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"Latar Belakang : External counterpulsation (ECP) ditunjukkan dapat mengurangi gejala angina dan memperbaiki kualitas hidup pasien penyakit jantung koroner (PJK) dengan angina refrakter. Efek protektif jangka panjang ini dipikirkan merupakan efek dari peningkatan pulsatile shear stress pada endotel vaskular sehingga terjadi perbaikan pada fungsi endotel. Dalam proses ini, sekelompok miRNA berfungsi meregulasi ekspresi gen dan dipengaruhi oleh shear stress, diantaranya adalah miR-92a yang bersifat proatherosklerosis. Tujuan : Mengetahui pengaruh ECP terhadap kadar miR-92a di plasma pada pasien PJK dengan angina refrakter. Metode : Sebanyak 50 pasien PJK dan angina refrakter direkrut dan diacak ke salah satu dari kelompok terapi ECP atau sham (1:1), dan menjalani 35 sesi yang berdurasi 1 jam tiap sesi. Terapi sham serupa dengan terapi ECP namun memberikan tekanan yang jauh lebih rendah. Level miR-92a di sirkulasi diukur di plasma darah sebelum dan sesudah selesai seluruh terapi, kemudian besar perubahan pada kedua kelompok dibandingkan. Hubungan antara keluaran klinis seperti keluhan angina, kapasitas fisik dan ejection fraction (EF) ventrikel kiri dengan kadar miR-92a juga dinilai.Hasil : miR-92a di plasma meningkat bermakna pada kelompok ECP [+5.1 (+4.2 s.d +6.4) menjadi +5.9 (+4.8 s.d +6.4), p value <0.001] dan sham [+5.2 (+4.1 s.d +9.4) menjadi +5.6 (+4.8 s.d +6.3), p value 0.008]. Besar perubahan dan fold changes cenderung lebih besar pada kelompok ECP namun tidak berbeda bermakna secara statistik dibandingkan kelompok sham. Kadar miR-92a post intervensi berkorelasi signifikan dengan rasio diastolik/sistolik selama terapi dan perbaikan EF pasca intervensi. Selain itu, perubahan miR-92a berkorelasi positif dengan perbaikan kapasitas fisik.

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Background : Noninvasive modality External counterpulsation (ECP) can improve angina frequency and exercise capacity in refractory angina (RA) patients. The long term benefit is thought to be the result of increase in shear stress on vascular endothelial cells resulting in improvement of endothelial dysfunction. In this process, a group of miRNA regulating gene expression in relation to shear stress is called flow-sensitive miRNA, among them is miR-92a. Aim : To evaluate ECP effect on plasma miR-92a level in RA patients. Method : Fifty subjects with RA were enrolled and randomized to either one of ECP or sham therapy (1:1 randomization). Each therapy session was one hour, for a total of 35 sessions. As a control, sham gave same sensation as ECP but with lower pressure. Plasma miR-92a level was measured before and after therapy and delta changes was compared between group. Secondary clinical outcome such as angina class, physical capacity and left ventricle Ejection Fraction (EF) were also measured and correlated with miR-92a level.

Result : Plasma miR-92a level increased in both treatment groups [in ECP group +5.1 (+4.2 to +6.4) to +5.9 (+4.8 to +6.4), p value <0.001, in sham group +5.2 (4.+1 to 9.4) to +5.6 (+4.8 to +6.3), p value =0.008]. There was higher delta increase and fold changes in ECP group, however the difference did not reach statistically significant. miR-92a level post intervention correlated significantly with Diastolic/Systolic ratio during intervention and improvement in ejection fraction (EF) post intervention. Moreover, changes in miR- 92a correlated positively with improvement in physical capacity. Conclusion : ECP did not cause significant different increase of miR-92a compared to sham."

