cover
Contact Name
Mohammad Saifur Rohman
Contact Email
hsj@ub.ac.id
Phone
+628973247705
Journal Mail Official
hsj@ub.ac.id
Editorial Address
Department of Cardiology and Vascular Medicine, Dr. Saiful Anwar General Hospital, 3rd Floor CVCU Jl. Jaksa Agung Suprapto No. 2, Malang, Indonesia
Location
Kota malang,
Jawa timur
INDONESIA
Heart Science Journal
Published by Universitas Brawijaya
Core Subject : Health, Science,
HEART SCIENCE is the official open access journal of Brawijaya Cardiovascular Research Center, Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia. The journal publishes articles three times per year in January, May, and September. The journal is a peer reviewed publication and accepts articles for publication from across the world. HEART SCIENCE accepts and publishes articles in the English language only. The primary goal of this journal is to publish clinical and basic research relevant to cardiovascular medicine. The journal covers the following topics: clinical cardiology, interventional cardiology, intensive and acute cardiovascular care, vascular diseases, non-invasive cardiology, pediatric cardiology, cardiac nuclear medicine imaging, arrhythmia, cardiac prevention and rehabilitation, and cardiac surgery. Animal studies are also considered for publication in HEART SCIENCE. To serve the interest of both practicing clinicians and researchers, the journal provides platform or forum for research scholars, intellectuals, and cardiologists to reveal their views and research work for dialogue, education, and interaction to the entire world. HEART SCIENCE publishes original research, reviews, brief reports, case reports, case series, editorial, and commentary. HEART SCIENCE also publishes the special issues and abstracts of papers presented at the annual meeting of the Cardiological Society of Malang.
Articles 325 Documents
Determinants of cost discrepancies in inpatients with acute decompensated heart failure Arisandi, Jeffri; Lorensia, Amelia; Rahem, Abdul
Heart Science Journal Vol. 6 No. 1 (2025): Challenges in Managing Acute Heart Failure
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2025.006.01.13

Abstract

BACKGROUND: Acute decompensated heart failure (ADHF) is a prevalent and complex condition that significantly burdens healthcare systems, requiring intensive care and leading to high treatment costs. OBJECTIVES: This study aims to identify factors influencing cost discrepancies in hospitalized ADHF patients. METHODS: This retrospective study was conducted at Universitas Brawijaya Hospital from July to August 2024. Data were collected from 86 ADHF patients who were hospitalized between January 2021 and December 2023. Information regarding the patients' clinical conditions, comorbidities, and medical procedures was extracted from their case histories. Statistical analyses included t-tests and Mann-Whitney tests. RESULTS: In this study of 86 individuals with ADHF, 58.1% were over 65 years old, 31.4% were between 45 and 64 years old, and 10.5% were between 18 and 44 years old. By classification of care, 58.1% were admitted for Class 1 care, 30.2% for Class 2, and 11.6% for Class 3. Our findings indicated that the costs of treatment for patients with moderate and severe diseases were higher as compared to those of mild severity. Patients who had a length of stay over 7 days had higher costs than the ones whose length of stay was 1 to 3 days. Furthermore, Class 2 care was associated with higher costs than Class 3 care. The analysis also revealed that an increase in the number of comorbidities and medical procedures corresponded with higher treatment costs. CONCLUSION: This study identified factors that increase the cost of treatment for patients with ADHF.
The current perspective of oxygen therapy and ventilatory support in acute heart failure Waranugraha, Yoga
Heart Science Journal Vol. 6 No. 1 (2025): Challenges in Managing Acute Heart Failure
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2025.006.01.1

