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All Journal Heart Science Journal Jurnal Klinik dan Riset Kesehatan
Yogibuana, Valerinna
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Biochemistry, Genetics & Molecular Biology Health Professions Immunology & microbiology Medicine & Pharmacology Nursing Public Health

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Acute Hemodynamic Index as a Predictor of In-Hospital Mortality in Mechanical Ventilated Acute Decompensated Heart Failure Patients Kurniawan, Dea Arie; Anjarwani, Setyasih; Rizal, Ardian; Satrijo, Budi; Yogibuana, Valerinna
Heart Science Journal Vol. 4 No. 1 (2023): Optimizing Outcome in Acute Cardiac Care
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2023.004.01.4

Abstract

Background: The likelihood of a poor clinical outcome is significantly increased in patients with acute decompensated heart failure. Mechanical ventilation was necessary for 23% of ADHF patients receiving treatment. The simple parameters of blood pressure and heart rate have good accuracy and repeatability. The development of the Acute Hemodynamic Index allowed for the calculation of pulse pressure and heart rate to be used as a basis for predicting intrahospital mortality.Methods: The medical records of patients who received care at CVCU RSSA were used in this retrospective, single-center study. ROC analysis and multivariate regression analysis were used to evaluate the prognostic performance of AHI. Statistical significance was determined by the P value of 0.05 or lower.Results: 252 patients with heart failure and low ejection fraction had their data analyzed. Hospital mortality is 82 percent. The cut-off was 4.19 mmHg/bpm, which was the AHI value. 68.8% of patients with fatal illnesses had low AHIs ( 4.19 mmHgbpm). AHI > 4.19 mmHgbpm patients have a 9-fold increased risk of dying in the hospital than patients with low AHI. AUC: 0.825 [0.743-0.907]; sensitivity: 0.814; specificity: 0.689; AUC: 0.825 [0.743-0.907; p = 0.000]; demonstrate the high predictive power of AHI.Conclusion: AHI has a strong degree of association with the likelihood of dying in the hospital from acute decompensated heart failure.
The role of green tea and green coffee extract, empagliflozin and metformin treatment on FGF23 mRNA expression in calcified aorta tissue in metabolic syndrome model Sprague-Dawley rat Kurniawan, Ary; Mohammad Saifur Rohman; Yogibuana, Valerinna
Heart Science Journal Vol. 7 No. 1 (2026): Accelerating Clinical Breakthroughs: The Journey from Molecular Discovery to Pa
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2026.007.01.11

Abstract

Background: Metabolic syndrome (MetS), encompassing dyslipidemia, glucose intolerance, hypertension, and central obesity, increases cardiovascular risk, including vascular calcification. Fibroblast growth factor 23 (FGF23), a bone-derived regulator of phosphate and vitamin D, is implicated in vascular calcification in kidney disease, but its role in MetS-related calcification is unclear. Objective: To determine if MetS promotes vascular calcification and alters aortic FGF23 mRNA expression in rats, and to assess effects of green tea/coffee extract, metformin, and empagliflozin on FGF23 mRNA modulation. Methods: Twenty-five Sprague-Dawley rats were divided into five groups: negative control, MetS (induced via high-fat/high-sucrose diet and streptozotocin), and three treatment groups (green tea/coffee extract, metformin 500mg/kg, empagliflozin 30mg/kg). Aortic calcification (hematoxylin-eosin staining) and FGF23 mRNA expression (qRT-PCR) were analyzed after 9 weeks. ANOVA with LSD post-hoc tests was used. Results: This study found MetS induction promoted vascular calcification. FGF23 mRNA expression increased in the MetS group compared to controls, though not statistically significant. All treatments reduced FGF23 mRNA levels modestly, but effects lacked statistical significance (p = 0.851–0.989), likely due to complex, tissue specific regulation of FGF23. Conclusion: Metabolic disturbances in MetS may prime vascular tissues for calcification without significantly altering local FGF23 mRNA expression. Interventions targeting oxidative stress, inflammation, or glucose metabolism could modulate FGF23-related pathways, warranting further investigation into the underlying signaling mechanisms.
A review of RUNX2 genetic interactions and their role in cardiovascular disease Christine, Anastasia; Rohman, Mohammad Saifur; Yogibuana, Valerinna
Heart Science Journal Vol. 7 No. 2 (2026): The Evolving Landscape of Heart Failure
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2026.007.02.5

