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"Latar belakang. Stenosis mitral masih menjadi masalah kesehatan di negara berkembang dengan hipertensi pulmoner sebagai salah satu komplikasinya. Disfungsi endothelium berperan penting pada hipertensi pulmoner dimana terdapat peningkatan produksi mediator vasoaktif. Endotelin-1 merupakan vasokonstriktor yang kuat dan berperan penting dalam hipertensi pulmoner. Metode. Penelitian ini merupakan studi kohort pada 32 pasien stenosis mitral bermakna dengan hipertensi pulmoner sedang-berat yang menjalani pembedahan katup mitral di Pusat Jantung Nasional Harapan Kita dari bulan April hingga November 2014. Dilakukan analisa statistik untuk mencari hubungan antara kadar endotelin-1 dengan tekanan sistolik arteri pulmoner pasca operasi. Hasil. Terdapat korelasi antara kadar endotelin-1 pre operasi dengan tekanan sistolik arteri pulmoner pasca operasi (r 0,387 dengan p 0,029). Analisa regresi linear antara kadar endotelin-1 pre operasi dengan tekanan sistolik arteri pulmoner pasca operasi (adjusted analysis sesuai usia, jenis kelamin, hipertensi, diabetes melitus, dislipidemia, atrial fibrilasi dan waktu cross clamp aorta dan penggunaan mesin cardiopulmonay bypass menunjukan nilai koefisien β 11,4 dengan IK 95% 2,9-19,9 dan nilai p 0,011. Analisa regresi linear antara kadar endotelin-1 pasca operasi dengan tekanan sistolik arteri pulmoner pasca operasi (adjusted analysis) menunjukan nilai koefisien β 4,3 dengan IK 95% -5,4-13,9 dan nilai p 0,367. Analisa regresi linear antara perubahan kadar endotelin-1 pre dan pasca operasi dengan tekanan sistolik arteri pulmoner pasca operasi (adjusted analysis) mendapatkan nilai koefisien β 12,5 dengan IK 95% 0,5-24,4 dan p 0,041. Kesimpulan. Kadar endotelin-1 pre operasi berhubungan dengan tekanan sistolik arteri pulmoner pasca operasi mitral pada pasien mitral stenosis dengan hipertensi pulmoner.

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Background. Mitral stenosis is still the major health problem in developing countries with pulmonary hypertension as one of the complications. Endothelial dysfunction play significant role in pulmonary hypertension where the production of vasoactive mediators increase. Endothelin-1 is a very strong vasoconstrictor which play role in pulmonary hypertension.

Methods. A cohort study in 32 patients with significant mitral stenosis complicated with moderate-severe pulmonary hypertension who underwent mitral valve surgery in National Cardiovascular Center Harapan Kita from April to November 2014. Statistical analysis is done to explore the correlation between endothelin-1 level and systolic pulmonary arterial pressure post surgery.

Results. There was correlation between endothelin-1 pre surgery with systolic pulmonary arterypressure after surgery (r 0,387 and p value 0,029). Linear regression analysis of the endothelin-1 level pre surgery with systolic pulmonary artery pressure post surgery (adjusted analysis to age, sex, hypertension, diabetes mellitus, dyslipidemia atrial fibrillation, aortic cross clamp time and cardio-pulmonary bypass time) with β coefficient 11,4 with 95% confidence interval 2,9-19,9 and p 0,011. Linear regression analysis between endothelin-1 level post surgery with systolic pulmonary artery pressure (adjusted analysis) showed β coefficient 4,3 with 95% confidence interval -5,4-13,9 and p 0,367. Linear regression analysis between the difference of endothelin-1 level post and pre surgery and systolic pulmonary artery pressure post surgery (adjusted analysis) showed β coefficient 4,3 with 95% confidence interval 0,5-24,4 and p 0,041.

Conclusion. Endothelin-1 level pre surgery is correlated with systolic pulmonary artery pressure post mitral valve surgery in mitral stenosis patients with pulmonary hypertension."