"Latar Belakang: ECP mampu menurunkan frekuensi angina, meningkatkan kualitas hidup, serta memperbaiki exercise–induced ischemia time. Manfaat tersebut dapat bertahan beberapa tahun setelah ECP. Mekanisme manfaat jangka panjang ECP tersebut telah dibuktikan akibat adanya angiogenesis yang diduga diperankan VEGF-A, VEGFR-2, dan miR-92a.Tujuan: Mengetahui efek ECP terhadap VEGF-A dan VEGFR-2, serta hubungannya dengan miR-92a pada pasien angina refrakter.Metode: Studi ini merupakan uji klinis acak tersamar ganda yang melibatkan 50 subjek dengan angina refrakter. Subjek dirandomisasi (1:1) ke dalam kelompok terapi ECP atau sham, yang masing-masing dilakukan selama 1 jam, hingga 35 kali. Kadar VEGF-A, VEGFR-2, dan miR-92a plasma diukur sebelum dan sesudah terapi menggunakan metode enzyme-linked immunosorbent assay (ELISA) untuk VEGF-A dan VEGFR-2, serta quantitative reverse transcription-polymerase chain reaction (qRT-PCR) untuk miR-92a. Keluaran klinis sekunder seperti derajat angina, kualitas hidup, 6-minutes walk test (6MWT), dan ejection fraction (EF) juga dinilai.Hasil: Kadar VEGF-A dan VEGFR-2 dipertahankan pada kelompok ECP, sedangkan kadar VEGF-A dan VEGFR-2 mengalami penurunan yang signifikan pada kelompok sham [ΔVEGF-A ECP vs sham: 1 (-139 to160) vs -136 (-237 to 67) pg/ml, p = 0.026; ΔVEGFR-2 ECP vs sham: -171(-844 to +1166) vs -517(-1549 to +1407) pg/ml, p = 0.021, respectively]. Kadar miR-92a meningkat secara signifikan pada kelompok ECP [5.1 (4.2 – 6.4) to 5.9 (4.8 – 6.4), p<0.001] and sham [5.2 (4.1 – 9.4) to 5.6 (4.8 – 6.3), p=0.008]. Tidak terdapat korelasi antara perubahan kadar VEGF-A, VEGFR-2, dan miR-92a [VEGF-A vs VEGFR-2 (r = 0.243, p = 0.09; uji Spearman), VEGF-A vs miR92-a (r = 0.229, p = 0.11; uji Spearman), dan VEGR-2 vs miR92-a (r = 0.08, p = 0.581; uji Spearman)].Kesimpulan: ECP mampu mempertahankan angiogenesis dengan cara mempertahankan kadar VEGF-A dan VEGFR-2. Pada kondisi iskemia, baik high shear stress (ECP) maupun low shear stress (sham) dapat menginduksi pelepasan miR-92a. ECP mempengaruhi VEGF-A, VEGFR-2, dan miR-92a secara independen.

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Background: ECP is able to reduce angina frequency, improve quality of life, and improve exercise time-induced ischemia time. These benefits can last several years after the ECP. The mechanism for the long-term benefit of ECP has been proven by the presence of angiogenesis, which is thought to be mediated by VEGF-A, VEGFR-2, and miR-92a.

Objective: To determine the effect of ECP on VEGF-A and VEGFR-2, and its relationship with miR-92a in patients with refractory angina.

Methods: This study was a double-blind randomized clinical trial involving 50 subjects with refractory angina. Subjects were randomized (1:1) into either ECP or sham therapy groups, each administered for 1 hour, up to 35 times. Plasma VEGF-A, VEGFR-2, and miR-92a levels were measured before and after therapy using the enzyme-linked immunosorbent assay (ELISA) method for VEGF-A and VEGFR-2, as well as quantitative reverse transcription-polymerase chain reaction (qRT-PCR). ) for miR-92a. Secondary clinical outcomes such as degree of angina, quality of life, 6-minute walk test (6MWT), and ejection fraction (EF) were also assessed.

Results: VEGF-A and VEGFR-2 levels are maintained in the ECP group, while VEGF-A and VEGFR-2 levels decrease in the sham group [ΔVEGF-A ECP vs sham: 1 (-139 to160) vs -136 (-237 to 67) pg/ml, p = 0.026; VEGFR-2 ECP vs sham: -171(-844 to +1166) vs -517(-1549 to +1407) pg/ml, p = 0.021, respectively]. MiR-92a levels increase significantly in the ECP group [5.1 (4.2 – 6.4) to 5.9 (4.8 – 6.4), p<0.001] and sham [5.2 (4.1 – 9.4) to 5.6 (4.8 – 6.3), p=0.008]. There is no correlation between changes in VEGF-A, VEGFR-2, and miR-92a levels [VEGF-A vs VEGFR-2 (r = 0.243, p = 0.09; Spearman's test), VEGF-A vs miR92-a (r = 0.229 , p = 0.11; Spearman's test), and VEGR-2 vs. miR92-a (r = 0.08, p = 0.581; Spearman's test)].

Conclusion: ECP therapy is able to maintain angiogenesis by maintaining VEGF-A and VEGFR-2 levels. In ischemic conditions, both high shear stress (ECP) and low shear stress (sham) can induce the release of miR-92a. ECP affects VEGF-A, VEGFR-2, and miR-92a independently."