Abstract

Cardiovascular diseases (CVD) remain the leading cause of global mortality, with underlying factors such as genetics, environment, and lifestyle interacting in complex and multiple ways. Runt-related transcription factor 2 (RUNX2), traditionally associated with osteogenesis, has gained recognition for its critical role in cardiovascular health. RUNX2 contributes to vascular calcification (VC), endothelial dysfunction, and myocardial fibrosis, thereby accelerating CVD progression. Its expression is influenced by multiple upstream regulators relevant to vascular pathology, such as BMP2/SMAD, Wnt/β-catenin, and ERK signaling, along with epigenetic mechanisms and gene-environment interactions such as oxidative stress, hyperglycemia, and dyslipidemia. Genetic variants in RUNX2 and environmental variables including diet and physical inactivity, amplify its activation, worsening VC and cardiovascular risk. RUNX2 reduces endothelial nitric oxide bioavailability, enhances vascular inflammation, and activates profibrotic signaling in cardiac tissue, promoting vascular dysfunction and myocardial remodeling. Circulating RUNX2 levels and genetic variations exhibit potential as diagnostic and predictive indicators for cardiovascular disease. Severalpharmaceutical agents including metformin, empagliflozin, and statins,   as well as natural substances such green tea polyphenols and green coffee extract, have demonstrated partial modulatory effects on RUNX2 activity. Moreover, genome-editing tools such as CRISPR-Cas9 present future opportunities for selective RUNX2 targeting. Comprehensive understanding of RUNX2 regulation and its interaction with genetic and environmental factors offers novel opportunities for personalized CVD prevention and treatment approaches through lifestyle modification, pharmacotherapy, and gene-based interventions in the future.
Prognostic implications of pulmonary hypertension in heart failure preserved and reduced ejection fraction Rosyidi, Muhammad Azhar; Yogibuana, Valerinna
Heart Science Journal Vol. 7 No. 2 (2026): The Evolving Landscape of Heart Failure
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2026.007.02.3

Abstract

Pulmonary hypertension (PH) attributable to left heart disease (PH associated with left heart disease, PH-LHD) is the most common type of PH. PH-LHD is an important indicator of elevated morbidity and mortality in individuals with heart failure, both heart failure with preserved and reduced ejection fraction despite receive adequate therapy. Literature was sourced from major scientific databases and studies relevant to symptoms, examinations, management, and prognostic implications of PH-LHD. Pathophysiologically, PH-LHD is a gradual process that begins with increased left-heart pressure (postcapillary component), which triggers a series of biological changes in the pulmonary vasculature (precapillary component). This process ultimately places an excessive burden on the right ventricle, resulting in right ventricular dysfunction and failure, which are the main determinants of prognosis. Symptoms of PH-LHD are usually characterized by disproportionate dyspnea that is not consistent with left ventricular ejection fraction and other comorbidities. Echocardiography can noninvasively assess the probability of pulmonary hypertension in heart failure patients. A definitive diagnosis of PH-LHD requires confirmation through right heart catheterization. The most important prognostic factors are not only determined by the degree of hemodynamic severity, but also depend heavily on the degree of right ventricular dysfunction and the status of right ventricle–pulmonary artery coupling. Management of PH-LHD is through optimization of basic Guideline-Directed Medical Therapy (GDMT) to reduce mortality and morbidity.
Co-Authors Akbar, Akita Rukmana Anjarwani, Setyasih Anna Fuji Rahimah Bambang Rahardjo Cholid Tri Tjahjono Christine, Anastasia Gultom, Yosafat Harumsari, Stefani Indra Prasetya Karolina, Wella KURNIAWAN, ARY Kurniawan, Dea Arie Martini, Heny Mohammad Saifur Rohman Noverike, Nikhen Novi Rahmawati Nugrahanti Prasetyorini Nurudinulloh, Akhmad Isna Pande Made Dwijayasa Rahimah, Anna Fuji Rizal, Ardian Rosyidi, Muhammad Azhar Saputri, Vemmy Lian Satrijo, Budi Setyowati, Danti Utami Triatmojo, Nicodemus