"ABSTRAK Latar belakang: disglikemia adalah keadaan intoleransi glukosa berupa peningkatan kadar gula darah yang berhubungan dengan risiko penyakit kardiovaskular. Seiring dengan waktu, pada akhirnya diabetes akan menimbulkan kerusakan pada target organ, salah satu yang penting adalah pada sistem organ kardiovaskular, dapat berupa penyakit jantung koroner, kardiomiopati diabetes, penyakit serebrovaskuler, dan penyakit arteri perifer. Diabetes juga meningkatkan risiko terjadinya gagal jantung. Pada kardiomiopati diabetes, proses fibrosis yang masih reversibel sudah mulai terjadi bahkan ketika penderita masih asimtomatik. Pemeriksaan baku emas untuk mendeteksi terjadinya fibrosis miokard secara dini adalah pemeriksaan histopatologi jaringan miokardium melalui biopsi. Akan tetapi pemeriksaan ini sangat invasif dan tidak nyaman bagi subjek. Pemeriksaan yang kemudian berkembang adalah pencitraan menggunakan Cardiac Magnetic Resonance Imaging (CMRI). Akan tetapi pemeriksaan ini cukup mahal, dan tidak tersedia pada semua fasilitas kesehatan. Sementara itu, ST2 adalah penanda enzim jantung yang menggambarkan derajat proses fibrosis yang sedang terjadi pada miokard, terutama pada keadaan gagal jantung. Pemeriksaan menggunakan penanda enzim dapat menjadi alternatif dengan keuntungan lebih murah, dapat terjangkau luas dan mudah tersedia. Tujuan: Mengetahui hubungan antara kadar ST2 serum dengan fibrosis miokard interstisial pada penderita disglikemia. Metode: Pasien disglikemia yang lolos kriteria eksklusi berupa komorbid kardiovaskular akan menjalani pemeriksaan kadar ST2 serum dan T1 relaxation time menggunakan Cardiac MRI. Selanjutnya dilakukan analisis hubungan antara kadar ST2 serum dan T1 relaxation time. Hasil penelitian: Sebanyak 34 pasien diikutsertakan ke dalam penelitian ini. Didapatkan kisaran nilai kadar ST2 serum antara 12.40-53.22 ng/dL (median 19.95 ng/dL). Rerata nilai T1 relaxation time didapatkan sebesar 443.39 ± 113.35 ms. Terdapat korelasi bermakna antara kadar ST2 serum dengan fibrosis diffuse miokardium (Spearman correlation r = -0,547, p < 0.01). Pada analisa multivariat hubungan antara kadar ST2 serum dan T1 relaxation time tidak dipengaruhi oleh faktor perancu yang telah ditetapkan (r = -0,44, p = 0,033). Kesimpulan: Hasil penelitian ini menunjukkan kadar ST2 serum berkolerasi dengan fibrosis diffuse miokardium pada populasi disglikemia.ABSTRACT Background: disglycemia is a state of glucose intolerance include increased blood sugar levels associated with risk of cardiovascular disease. Over time, eventually diabetes will cause damage to the target organ, especially the cardiovascular system, which include coronary heart disease, diabetic cardiomyopathy, diabetes, cerebrovascular disease, and peripheral arterial disease. Diabetes also increases the risk of heart failure. The clinical appearance of the disease is wide ranging from asymptomatic to symptomatic heart failure. Gold standard examination to detect the occurrence of early myocardial fibrosis is histopathological examination of myocardial tissue via biopsy. However, these tests are very invasive and uncomfortable for the subject. Examination which later evolved is imaging using cardiac magnetic resonance imaging (CMRI). However, these tests are quite expensive, and not available at all health facilities. Meanwhile, ST2 is a cardiac enzyme marker that describes the degree of fibrosis process in the myocardium, especially in the state of heart failure. Examination using enzyme markers can be a cheaper alternative, widely accessible and readily available. Aim: Knowing the relationship between serum levels of ST2 with myocardial interstitial fibrosis in disglycemic patients. Methods: Disglycemic patients who passed from the exclusion criteria (cardiovascular comorbid), will undergo a serum ST2 levels and T1 relaxation time using cardiac MRI. Then we analyzed the relationship between serum levels of ST2 and T1 relaxation time. Results: A total of 34 patients were included in this study. The range values of serum ST2 levels were between 12.40-53.22 ng/dL (median 19.95 ng/dL). The mean value of T1 relaxation time were 443.39 ± 113.35 ms. There is a significant correlation between serum levels of ST2 with diffuse myocardial fibrosis (Spearman correlation r = -0.547, p <0:01). Multivariate analysis showed the relationship between serum levels of ST2 and T1 relaxation time is not influenced by confounding factors (r = -0.44, p = 0.033). Conclusion: ST2 serum levels correlates with diffuse myocardial fibrosis on disglycemic population.;Background: disglycemia is a state of glucose intolerance include increased blood sugar levels associated with risk of cardiovascular disease. Over time, eventually diabetes will cause damage to the target organ, especially the cardiovascular system, which include coronary heart disease, diabetic cardiomyopathy, diabetes, cerebrovascular disease, and peripheral arterial disease. Diabetes also increases the risk of heart failure. The clinical appearance of the disease is wide ranging from asymptomatic to symptomatic heart failure. Gold standard examination to detect the occurrence of early myocardial fibrosis is histopathological examination of myocardial tissue via biopsy. However, these tests are very invasive and uncomfortable for the subject. Examination which later evolved is imaging using cardiac magnetic resonance imaging (CMRI). However, these tests are quite expensive, and not available at all health facilities. Meanwhile, ST2 is a cardiac enzyme marker that describes the degree of fibrosis process in the myocardium, especially in the state of heart failure. Examination using enzyme markers can be a cheaper alternative, widely accessible and readily available. Aim: Knowing the relationship between serum levels of ST2 with myocardial interstitial fibrosis in disglycemic patients. Methods: Disglycemic patients who passed from the exclusion criteria (cardiovascular comorbid), will undergo a serum ST2 levels and T1 relaxation time using cardiac MRI. Then we analyzed the relationship between serum levels of ST2 and T1 relaxation time. Results: A total of 34 patients were included in this study. The range values of serum ST2 levels were between 12.40-53.22 ng/dL (median 19.95 ng/dL). The mean value of T1 relaxation time were 443.39 ± 113.35 ms. There is a significant correlation between serum levels of ST2 with diffuse myocardial fibrosis (Spearman correlation r = -0.547, p <0:01). Multivariate analysis showed the relationship between serum levels of ST2 and T1 relaxation time is not influenced by confounding factors (r = -0.44, p = 0.033). Conclusion: ST2 serum levels correlates with diffuse myocardial fibrosis on disglycemic population.;Background: disglycemia is a state of glucose intolerance include increased blood sugar levels associated with risk of cardiovascular disease. Over time, eventually diabetes will cause damage to the target organ, especially the cardiovascular system, which include coronary heart disease, diabetic cardiomyopathy, diabetes, cerebrovascular disease, and peripheral arterial disease. Diabetes also increases the risk of heart failure. The clinical appearance of the disease is wide ranging from asymptomatic to symptomatic heart failure. Gold standard examination to detect the occurrence of early myocardial fibrosis is histopathological examination of myocardial tissue via biopsy. However, these tests are very invasive and uncomfortable for the subject. Examination which later evolved is imaging using cardiac magnetic resonance imaging (CMRI). However, these tests are quite expensive, and not available at all health facilities. Meanwhile, ST2 is a cardiac enzyme marker that describes the degree of fibrosis process in the myocardium, especially in the state of heart failure. Examination using enzyme markers can be a cheaper alternative, widely accessible and readily available. Aim: Knowing the relationship between serum levels of ST2 with myocardial interstitial fibrosis in disglycemic patients. Methods: Disglycemic patients who passed from the exclusion criteria (cardiovascular comorbid), will undergo a serum ST2 levels and T1 relaxation time using cardiac MRI. Then we analyzed the relationship between serum levels of ST2 and T1 relaxation time. Results: A total of 34 patients were included in this study. The range values of serum ST2 levels were between 12.40-53.22 ng/dL (median 19.95 ng/dL). The mean value of T1 relaxation time were 443.39 ± 113.35 ms. There is a significant correlation between serum levels of ST2 with diffuse myocardial fibrosis (Spearman correlation r = -0.547, p <0:01). Multivariate analysis showed the relationship between serum levels of ST2 and T1 relaxation time is not influenced by confounding factors (r = -0.44, p = 0.033). Conclusion: ST2 serum levels correlates with diffuse myocardial fibrosis on disglycemic population.;Background: disglycemia is a state of glucose intolerance include increased blood sugar levels associated with risk of cardiovascular disease. Over time, eventually diabetes will cause damage to the target organ, especially the cardiovascular system, which include coronary heart disease, diabetic cardiomyopathy, diabetes, cerebrovascular disease, and peripheral arterial disease. Diabetes also increases the risk of heart failure. The clinical appearance of the disease is wide ranging from asymptomatic to symptomatic heart failure. Gold standard examination to detect the occurrence of early myocardial fibrosis is histopathological examination of myocardial tissue via biopsy. However, these tests are very invasive and uncomfortable for the subject. Examination which later evolved is imaging using cardiac magnetic resonance imaging (CMRI). However, these tests are quite expensive, and not available at all health facilities. Meanwhile, ST2 is a cardiac enzyme marker that describes the degree of fibrosis process in the myocardium, especially in the state of heart failure. Examination using enzyme markers can be a cheaper alternative, widely accessible and readily available. Aim: Knowing the relationship between serum levels of ST2 with myocardial interstitial fibrosis in disglycemic patients. Methods: Disglycemic patients who passed from the exclusion criteria (cardiovascular comorbid), will undergo a serum ST2 levels and T1 relaxation time using cardiac MRI. Then we analyzed the relationship between serum levels of ST2 and T1 relaxation time. Results: A total of 34 patients were included in this study. The range values of serum ST2 levels were between 12.40-53.22 ng/dL (median 19.95 ng/dL). The mean value of T1 relaxation time were 443.39 ± 113.35 ms. There is a significant correlation between serum levels of ST2 with diffuse myocardial fibrosis (Spearman correlation r = -0.547, p <0:01). Multivariate analysis showed the relationship between serum levels of ST2 and T1 relaxation time is not influenced by confounding factors (r = -0.44, p = 0.033). Conclusion: ST2 serum levels correlates with diffuse myocardial fibrosis on disglycemic population."