Abstract

Oxygen (O2) therapy in acute heart failure (AHF) is purposed to address hypoxemia and thereby avert irreversible harm to essential organs caused by cellular hypoxemia. The O2 therapy is recommended for patients with AHF who have an oxygen saturation (SpO2) level below 90% or an oxygen partial pressure (PaO2) below 60 mmHg. The initial strategy of O2 therapy in AHF involves administering O2 using the nasal, face mask, or non-rebreathing mask (NRBM). In more severe clinical conditions or respiratory distress, non-invasive positive pressure ventilation (NIPPV) or intubation with mechanical ventilation may needed.
Molecular mechanisms of vascular calcification in diabetes mellitus: insights from human aortic smooth muscle cells, a systematic review Weningtyas, Anditri; Rohman, Mohammad Saifur; Chomsy, Indah Nur; Hose, Victor Alvianoes Guterez; Riza, Mochamad Faishal; Purbaningroom, Dian Laila; Rudijanto, Achmad; Nugrahenny, Dian
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.2026.007.01.2

Abstract

Background: Vascular calcification is a significant contributor to cardiovascular complications in diabetes mellitus (DM), particularly affecting the prognosis of patients.   Objectives: To conduct a comprehensive analysis of the molecular mechanisms underlying vascular calcification in DM, with a focus on insights from human aortic smooth muscle cells (HASMCs). Methods: The search was conducted following the PRISMA guidelines, utilizing databases such as MEDLINE/PubMed, Science Direct, and Google Scholar. The search focused on articles published within the last 5 years that discussed the molecular mechanisms of vascular calcification in DM, specifically in HASMCs. Results: Five selected reviews were found in a total of 637 articles. DM significantly accelerates vascular calcification in HASMCs through the upregulation of osteogenic markers and activation of the Wnt/β-catenin signaling pathway. Other identified mechanisms include inflammation, ferroptosis, and endothelial dysfunction, contributing to the complex interplay of factors that drive vascular calcification in diabetic patients. Conclusion: It is concluded that DM significantly accelerates vascular calcification in enhanced expression of osteogenic markers and activation of the Wnt/β-catenin signaling pathway in human aortic smooth muscle cells. Patients with diabetes are more likely to have cardiovascular issues as a result of this pathological process.
The role of oxidative stress on cardiovascular disease in metabolic syndrome: Efficacy and safety of EGCG and CGA Nugroho, Ira Vori; Rohman, Mohammad Saifur
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.2026.007.01.3

Abstract

The challenge of cardiovascular disease has spread across the globe, especially concerning metabolic syndrome and its components. There is a need to look for new treatment strategies that attack underlying pathophysiological mechanisms. This review discusses the role of oxidative stress in the development and progression of cardiovascular complications in metabolic syndrome while evaluating the therapeutic potential of two natural compounds as antioxidants: epigallocatechin gallate (EGCG) from green tea and chlorogenic acid (CGA) from coffee. Oxidative stress disrupts normal cellular function through multiple pathways, including LDL oxidation, nitric oxide function, glycolysis, modified TCA cycle activity, and activation of inflammatory cascades. These mechanisms contribute to CVD's endothelial dysfunction, atherosclerosis, and cardiac remodelling. Despite its limited bioavailability and concentration-dependent effects, EGCG demonstrates significant cardiovascular benefits through enhanced NO bioavailability, activation of antioxidant pathways, and suppression of inflammatory responses. CGA shows promising results in hypertension management and endothelial function improvement, with clinical studies reporting significant blood pressure reductions and improved vascular function. These natural compounds could serve as valuable add-on therapeutic agents for treating cardiovascular disease associated with metabolic syndrome. However, optimal dosing strategies and individual patient factors require further investigation
Pain symptoms and delays healthcare decision-making in acute myocardial infarction Ainan, Shafa; Lukitasari, Mifetika; Sari, Efris Kartika; Ahsan, Ahsan; Rohman, Mohammad Saifur; Satrijo, Budi
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.2026.007.01.16

