syndrome yang dinilai dengan penggunaan inotropik dan IABP pasca operasi kematian dalam masa rawat perioperatif infark miokard dan aritmia pada pasien PJK dengan disfungsi ventrikel kiriMetode: Penelitian ini adalah uji klinis tersamar ganda 34 subjek dipilih secara konsekutif pada September November 2015 Subjek dibagi menjadi dua kelompok yaitu 16 orang mendapat allopurinol 600mg dan 18 orang mendapat plasebo Obat per oral diberikan 1 hari sebelum dan 6 jam sebelum operasi Pengamatan kejadian komplikasi pasca operasi dimulai sejak pelepasan klem silang aorta hingga pasien selesai perawatanHasil: Penggunaan inotropik dan IABP pasca operasi menunjukkan perbedaan yang bermakna pada kedua kelompok p 0 047 Ini berarti penggunaan allopurinol berpotensi mengurangi penggunaan inotropik dan IABP pasca operasi BPAK Proporsi kematian dalam masa rawat pasca operasi BPAK pada kedua kelompok tidak berbeda bermakna yaitu 6 25 vs 5 6 p 1 000 Sedangkan untuk kejadian aritmia pada kedua kelompok terdapat perbedaan bermakna dengan total proporsi 31 vs 66 p 0 039 dengan jumlah aritmia terbanyak pada kedua kelompok adalah fibrilasi atrium Kejadian perioperatif infark miokard tidak didapatkan pada penelitian ini sehingga efek pemberian allopurinol terhadap kejadian tersebut tidak dapat dinilaiKesimpulan: Pemberian allopurinol sebelum operasi pada pasien PJK dengan disfungsi ventrikel kiri berpotensi menurunkan kejadian low cardiac output syndrome LCOS yang terlihat dari rendahnya penggunaan obat inotropik dan IABP pasca operasi dan menurunkan kejadian aritmia pasca operasi BPAK

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Background: Reperfusion of coronary blood flow is important to resuscitate the ischemic or hypoxic myocardium However the return of blood flow to the ischemic area can result paradoxical cardiomyocyte dysfunction this is referred to as ldquo reperfusion injury rdquo Clinical manifestations of reperfusion injury post CABG surgery are arrhythmias decrease cardiac output and perioperative myocardial infarct Oxidative stress has been confirmed as one of the main initiator in myocardial injury at ischemic and reperfusion state Allopurinol as an effective inhibitor of xanthine oxidase XO can reduce the oxidative stress by blocking the formation of reactive oxygen species ROS Pre operative allopurinol on CAD's patient with LV dysfunction is expected reduce the complications of post CABG surgery

Objective: To analyze effects of pre operative administration of allopurinol on complications of post CABG surgery low cardiac output syndrome which is measured by the use of post surgery inotropic and IABP hospital mortality perioperative myocardial infarction and arrhythmias in CAD's patient with LV dysfunction

Methods: This study is a double randomized clinical trial 34 CAD's patients with LV dysfunction were randomly selected by consecutive sampling methods from September November 2015 They were divided into two groups Sixteen patients were given 600 mg dose of allopurinol per oral one day before and 6 hours before surgery and the rest received placebo Complications of post CABG surgery were observed since the aortic cross clamp off until discharged

Results: The use of post surgery inotropic and IABP found significantly lower in allopurinol group p 0 047 There was no significant difference in proportion of death in post operative hospitalization period in both groups 6 25 vs 5 6 p 1 000 While for the incidence of arrhythmias was found significantly different in the two groups 31 vs 66 p 0 039 with atrial fibrillation as the most common arrhythmia No perioperative myocardial infarction was found in this study therefore effects of allopurinol to the event is unknown

Conclusions: Pre operative administration of allopurinol may reduce the complications of post CABG especially the use of inotropic and IABP and occurrence of arrhythmias"