"Latar belakang: PCSK9 telah diketahui sebagai molekul yang berperan dalam regulasi kadar kolesterol LDL darah. Dua dekade ini, PCSK9 diketahui memiliki mekanisme kerja lain yang melibatkan proses inflamasi, peningkatan Lp(a), aktivasi jaras protrombotik dan platelet, metabolisme triglyceride-rich lipoprotein, serta modifikasi plak yang juga dapat berperan dalam patogenesis berbagai spektrum penyakit aterosklerotik, termasuk IMA-EST. Kemajuan dalam strategi penatalaksanaan IMA-EST telah berhasil meningkatkan kesintasan, akan tetapi sekelompok pasien masih mengalami luaran klinis buruk meski telah mendapatkan tatalaksana optimal. Adanya polimorfisme gain of function E670G PCSK9 dipikirkan dapat memiliki peranan dalam risiko residual pasien-pasien tersebut Tujuan: Penelitian ini bertujuan untuk mempelajari hubungan antara polimorfisme PCSK9 pada pasien IMA-EST yang menjalani IKPP dengan luaran kardioserebrovaskular mayor. Metode: Sebanyak 423 pasien dengan IMA-EST yang menjalani IKPP diperiksakan polimorfisme PCSK9 pada saat admisi. Pemeriksaan polimorfisme PCSK9 didapatkan dengan menggunakan Real Time PCR. Data luaran kardioserebrovaskular mayor dan data penunjang lain didapatkan dari rekam medik dan follow-up telepon. Hasil: Terdapat 2,1 % polimorfisme berupa alel mutan (AG). Terdapat 65 (15,4%) subjek penelitian yang mengalami luaran kardioserebrovaskular mayor dalam 180 hari. Didapatkan analisis kesintasan menunjukkan adanya hubungan yang bermakna secara statistik antara polimorfisme E670G PCSK9 dengan luaran kardioserebrovaskular mayor dalam 180 hari (HR 7,486; IK95% 3.57-15.697; P=0,0000). Kesimpulan: Pada pasien IMA-EST yang menjalani IKPP, terdapat hubungan yang bermakna antara polimorfisme E670G PCSK9 dengan luaran kardioserebrovaskular mayor dalam 180 hari.