Abstract

Background: Rapid initiation of reperfusion therapy in acute myocardial infarction (AMI) is vital for a favourable prognosis and is significantly affected by the duration from symptom onset to hospital arrival. Previous studies have indicated that cardiac autonomic neuropathy (CAN), prevalent in diabetic patients, may impair pain perception, potentially delaying healthcare-seeking behaviour Objective: This study aimed to compare chest pain characteristics and healthcare-seeking delays between patients with diabetes mellitus (DM) and without DM (non-DM) myocardial infarction. Methods: A cross-sectional study was conducted involving 93 subjects (35 DM and 58 non-DM) diagnosed with either ST-elevation myocardial infarction (STEMI, n=78) or non-ST elevation myocardial infarction (NSTEMI, n=15). Data on symptoms, including pain quality and healthcare-seeking timing within 72 hours of admission, were gathered via a standardized questionnaire. Result: Logistic regression analysis highlighted stabbing pain as a strong predictor (OR = 3.296, p-Value = 0.038), indicating that patients with this symptom are more than three times more likely to delay seeking care. Patients with DM are more frequently reported back-radiating stabbing pain (p<0.05). No significant differences between the groups were observed in pain symptomatology and decision-making delay, although DM patients were more likely to delay seeking care for over two hours. Conclusion: While pain characteristics showed no significant differences between DM and non-DM myocardial infarction patients, DM patients were prone to later healthcare engagement. This delay could be attributed to the misinterpretation of cardiac symptoms as diabetic complications, underscoring the need for targeted patient education. Therefore, strengthened patient education and routine screening for cardiovascular symptoms in individuals with diabetes are essential to support early detection and timely management.
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.
The role of FGF23 in cardiovascular disease: From pathophysiology to biomarker and therapeutic implications Kurniawan, Ary; Rohman, Mohammad Saifur
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.2026.007.01.4

Abstract

Cardiovascular disease (CVD) remains a leading global cause of mortality, necessitating deeper insights into non-traditional risk factors. Fibroblast growth factor 23 (FGF23), a hormone central to phosphate and vitamin D regulation, has emerged as a pivotal contributor to CVD pathogenesis. This review synthesizes evidence linking elevated FGF23 levels to adverse cardiovascular outcomes, including left ventricular hypertrophy, vascular calcification, hypertension, and atrial fibrillation in both chronic kidney disease (CKD) and individuals with preserved renal function. Mechanistically, FGF23 exerts direct effects on cardiac remodeling and calcium handling while indirectly promoting CVD via dysregulated mineral metabolism, renin-angiotensin-aldosterone system (RAAS) activation, and inflammatory pathways. Paradoxically, its compensatory rise in CKD to counteract hyperphosphatemia becomes maladaptive, accelerating cardiovascular pathology.  Despite its potential as a biomarker, challenges persist in establishing causality, disentangling confounding factors (e.g., inflammation, renal function), and developing targeted therapies that mitigate pathological effects without disrupting physiological phosphate homeostasis. Future research must prioritize defining context-specific FGF23 thresholds, elucidating cardiac versus systemic signaling mechanisms, and advancing receptor-specific interventions. Bridging these gaps will require multidisciplinary collaboration to translate FGF23’s dual roles, as both a compensatory hormone and a disease mediator into clinical strategies for CVD risk stratification and management.
Bibliometric analysis of acute limb ischemia research: Global trends and key insights from 2000-2024 Abiseka Panji Baskoro; Enrico Ananda Budiono; Heru Sulastomo; An Aldia Asrial
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.2026.007.01.17