"[ABSTRAKLatar belakang. Pada stenosis mitral sering timbul komplikasi hipertensi pulmoner dan disfungsi ventikel kanan. Belum ada penelitian yang menghubungkan antara resistensi vaskular paru sebelum operasi dengan fungsi jantung kanan saat pasca operasi serta perubahannya pasca operasi stenosis mitral rematik.Metode. Studi ini merupakan studi kohort prospektif pada 31 pasien stenosis mitral rematik yang menjalani operasi katup mitral di Rumah Sakit Jantung dan Pembuluh Darah Harapan Kita sejak April 2014 sampai Maret 2015. Pasien menjalani pemeriksaan ekokardiografi sebelum operasi, sebelum pulang perawatan pasca operasi serta saat follow up mid term di poliklinik. Dilakukan analisa statistik untuk melihat hubungan antara resistensi vaskular paru (RVP) pra operasi dengan strain longitudinal ventrikel kanan saat follow up mid term serta perubahan strain longitudinal ventrikel kanan pasca operasi (delta strain).Hasil. Tidak terdapat korelasi antara RVP pra operasi dengan strain longitudinal speckle tracking ventrikel kanan saat follow up mid term pasca operasi (r 0,199 p 0,264) serta dengan perubahan strain longitudinal ventrikel kanan pasca operasi atau delta strain (r 0,174 p 0,350).Kesimpulan. Resistensi vaskular paru pra operasi tidak berhubungan dengan strain longitudinal speckle tracking ventrikel kanan saat follow up mid term pasca operasi serta dengan perubahan strain longitudinal ventrikel kanan pasca operasi atau delta strain.

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ABSTRACTBackground. In MS right ventikel (RV) dysfunction and pulmonary hypertension often occur as complication. There is no research that connects the pulmonary vascular resistance before surgery with RV function and its changes in the case of rheumatic mitral stenosis who underwent mitral valve surgery.Methods. This study is a prospective cohort study which involves 31 patients with rheumatic mitral stenosis who underwent surgery at National Cardiovaskular Center Harapan Kita Hospital from April 2014 to March 2015. Patients underwent echocardiography before surgery, after surgery pre-hospital discharge and mid-term follow-up at clinic. Statistical analysis was performed to see the relationship between preoperative pulmonary vascular resistance (PVR) with RV function at mid term follow up, which is assessed using echocardiographic parameters right ventricular longitudinal speckle strain, and also with right ventricle longitudinal speckle strain postoperative changes (delta strain).Results. There is no correlation between pre operative PVR with RV longitudinal speckle strain at mid term follow-up (r 0,199 p 0,264), and post operative changes or delta strain (r 0.174 p 0.350).Conclusion. RVP before surgery is not associated with right ventricle longitudinal speckle strain at follow up mid term and post operative changes or delta strain., Background. Acute rheumatic fever and rheumatic heart disease is still regarded as animportant public health problem especially in developing countries. Mitral stenosis (MS) is asequale of rheumatic fever which are most commonly found. In MS right ventikel (RV)dysfunction and pulmonary hypertension often occur as complication. The right ventricle hasa smaller muscle mass so it is more sensitive to changes in pressure loads. There is noresearch that connects the pulmonary vaskular resistance before surgery with RV functionand also changes in the case of rheumatic mitral stenosis who underwent mitral valvesurgery.Methods. This study is a prospective cohort study which involves 31 patients with rheumaticmitral stenosis who underwent surgery at National Cardiovaskular Center Harapan Kita Hospital from April 2014 to March 2015. Patients underwent echocardiography before surgery, after surgery pre-hospital discharge and mid-term follow-up at clinic. Statisticalanalysis was performed to see changes in RV function with longitudinal speckle strain, aftersurgery pre-hospital discharge and mid-term follow-up at clinic. Analysis also performed tosee the relationship between preoperative pulmonary vascular resistance (PVR) with RVfunction at mid term follow up, which is assessed using echocardiographic parameters rightventricular longitudinal speckle strain, and also with right ventricle longitudinal specklestrain postoperative changes (delta strain). Results. Right ventricular function after surgery seen with longitudinal speckle strainimproved from -12.94 ± 3.63 preoperatively into -13.06 ± 3.63 after surgery pre hospitaldischarge, and -15.25 ± 3.75 at follow-up evaluation (p 0.007). There is no correlationbetween pre operative PVR with longitudinal speckle strain at mid term follow-up (r 0,199 p0,264), and RV longitudinal speckle strain post operative changes or delta strain (r 0.174 p0.350). Conclusion. After mitral valve surgery, right ventricle longitudinal speckle strain improves.RVP before surgery is not associated with right ventricle longitudinal speckle strain at follow up mid term and right ventricle longitudinal speckle strain post operative changes or deltastrain. ]"