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Background: PCSK9 is a molecule that regulates blood LDL cholesterol level. Recent evidences suggest that PCSK9 may also have other mechanisms, such as inflammation, increased Lp(a), triglyceride-rich lipoprotein metabolism, activation of prothrombotic pathways and platelets, and modification of atherosclerotic plaque, which all may play a role in the pathogenesis of atherosclerotic diseases, including STEMI. Previous advances in the management of STEMI had succeed in increasing survival. However, some STEMI patients still experienced adverse outcomes eventhough they already received optimal management in accordance with the guidelines. Polimorphysm gain of function PCSK9 may have a role in the residual risk that those patients have. However, our knowledge regarding this association between polymorphism gain of function E670G PCSK9 and MACCE in STEMI is still unknown. Objective: The aim of this study is to evaluate the association between polymorphism Gain of Function E670G PCSK9 with MACCE in STEMI patients who underwent primary PCI. Methods: In total, 423 patients with STEMI who were treated with primary PCI had their plasma sample drawn during admission and evaluated for Polymorphism PCSK9. PCSK9 Polymophism was measured with PCR RT. MACCE and other supportive data were taken from the medical records and telephone follow-up. Results: The prevalence of Poymorphisme E670G PCSK9 in STEMI patient who underwent PPCI is 2,1 %. There were 65 (15,4%) study participants who experienced MACCE in 180 days. Survival analysis shows a significant association between Polymorphsm Gain of Function E670G PCSK9 and MACCE in 180 days. (HR 7,486; IK95% 3.57-15.697; P=0,0000). Conclusion: There was significant association between Polymorphsm gain of function E670G PCSK9 and 180 days MACCE in STEMI patients treated with primary PCI."

"Latar belakang: Gagal jantung merupakan beban baik dalam hal prognostik maupun sosial ekonomi. Gagal jantung dan diabetes melitus tipe 2 (DMT2) saling mempengaruhi luaran klinis pasien. Empagliflozin, suatu penghambat SGLT2, merupakan agen antihiperglikemia baru yang terbukti dapat menurunkan mortalitas dan hospitalisasi akibat gagal jantung. Beberapa mekanisme efek proteksi empagliflozin terhadap kardiovaskular telah dibuktikan melalui studi pada hewan. Empagliflozin memiliki efek meningkatkan fungsi sistolik ventrikel kiri pada hewan coba. Namun efek Empagliflozin terhadap fungsi sistolik intrinsik ventrikel kiri pada pasien DMT2 dengan gagal jantung belum diketahui.Tujuan: Mengetahui pengaruh pemberian Empagliflozin terhadap fungsi sistolik intrinsik ventrikel kiri pada pasien DMT2 dengan gagal jantungMetode: Penelitian ini merupakan uji klinis acak tidak tersamar yang dilakukan di poliklinik Rumah Sakit Jantung dan Pembuluh Darah Harapan Kita (RSJPDHK) pada pasien DMT2 dengan gagal jantung. Kelompok yang mendapat Empagliflozin 10 mg selama 3 bulan dibandingkan terhadap kelompok kontrol dengan terapi standar. Dilakukan pemeriksaaan global longitudinal strain (GLS) dengan speckle tracking echocardiography (STE) sebelum dan setelah terapi diberikan.Hasil: Total terdapat 41 pasien menyelesaikan penelitian (21 kelompok empagliflozin, 20 kelompok kontrol). Setelah 3 bulan follow up, nilai GLS kelompok empagliflozin cenderung tetap (rerata perubahan GLS 0,06%), sedangkan pada kelompok kontrol terdapat perburukan nilai GLS dengan rerata 1,5%, perbedaan kedua kelompok bermakna secara statistik (p 0,04). Kesimpulan: Terdapat perbedaan perubahan fungsi sistolik intrinsik ventrikel kiri setelah pemberian empagliflozin pada pasien diabetes melitus tipe 2 dengan gagal jantung dibandingkan terapi standar.

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Background: Heart failure is a burden both in terms of prognostic and socio-economic. Heart failure and type 2 diabetes mellitus (T2DM) have a strong relationship in influencing patient s clinical outcome. Empagliflozin, an SGLT2 inhibitor, is a new antihyperlglycemic agent that has been shown to reduce mortality and hospitalization due to heart failure. Several mechanisms of cardioprotective effect of empagliflozin have been demonstrated in animal studies. Empagliflozin has proven to increase left ventricular systolic function in animal study. However, its effect on left ventricular intrinsic systolic function in T2DM patients with heart failure is unknown.

Objectives: Knowing the effect of empagliflozin on left ventricular intrinsic systolic function in T2DM patients with heart failure.

Methods: This is a randomized, open label, clinical trial, which was conducted at National Cardiovascular Center Harapan Kita (NCCHK) hospital outpatient clinic. The group who received 10 mg empagliflozin for 3 months was compared with control group. Global longitudinal strain (GLS) by speckle tracking echocardiography was examined before and after therapy was given.

Results: A total of 41 patients completed the study (21 in empagliflozin group, and 20 in control group). After 3 months of follow-up, the GLS in empagliflozin group remained constant (mean changes in GLS was 0.06%), whereas in the control group there was a deterioration in GLS with an average of 1.5%, the difference between the two groups was statistically significant (p 0.04).

Conclusion: There is a difference in left ventricular intrinsic systolic function after administration of empagliflozin in T2DM patients with heart failure compared to standard therapy."

