Coronary microvascular dysfunction (DMK) is a condition of patients who are accompanied by complaints of chest pain where the results of coronary angiography examination are normal and this is almost 49% with 60% of patients diagnosed with DMK. Another study said that about 40% of patients with DMK showed coronary flow reserve (CFR <2) of about 40% and the WISE study (Women's Ischaemia Syndrome Evaluation) showed that about 47% of patients with chest pain had normal coronary arteries. DMK can be divided into 4 groups; DMK with no coronary arterial disease (CAD) obstruction and myocardial disease, DMK with myocardial disease where this occurs due to remodeling of intramural coronary arteries, DMK with CAD (coronary arterial disease) or acute myocardial infarction with or without ST segment, iatrogenic typhoid DMK occurs after coronary recanalization caused by vasoconstriction and distal embolization. The mechanism of action of DMK can be caused by several factors, namely endothelial dysfunction, smooth muscle dysfunction, decreased diastolic perfusion time, damage to blood vessels and damage to the vascular and microvascular remodeling. And to enforce this DMK, there are several tests carried out in diagnosing the disease, some of which are invasive and non-invasive so that by enforcing the diagnosis of this disease, treatment for DMK can be done immediately and optimally.
Pendahuluan. Adanya polimorfisme gen angiotensin converting enzyme (ACE) diduga berperan terhadap penyakit kardiovaskular, termasuk coronary slow flow phenomenon (CSFP). Polimorfisme gen ACE juga merupakan faktor penting dalam peningkatan kadar angiotensin II. Penelitian ini bertujuan untuk mengetahui pengaruh polimorfisme insersi/delesi (I/D) 287 bp alu repetitive sequence pada intron 16 gen ACE dan kadar angiotensin II terhadap CSFP di RSUP Dr. Mohammad Hoesin Palembang.Metode. Studi kasus kontrol dimulai dari Juli 2019 sampai Juli 2020 di RSMH Palembang dengan masing-masing 32 subjek pada kelompok kasus (pasien CSFP) dan kontrol (non-CSF). Penelitian ini menggunakan sepasang primer dan satu kali PCR untuk deteksi polimorfisme I/D gen ACE. Analisis genetik dilakukan di Laboratorium Bioteknologi Fakultas Kedokteran Universitas Sriwijaya. Data yang terkumpul dianalisis dengan uji korelasi Spearman.Hasil. Dari 32 subjek kelompok CSFP, didapatkan distribusi genotip II pada 17 subjek (53,1%), genotip ID pada 14 subjek (43,8%), dan genotip DD pada 1 subjek (3,1 %). Sementara dari 32 subjek kelompok non-CSF, didapatkan distribusi genotip II pada 11 subjek (34,4%), genotip ID pada 13 subjek (42,2%), dan genotip DD pada 9 subjek (14,1%). Nilai median kadar angiotensin II pada kelompok CSFP 58 pg/mL dan pada kelompok Non-CSF 32,8 pg/mL. Hasil analisis menunjukkan terdapat pengaruh kadar angiotensin II terhadap kejadian CSFP (p=0,001). Analisis lebih lanjut menunjukkan adanya korelasi kadar angiotensin II dengan polimorfisme I/D 287 bp alu repetitive sequence pada intron 16 gen ace (p=0,030, r=0,822). Simpulan.Terdapat korelasi antara polimorfisme I/D 287 bp alu repetitive sequence pada intron 16 gen ACE dan kadar angiotensin II terhadap kejadian coronary slow flow phenomenon di Rumah Sakit Dr. Mohammad Hoesin Palembang.
e 29monitoring. Plasma AGT and angiotensin II level were performed at baseline and after 4 months of ARB therapy. Results:Significantly reduced blood pressure in both daytime and 24 hours mean systolic/diastolic blood pressure were observed in patients with -217 AA/AG genotype who received telmisartan, but not valsartan, compared to those carrying GG genotype. The change of plasma AGT and angiotensin II level in those who had -217 AA/AG genotype showed no difference as compared to GG genotype after received telmisartan or valsartan.Conclusion: AGT G-217A polymorphism is associated with antihypertensive response to telmisartan, but not valsartan, in hypertensive patients.Introduction: Hypertension may affect any age, including young adults. Acute coronary syndrome (ACS) is one of the devastating complicationsof hypertension, and a common reason for hospitalization. Previous studies have found that having 2 or more risk factors increases the risk for multivessel disease.Objective: To review the role of hypertensionas a predictor for multivessel disease inhypertensive young adults with ACS at National Cardiovascular Centre Harapan Kita (NCCHK) Methods:A retrospective study ofhypertensive young adults (18-40 years old)hospitalized due to ACS atNCCHK. The data were collected from medical records. The coronary angiography data from patients with at least 2 or more risk factors were analyzed.Results: From 194 hypertensive young adults hospitalized in NCCHK during 2011-2013, 100 patients (51.5%) were admitted with ACS. 61 patient underwent coronary angiography, and the result was 10 patients with normal coronary artery, 23 patients with single vessel disease, and 28 patients with multivessel disease. The odds of multivessel disease were 1.06 in patients with uncontrolled blood pressure (95% CI = 0.33-3.45), 0.91 in patients with diabetes (95% CI = 0.29-2.88), 1.04 in patients with family history of CAD (95% CI = 0.34-3.19), 0.9 in smokers(95% CI = 0.28-2.89), and 0.12 in patients with dyslipidemia(95% CI = 0.02-0.61).Conclusion: ACS was the most common reason for hospitalization of hypertensive young adults in NCCHK. Among the traditional risk factors, uncontrolled blood pressure has the highest odds in the development of multivessel disease.Background: Hypertension and hyperuricemia are factors related to cardiovascular disease risk. Hyperuricemia is found in approximately 25% patients with hypertension while hypertension is found in 30% patients with hyperuricemia or gout. The link between hypertension and hyperuricemia theoretically explained by the effect of uric acid on renal and vascular smooth muscle cells. Hyperuricemia leads to inflammation and endothelial dysfunction. Losartan is an angiotensin renin blocker that has other effects as an anti-inflammatory and uricosuric agent.Objective: This study to determine the effect of losartan on serum IL-6 levels in hypertensive patients with asymptomatic hyperuricemia in DR. Mohammad Hoesin Hospital Palembang.Result: Research subjects were 30 patients with 53.3% men and ...
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