"Latar belakang: Penyakit jantung bawaan (PJB) pirau kiri ke kanan adalah penyebab penting gagal tumbuh pada anak. Koreksi terhadap defek tersebut diketahui memperbaiki prognosis pertumbuhan berat maupun tinggi badan. Tujuan. Mengetahui korelasi usia koreksi defek dengan pertambahan tinggi badan pada pasien PJB pirau kiri ke kanan pasca-koreksi terhadap prognosis pertumbuhan. Metode: Penelitian dilakukan secara potong lintang dengan menggunakan rekam medis pada subyek dengan PJB pirau kiri ke kanan yang dikoreksi kurang dari 2 tahun di Rumah Sakit Cipto Mangunkusumo (RSCM) dengan variabel bebas usia koreksi defek dan variabel terikat z-skor dan Δz-skor TB/U pasca-koreksi. Referensi pertumbuhan menggunakan kurva WHO 2006. Perhitungan korelasi dilakukan menggunakan korelasi Spearman dan kemaknaan ditetapkan dengan p<0,05. Hasil: Median usia koreksi defek pada penelitian ini adalah 8 bulan dengan usia koreksi terbanyak adalah kurang dari 6 bulan dan usia 6-12 bulan masing-masing sebanyak 11 orang. Defek terbanyak adalah VSD. Usia koreksi defek tidak berkorelasi dengan z-skor TB/U pasca-koreksi berdasarkan uji korelasi Spearman (r= 0,093) dengan nilai p=0,642. Usia koreksi defek dengan Δ z-skor TB/U tidak ditemukan korelasi berdasarkan uji korelasi Spearman (r=0,143) dengan nilai p=0,452. Kesimpulan: Usia koreksi defek tidak terbukti berkorelasi baik dengan z-skor TB/U maupun Δ z-skor TB/U pasca-koreksi.

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Background: Congenital heart disease (CHD) left-to-right shunt is an important cause of growth failure in children. Correction of these abnormalities is known to improve the prognosis of growth in weight and height.

Objectives: Identify correlation between age of defect correction and height gain in patients with left-to-right shunt CHD after correction of growth prognosis Methods. This was a cross sectional study with reviewing medical records on subjects with CHD with left-to-right shunts who were corrected for less than 2 years at Cipto Mangunkusumo hospital with the independent variable being the age of defect correction and the dependent variable were z-score of post-correction height-for-age (H/A) and height gain (Δz-score H/A). The WHO 2006 growth chart were used as the growth reference. The correlation analysis was performed using the Spearman correlation and the significance was determined with p<0.05.

Results: The median age of defect correction in this study was 8 months. Most of the subjects were less than 6 months (11 subjects) and 6-12 months (11 subjects) in corrected ages. The most defects were ventricular septal defects (VSD). The age of defect correction did not correlate with the post-correction H/A z-score based on the Spearman correlation test (r= 0.093) with p value = 0.642 while the defect correction age with z-score H/A was not found to be correlated based on the Spearman correlation test (r = 0.143) with p value = 0.452.

Conclusion: The age of defect correction did not prove correlate with either the z-score for H/A or height gain."