"Latar belakang: Polimorfisme Gly972Arg pada gen IRS1 dapat mengganggufungsi normal endotel dan menyebabkan disfungsi endotel. TIMI flow pascaprosedur IKPP dan jumlah pembuluh darah yang terlibat pada pasien IMA-ESTmerupakan prediktor mortalitas dan morbiditas selama perawatan. Mekanismeyang menyebabkan adanya perbedaan profil angiografi ini salah satunyadipengaruhi oleh difungsi endotel di tingkat mikrovaskular dan makrovaskular.Penelitian mengenai hubungan antara polimorfisme Gly972Arg pada gen IRS1dengan TIMI flow pasca prosedur dan jumlah keterlibatan pembuluh darah belumpernah dilakukan.Tujuan: Penelitian ini bertujuan untuk mengetahui hubungan antara polimorfismeGly972Arg pada IRS1 dengan TIMI flow pasca IKPP dan jumlah keterlibatanpembuluh darah pada pasien IMA-EST.Metode: Studi potong lintang pada 104 pasien IMA-EST RSJPDHK yangmenjalani IKPP yang masuk pada registri 2018. Pemeriksaan polimorfismeGly972Arg pada IRS1 dengan menggunakan metode Taqman.Hasil: Terdapat 104 subjek yang diikutsertakan dalam penelitian ini. Subjek dibagidalam 3 kelompok, yakni grup wildtype/CC (42,3%), heterozigot/CT (49,0%), danhomozigot mutan/TT (8,7%). Tidak terdapat hubungan yang bermakna antarakelompok mutan (TT) dengan TIMI flow pasca IKPP (OR 0,8; p = 1,000) danjumlah keterlibatan pembuluh darah (OR 0,3; p = 0,163).Kesimpulan: Tidak terdapat hubungan antara polimorfisme Gly972Arg gen IRS1dengan TIMI flow pasca IKPP dan jumlah keterlibatan pembuluh darah pasien IMAEST.

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Background: Gly972Arg polymorphism of IRS1 gene can interfere with normalendothelial function and cause endothelial dysfunction. TIMI flow after the primarypercutaneous intervention procedure and the number of coronary vessels involvedin STEMI patients are predictors that determine mortality and morbidity duringtreatment. The mechanism that causes this difference in angiographic profile isinfluenced by endothelial dysfunction at the microvascular and macrovascularlevels. Research on the relationship between Gly972Arg polymorphisms of IRS1gene with TIMI flow post procedure and the amount of blood vessel involvementhas not been carried out.Objective: We sought to define whether Gly972Arg polymorphisms of IRS1 genemay affect TIMI flow after primary percutaneous intervention and number ofcoronary vessel involved.Methods: Cross-sectional study design of 104 STEMI patients who underwentprimary PCI at National Cardiovascular Center Harapan Kita Hospital at year 2018.Examination of Gly972Arg polymorphism on IRS1 is using the Taqman methodPCR.Results: There were 104 of STEMI patients who underwent primary PCI andrecruited for the study. The subjects then divided into 3 categories, which arewildtype/CC (42,3%), carrier/CT (49,0%) and mutant/TT (8,7%). There were nosignificant relationship between the mutant group (TT) with TIMI flow afterprimary PCI (OR 0.8; p = 1,000) and the number of coronary vessel involvement(OR 0.3; p = 0.163).Conclusion: There were no relationship between the Gly972Arg polymorphism ofIRS1 gene with TIMI flow after primary PCI and the number of coronary vesselinvolvement of STEMI patients."

"Latar Belakang : Setengah pasien IMA-EST yang menjalani intervensi koroner perkutan primer(IKPP) memiliki multivessel disease. Rekomendasi saat ini hanya menganjurkan intervensi pada arteri terkait infark pada saat IKPP. Revaskularisasi selanjutnya pada stenosis signifikan lainnya dapat dilakukan dengan intervensi koroner perkutan (IKP) atau bedah pintas arteri koroner (BPAK). Namun sampai saat ini belum ada panduan pemilihan tindakan paska IKPP dengan multivessel disease. Tujuan : Mendapatkan data yang akurat tentang mortalitas IKP dan BPAK pada stenosis multipel paska IKPP. Melalui data ini diharapkan didapatkan rekomendasi yang sesuai tentang pilihan strategi pada stenosis multipel paska IKPP. Metode : Penelitian ini merupakan studi kohort retrospektif observasional. Penelitian dilakukan di Rumah Sakit Jantung dan Pembuluh Darah Harapan Kita (RSJPDHK) dengan mengambil data dari rekam medis. Durasi data yang diambil dari 01 Januari 2011 - 31 Desember 2014. Data karakteristik dasar, data klinis, dan angiografi dicatat dari rekam medis dan melalui wawancara melalui telepon. Data kemudian diolah dengan analisis bivariat dan multivariat untuk melihat hubungan kedua jenis tindakan dan mortalitas. Hasil Penelitian : Terdapat 177 pasien yang memenuhi kriteria dengan 141 pasien yang dilakukan IKP dan 36 pasien dilakukan BPAK paska IKPP. Karakteristik dasar tidak berbeda diantara kedua kelompok. Data klinis dan angiografi menunjukkan perbedaan culprit lesion (p=0,007), residual lesion (p<0,001), dan jumlah vessel (p<0,001). Data pre tindakan ulang menunjukkan perbedaan interval waktu tindakan (p=0,042) dan lesi Left Main (LM) atau proksimal left anterior descending (LAD) (p=0,032). Mortalitas terjadi pada 14,2% pada kelompok IKP dan 27,8% pada kelompok BPAK (RR 1,96; 95% IK 1,01-3,81). Hasil analisis bivariat menunjukkan bahwa diabetes mellitus (RR 1,18; 95% IK 1,03-1,36), fraksi ejeksi (RR 1,18; 95% IK 1,01-1,38), lesi residual LM atau proksimal LAD (RR 2,43; 95% IK 1,08-5,48), dan nilai kreatinin saat tindakan ulang (p=0,027) memiliki pengaruh terhadap mortalitas selain BPAK. Hasil multivariat regresi logistik biner dan cox regression didapatkan bahwa DM (aOR 2,67; 95% IK 1,145-6,248), lesi LM atau proksimal LAD (aOR 2,49; 95% IK 1,078-5,762), dan fraksi ejeksi (aOR 2,43; 95% IK 1,067-5,567) yang berpengaruh terhadap mortalitas. Kesimpulan : Mortalitas BPAK dan IKP tidak berbeda secara statistik pada pasien paska IKPP dengan multivessel disease. Perbedaan angka mortalitas disebabkan karena adanya perbedaan lesi residual pada LM atau proksimal LAD yang dari awal merupakan karakteristik pre tindakan ulang yang berbeda diantara kedua kelompok. DM dan fraksi ejeksi konsisten menyebabkan mortalitas pada kedua kelompok dan tidak berbeda bermakna pada kedua kelompok.

