Background: Since first reported having the association with essential hypertension, angiotensin II type 1 receptor (AT1R) A1166C was globally investigated worldwide. However, controversy was found. Furthermore, previous metaanalyses did not adequate to clarify the precise correlation due to some limitations. Therefore, we aimed to perform a meta-analysis concerning the association between AT1R A1166C single-nucleotide polymorphism (SNP) and the risk of essential hypertension with eliminating the limitations of previous studies. Methods: A meta-analysis was conducted from February to March 2019. Some information related to sample size of hypertension and control groups and genotype frequencies of hypertension and control groups were extracted from each study. Data were analyzed using fixed or random effect model to determine the overall correlation. Results: A total of 45 papers consisting of 11911 cases and 1340 controls were enrolled for the study. Our overall analysis showed that C allele and AC genotype of AT1R A1166C was associated with 1.18-fold and 1.15-fold respectively increased risk of essential hypertension, while the decreased risk of essential hypertension was observed in A allele and AA genotype. In subgroup analysis, increased risk of essential hypertension was found in C allele, AC genotype, and CC genotype of both Asian population and PCR-RFLP subgroups , while decreased risk was observed in A allele and AA genotype. Conclusions: Our meta-analysis reveals that AT1R A1166C remains a valuable SNP having an association with the risk of essential hypertension.

This study aims to investigate the migration capability of endothelial progenitor cells (EPCs) under hyperglycemia conditions, which is expected to mimic the metabolic disturbance that occurs in patients with type 2 diabetes mellitus. MATERIALS AND METHODS Sample criteria This is an in-vitro study, with true experimental posttest only control group design. The blood sample was obtained from CAD patients in Dr. Soetomo General ABSTRACT Hyperglycemia state is harmful to body's homeostasis. Uncontrolled hyperglycemic patients, especially patients with diabetes mellitus have a higher mortality risk of heart disease 2 to 4 times compared to non-hyperglycemic patients. Vascular endothelial impairment always been observed and found as a key feature of hyperglycemia state, which is correlated with reduced numbers and dysfunction of endothelial progenitor cells (EPCs). Objective: This paper aims to investigate the effect of hUCB-MSCs derived secretome treatment on the EPCs migration under hyperglycemia state. Material and Method: EPCs were isolated and cultured from peripheral blood samples and cultured for three days. Cultured EPCs were cultivated in 6-well plates until confluence and incubated with high glucose for 5 days, then placed in the modified Boyden chamber at the upper chamber with basal media. The lower chamber was supplemented with basal media and secretome at 2%, 10%, and 20% concentration and VEGF treated group as a control. EPCS migration was evaluated using a Boyden chamber assay. Statistical analysis was performed using SPS 25.0. Results: EPCs migration were significantly higher when hUCB-MSCs-derived secretome was given in high glucose concentrations compared to the and control group (79.80 ± 5.07 vs 51.00 ± 5.15, p<0.000). This study also showed that hUCB-MSCs-derived secretome increase EPCs migration under high glucose concentrations in a dose-dependent manner (p<0.05). Conclusion: hUCB-MSCsderived secretome enhances EPCs migration under hyperglycemic state. This result may be of relevance for cell-free and regenerative therapeutic modality for a diabetic patient with coronary artery disease (CAD).

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Background Systemic AA amyloidosis is a rare infiltrative disease representing a complication of chronic inflammatory disorders. Cardiac involvement is rare and is associated with a poor prognosis. Early recognition is imperative as appropriate measures, and treatment of the underlying disease may prevent death from refractory heart failure and fatal arrhythmias. Case Summary A 53-years-old male patient with psoriatic arthritis presented with heart failure and nephrotic syndrome. Electrocardiogram revealed first-degree AV block, low voltage QRS complexes, and prolonged QT interval. On echocardiography, a normal systolic function of hypertrophic left ventricle with signs of diastolic dysfunction was present. An abdominal fat pad punch biopsy was able to confirm amyloid deposition. Self-terminated polymorphic ventricular arrhythmia was recorded by 24-hour Holter. Immunosuppressive, anti-inflammatory, anti-arrhythmic, and heart failure agent were promptly instituted, which are ineffective. Discussion Restrictive cardiomyopathy is the hallmark finding in cardiac amyloidosis that caused by the interstitial deposits of amyloid fibrils. Clinically, this manifests in progressive diastolic dysfunction, elevated left ventricular filling pressures, and heart failure with preserved ejection. The presence of rapidly progressed heart and renal failure with characteristic features of ECG should prompt further evaluation to confirm an infiltrative cardiomyopathy. This is highly suggestive that the natural course of cardiac amyloidosis often unpredictable and can be aggressive if left undiagnosed and untreated.

Background Systemic AA amyloidosis is a rare infiltrative disease representing a complication of chronic inflammatory disorders. Cardiac involvement is rare and is associated with a poor prognosis. Early recognition is imperative as appropriate measures, and treatment of the underlying disease may prevent death from refractory heart failure and fatal arrhythmias. Case Summary A 53-years-old male patient with psoriatic arthritis presented with heart failure and nephrotic syndrome. Electrocardiogram revealed first-degree AV block, low voltage QRS complexes, and prolonged QT interval. On echocardiography, a normal systolic function of hypertrophic left ventricle with signs of diastolic dysfunction was present. An abdominal fat pad punch biopsy was able to confirm amyloid deposition. Self-terminated polymorphic ventricular arrhythmia was recorded by 24-hour Holter. Immunosuppressive, anti-inflammatory, anti-arrhythmic, and heart failure agent were promptly instituted, which are ineffective. Discussion Restrictive cardiomyopathy is the hallmark finding in cardiac amyloidosis that caused by the interstitial deposits of amyloid fibrils. Clinically, this manifests in progressive diastolic dysfunction, elevated left ventricular filling pressures, and heart failure with preserved ejection. The presence of rapidly progressed heart and renal failure with characteristic features of ECG should prompt further evaluation to confirm an infiltrative cardiomyopathy. This is highly suggestive that the natural course of cardiac amyloidosis often unpredictable and can be aggressive if left undiagnosed and untreated.