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Background : Almost half of the patients with STEMI that undergo Primary Percutaneous Coronary Intervention (PPCI) have multivessel disease. Currently, the only recommendation is to intervene in the infarct related artery at the time of PPCI. The next revascularization on other significant stenosis can be done with Percutaneous Coronary Intervention (PCI) or Coronary Artery Bypass Grafting (CABG). However, the guideline in selecting intervention post PPCI with multivessel disease is currently unavailable.

Objective : To obtain accurate data of mortality in PCI and CABG on patient with multivessel disease post PPCI. The data is expected to obtain reasonable recommendation of selection strategy on multiple stenosis post PPCI.

Methods : This study is an observational retrospective cohort. The research was done by retrieving medical record data of catheterization laboratory divison at the Rumah Sakit Jantung dan Pembuluh Darah Harapan Kita (RSJPDHK) from 1st January 2011 to 31st December 2014. Basic characteristics data, clinical data, and angiography were recorded from medical records and interviewes through telephone. The data is then processed by bivariate and multivariate analyzes to obtain the relationship between two types of modality and mortality.

Results : There were 177 eligible post PPCI patients, 141 patients undergoing PCI and 36 patients undergoing CABG. The baseline characteristics are no different between the two groups. Clinical data and angiography show a difference culprit lesion (p = 0.007), residual lesions (p<0.001), and the number of vessel (p <0.001). Pre intervention data shows the intervention time interval difference (p = 0.042) and the Left Main lesion (LM) or proximal left anterior descending (LAD) (p = 0.032). Mortality occurred in 14.2% and 27.8% in the PCI and CABG group (RR 1.96; 95% CI 1.01 to 3.81). The results of bivariate analyzes shows that diabetes mellitus (RR 1.18; 95% CI 1.03 to 1.36), ejection fraction (RR 1.18; 95% CI 1.01 to 1.38), residual lesions LM or proximal LAD (RR 2.43; 95% CI 1.08 to 5.48), and creatinine values before intervention (p = 0.027) had an significant influence on mortality other than CABG. The results of multivariate binary logistic regression and cox regression shows that DM (aOR 2.67; 95% CI 1.145 to 6.248), LM or proximal LAD lesion (aOR 2.49; 95% CI 1.078 to 5.762), and ejection fraction (aOR 2 , 43; 95% CI 1.067 to 5.567) effect on mortality.

Conclusion : Mortality in PCI and CABG were not statitically different for the post PPCI patients with multivessel disease. The difference on mortality was caused by the difference of residual lesions on the LM or proximal LAD which is the characteristic of different pre reintervention in the two types of modality. DM and the ejection fraction were consistently cause mortality in both groups and not significantly different in both groups."

"Polimorfisme gen Methylenetetrahydrofolate Reductase MTHFR C677T dihubungkan dengan kejadian hipertensi dan bergantung dengan etnis dan daerah geografis. Stratifikasi risiko dan potensi terapeutik menjadi alasan dilakukannya sejumlah studi pada gen MTHFR ini. Hingga saat ini belum ada studi yang menghubungkan polimorfisme MTHFR C677T dengan hipertensi di Indonesia. Penelitian ini bertujuan untuk menentukan hubungan antara polimorfisme C677T pada gen MTHFR dengan hipertensi pada masyarakat rural di desa Gunung Sari, Bogor-Indonesia. Total sebanyak 415 subyek yang terdiri dari 213 subyek dengan hipertensi dan 202 subyek normotensif sebagai kontrol, menjalani pemeriksaan polimorfisme MTHFR C677T dengan menggunakan metode Taqman. Terdapat perbedaan polimorfisme MTHFR C677T yang bermakna antara kelompok hipertensi dengan kelompok kontrol 62,9 CC; 34,3 CT; 2,8 TT vs 77,7 CC; 20,8 CT; 1,5 TT . Setelah disesuaikan dengan usia, indeks massa tubuh, lingkar pinggang, dan status diabetes mellitus, didapatkan hubungan antara polimorfisme MTHFR C677T dengan kejadian hipertensi OR 2,1; 95 IK 1,3-3,5 . Sebagai kesimpulan, terdapat hubungan antara polimorfisme MTHFR C677T dengan kejadian hipertensi pada populasi desa Gunung Sari, Kabupaten Bogor, Indonesia.

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Methylenetetrahydrofolate Reductase MTHFR C677T gene polymorphism is associated with hypertension depending on ethnic and geographic region. Risk stratification and therapeutic potential has become the common reason of recent studies on this gene. No study of MTHFR C677T polymorphism on hypertension is available in Indonesia. This study sought to determine the association of MTHFR C677T gene polymorphism and hypertension in rural population of Gunung Sari Village, Bogor Indonesia. A total of 415 subjects consisting of 213 hypertensive subjects and 202 normotensive subjects as a control group, underwent MTHFR C677T polymorphism examination using Taqman method. There was a significant difference of MTHFR C677T polymorphism between hypertensive group and control group 62,9 CC 34,3 CT 2,8 TT vs 77,7 CC 20,8 CT 1,5 TT . After adjustment of age, body mass index, waist circumference, and diabetes mellitus, there was an association between MTHFR C677T polymorphism with hypertension OR 2,1 95 CI 1,3 3,5 . As conclusion, there is an association between MTHFR C677T gene polymorphism and hypertension in rural population of Gunung Sari Village, Bogor Indonesia"

"Latar belakang: Intervensi endovaskular aorta perkutan rutin dilakukan dan menjadi pilihan tatalaksana invasif aneurisma atau diseksi aorta serta penyakit katup aorta. Komplikasi vaskular pasca intervensi sering terjadi pada pasien dengan diameter arteri femoralis komunis yang lebih kecil. Namun terdapat perbedaan bermakna dari diameter arteri femoralis komunis antara populasi Kaukasia dan Asia terkait komplikasi vaskular. Pada populasi Indonesia belum ada data terkait diameter arteri femoralis komunis dengan komplikasi vaskular. Tujuan: Mengetahui diameter minimal arteri femoralis komunis sebagai prediktor komplikasi vaskular pasca intervensi endovaskular aorta perkutan pada populasi Indonesia. Metode: Pasien yang dilakukan intervensi endovaskular aorta perkutan, diukur diameter arteri femoralis komunis dengan CT scan. Pasien dievaluasi kejadian komplikasi vaskular selama perawatan pasca tindakan. Hasil: Terdapat 101 pasien dengan 135 arteri femoralis komunis yang menjadi sampel penelitian. Dibagi menjadi dua kelompok ukuran diameter arteri femoralis komunis berdasarkan median 7,6 mm, yaitu diameter ≥7,6 mm dan diameter <7,6 mm. Dari analisis multivariat, tidak terdapat hubungan bermakna antara kategori diameter arteri femoralis komunis dengan komplikasi vaskular pasca intervensi endovaskular aorta perkutan (p 0,38). Variabel lain yang berhubungan dengan kejadian komplikasi vaskular adalah jenis kelamin perempuan (p 0,03) dan RSAF ≥0,82 (p <0,001). Kesimpulan: Diameter arteri femoralis komunis tidak dapat menjadi prediktor kejadian komplikasi vaskular pasca intervensi endovaskular aorta perkutan pada populasi Indonesia karena berdasarkan analisis multivariat tidak ditemukan hubungan yang bermakna.

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Background: Percutaneus endovascular aorta repair has been routinely performed and become the primary choice of invasive therapy for aortic aneurism, aortic dissection and aortic valve disease. The occurrence of vascular complications resulting from intervention, often occurs in patients with smaller common femoral artery. However there is a significant difference in the diameter of common femoral artery between the Caucasian and Asian populations related to the incidence of vascular complications. Objectives: To investigate the minimal diameter of common femoral artery as a predictor of vascular complications after percutaneus endovascular aorta repair in the Indonesian population. Methods: Patients who performed percutaneus endovascular aorta repair, measured the diameter of the common femoral artery with a CT scan and than evaluated for the occurrence of vascular complications after procedure. Results: 101 patients with 135 common femoral arteries are divided into two groups based on median of common femoral arteries (7,6 mm), diameter ≥7,6 mm and diameter <7,6 mm. From multivariate analysis, there is no significant association between the common femoral artery diameter and vascular complications after percutaneous aortic endovascular repair (p 0,38). Other variables that related to the incidence of vascular complications were female (p 0.03) and RSAF ≥0.82 (p <0.001). Conclusion: Diameter of common femoral artery can not be used as predictor of vascular complications after percutaneus endovascular aorta repair in the Indonesian population because based on multivariate analysis there was no significant relationship."

"Latar belakang: Gangguan pada regulasi transportasi natrium di ginjal merupakan salah satu patofisiologi hipertensi yang penting. Transportasi natrium diregulasi oleh jalur natriuresis dan antinatriuresis, salah satunya adalah dopamin, yang bekerja melalui G protein-coupled receptors (GPCRs). GPCR pada ginjal diatur oleh gen GRK4. Adanya polimorfisme GRK4 A486V akan meningkatkan aktivitas gen tersebut dan menurunkan fungsi dari reseptor dopamin sehingga terjadi retensi natrium. Dari berbagai studi dengan melibatkan hewan dan manusia, didapatkan adanya hubungan yang signifikan antara polimorfisme GRK4 A486V dengan hipertensi dan sifat sensitif garam. Stratifikasi risiko dan potensi preventif serta terapeutik menjadi alasan dilakukannya sejumlah studi pada gen GRK4 A486V ini. Hingga saat ini, belum ada penelitian yang memperlihatkan frekuensi dan hubungan antara polimorfisme pada gen GRK4 A486V dengan hipertensi pada populasi di Indonesia.Tujuan: Penelitian ini bertujuan untuk menentukan hubungan antara polimorfisme A486V pada gen G Protein-Coupled Receptor Kinase 4 (GRK4) dengan hipertensi pada masyarakat rural di desa Gunung Sari, Bogor-Indonesia.Metode: 412 subyek yang terdiri dari 211 subyek dengan hipertensi dan 201 subyek normotensif sebagai kontrol, menjalani pemeriksaan polimorfisme GRK4 A486V dengan menggunakan metode Taqman.Hasil: Setelah disesuaikan dengan usia, indeks massa tubuh, lingkar pinggang, dan status diabetes mellitus, didapatkan hubungan yang bermakna antara polimorfisme GRK4 A486V dengan kejadian hipertensi (OR 1.7; 95 IK 1,1-2,7) Kesimpulan: Terdapat hubungan antara polimorfisme GRK4 A486V dengan kejadian hipertensi pada populasi desa Gunung Sari, Kabupaten Bogor, Indonesia

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Background: Many studies have focused on the abnormal renal handling of natrium chloride in the pathogenesis of essential hypertension. Natrium transport is regulated by natriuretic and antinatriuretic pathways, one of them is dopamine, which exert their effects via G protein-coupled receptors (GPCRs). GPCRs in renal mainly regulated by GRK4 gene. GRK4 A486V polymorphism gene will increase it activity and down regulating dopamine receptor, and attenuate natrium retention. From many studies, GRK4 A486V polymorphism is associated with hypertension and salt sensitivity depending on ethnic and geographic region. Salt sensitivity is a trait in which blood pressure "changes parallel to changes in salt intake". It is counted as a risk factor for cardiovascular mortality and morbidity, independent of and as powerful as blood pressure. Risk stratification and therapeutic potential regarding salt sensitivity, have become the reasons of recent studies on this gene. No published study of GRK4 A486V polymorphism on hypertension is available in Indonesia.Objective: This study sought to determine the association of GRK4 A486V gene polymorphism and hypertension in rural population of Gunung Sari Village, Bogor-Indonesia.Methods: 412 subjects containing of 211 hypertensive subjects and 201 normotensive subjects as a control group, underwent GRK4 A486V polymorphism examination using Taqman method.Results: After adjustment of age, body mass index, waist circumference, and diabetes mellitus, there was an association between GRK4 A486V polymorphism with hypertension (OR 1,7; 95 CI 1,1-2,7) Conclusion: There is an association between GRK4 A486V gene polymorphism and hypertension in rural population of Gunung Sari Village, Bogor-Indonesia."

"Latar belakang: Elabela merupakan peptida baru yang ditemukan tahun 2013, bersama dengan apelin bertindak sebagai ligan endogen yang mengikat reseptor angiotensin receptor-like 1 (APJ), diekspresikan di berbagai jaringan tubuh terutama pembuluh darah dan memperlihatkan profil kardiovaskular yang mirip dengan apelin. Studi-studi ekperimental dan klinis telah memperlihatkan hubungan elabela dengan hipertensi, namun belum banyak diketahui mengenai peran elabela dalam proses aterosklerosis pada pasien hipertensi. Tujuan: Mengetahui hubungan konsentrasi peptida elabela dalam plasma dengan aterosklerosis subklinis pada populasi hipertensi. Metode: Sebanyak 104 subyek dengan hipertensi diikutkan dalam studi potong lintang. Konsentrasi elabela diperiksa dengan metode enzyme-linked immunosorbent assay (ELISA) dengan terlebih dahulu melakukan ekstraksi peptida sesuai protokol. Parameter aterosklerosis subklinis dinilai dengan pemeriksaan ketebalan intima-media (KIM) karotis menggunakan alat ultrasonografi. Hasil: Konsentrasi elabela pada kelompok hipertensi derajat 2 lebih rendah dibandingkan kelompok hipertensi stadium 1 (0.14 [0.09, 0.23] ng/ml vs. 0.23 [0.13, 0.45] ng/ml; P = 0.000). Konsentrasi elabela lebih rendah pada kelompok dengan KIM karotis yang meningkat (0.15 [0.10, 0.23] ng/dl vs. 0.24 [0.13, 0.38] ng/dl; P = 0.005). Elabela memiliki korelasi linier negatif bermakna terhadap tekanan darah sistolik (r = -0.340, P = 0.000) dan KIM karotis (r = -0.213; P = 0.030). Konsentrasi elabela yang rendah (cutoff 0.155 ng/dl) berhubungan dengan subkelompok risiko tinggi kardiovaskular (OR 5.0, IK 95% 1.8-13.5, P <0.001). Kesimpulan: Penelitian ini untuk pertama kalinya memperlihatkan hubungan elabela dengan aterosklerosis subklinis terkait hipertensi. Rendahnya konsentrasi elabela dikaitkan dengan patogenesis aterosklerosis terkait hipertensi sehingga menjadikan elabela sebagai kandidat penanda biologis (biomarker) vaskular yang baru.

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Introduction: Elabela is a newly identified peptide which, alongside apelin, acts as an endogenous ligand that activates the angiotensin receptor-like 1 receptor. Previous studies have shown the association of elabela with hypertension, but information about the role of elabela in hypertension-related subclinical atherosclerosis is scarce. Aim: To determine the elabela level in hypertensive patients and reveal its association with subclinical atherosclerosis. Methods: A total of 104 subjects with hypertension were included in the study. Elabela levels were measured using an enzyme-linked immunosorbent assay, by first extracting the peptide following the manufacturer's instructions. Subclinical atherosclerosis was assessed by measuring the carotid intima-media thickness (IMT) using ultrasound. Results: Compared to stage 1, elabela levels decreased in stage 2 hypertension (0.23 [0.13, 0.45] ng/ml vs. 0.14 [0.09, 0.23] ng/ml; P = 0.000), and in the group with increased carotid IMT compared to normal IMT (0.24 [0.13, 0.38] ng/ml vs. 0.15 [0.10, 0.23] ng/ml; P = 0.005). Additionally, a linear correlation analysis showed that elabela had a significant negative correlation with systolic blood pressure (r = -0.340, P = 0.000) and carotid IMT (r = -0.213; P = 0.030). In multivariate analysis, lower elabela levels were associated with a higher cardiovascular risk group in this study (OR 5.0, 95% CI 1.8-13.5, P < 0.001). Conclusions: This study demonstrated for the first time that circulating elabela declined in a higher stage of hypertension and hypertensive patients with increased carotid IMT, implicating that elabela may be involved in the pathogenesis of hypertension-associated subclinical atherosclerosis"