Abstract

Background: Acute Limb Ischemia (ALI) remains a critical vascular emergency, necessitating understanding to prevent devastating outcomes. Despite its clinical significance, a comprehensive understanding of global research trends, key contributors, and emerging themes in ALI remains underexplored. Objective: This study aims to perform a bibliometric analysis of ALI-related research, identifying trends, influential contributors, and areas for future exploration. Methods: Data were retrieved from the Scopus database using relevant keywords. Bibliometric metrics were analyzed using VOSviewer and Biblioshiny, focusing on publication trends, co-authorship networks, and keyword co-occurrence. Descriptive and visual analyses highlighted the leading journals, nations, and emerging research themes in ALI. Result: A total of 1,967 documents were identified, with a surge in publications from 2020 to 2021, likely driven by the COVID-19 pandemic's thrombotic implications. The United States led global research efforts with 28.5% of corresponding author articles and the highest citation impact. Annals of Vascular Surgery and Journal of Vascular Surgery emerged as the most relevant and influential journals, respectively. Keyword mapping identified "acute limb ischemia," "peripheral arterial disease," and "vascular surgery" as central themes, with emerging topics including novel anticoagulants, mechanical circulatory support, and congenital risk factors like persistent sciatic artery and congenital heart disease. Despite advancements, gaps persist in systematic reviews, meta-analyses, and evidence-based clinical evaluations. Conclusion: This study provides a comprehensive overview of ALI research, identifying trends and highlighting opportunities for further investigation. By addressing existing gaps and integrating emerging guidelines—such as the 2024 ESC and ACC recommendations—future research can advance clinical practice and improve outcomes for patients with ALI.
Effect of decaffeinated green tea and green coffee combination on improving blood glucose levels in metabolic syndrome patients Nugroho, Ira Vori; Rohman, Mohammad Saifur; Karolina, Wella; Tjahjono, Cholid Tri; Kurnianingsih, Novi
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.2026.007.01.12

Abstract

Background: Metabolic syndrome (MS) contributes to high mortality and morbidity not only in developing countries but also in developed countries, with central obesity and insulin resistance as primary risk factors. Our previous study demonstrated that combined decaffeinated green tea and green coffee extracts more effectively improved lipid and glucose profiles in an MS rat model. Objective: This study evaluates the efficacy of the extracts on top guideline-directed medical treatment optimal therapy in metabolic syndrome patients. Methods: The study was a randomized controlled trial (RCT) involving 90 patients diagnosed with metabolic syndrome, ages 45-70. Participants were randomly sorted into three groups: the first group received 2x2.5 g, the second group received 1x5 g, and the third one received a placebo. Researchers measured baseline and final values for fasting blood glucose (FBG), post-meal glucose levels (PPBG), and glycated hemoglobin (HbA1C) to evaluate treatment effects. Result: After 90 days of treatment with decaffeinated green tea and green coffee combination, both experimental groups (Groups 1 and 2) revealed significant decreases in PPBG and HbA1c compared to the control group. (-14.10 ± 2.00 vs. -28.63 ± 4.61 vs. -5.03 ± 0.74 mg/dL and -0.23 ± 0.01 vs. -0.22 ± 0.03 vs. -0.13 ± 0.01; p = < 0.05). FBG decreased across all groups but was not statistically significant. Conclusion: After 90 days, the combination of decaffeinated green tea and green coffee significantly reduced PPBG and HbA1C levels in patients with metabolic syndrome compared to the placebo. These findings suggest that this combination may serve as an effective adjunctive therapy for glucose management in metabolic syndrome, translating efficacious preclinical dosages to clinical application.
The role of SIRT1 activator in preventing endothelial dysfunction: A systematic review in vitro studies evaluating senescence markers and cellular senescence-associated outcomes Rahma, Oktivani Adelathifa; Rohman, Mohammad Saifur; Akbar, Naufal Zulfikar; Rohman, Ibrahim Abdur; Nurwidyaningtyas, Wiwit
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.2026.007.01.5

Abstract

Background: Endothelial dysfunction, largely driven by endothelial senescence, is a critical factor in the pathogenesis of cardiovascular diseases. SIRT1, a key regulator of vascular homeostasis, has been identified as a potential target for mitigating endothelial senescence. Activators of SIRT1 have shown promise in delaying cellular senescence by modulating senescence markers and inflammatory pathways. However, a comprehensive evaluation of their effectiveness in in vitro models is required. Methods: This systematic review follows PRISMA 2020 guidelines and SYRCLE’s risk of bias assessment. Studies from four databases (PubMed, ScienceDirect, SpringerLink, and Taylor & Francis) were screened based on eligibility criteria, focusing on in vitro studies using Human Umbilical Vein Endothelial Cells (HUVECs) treated with SIRT1 activators. Key outcomes analyzed included senescence-associated β-galactosidase (SA-β-gal), cyclin-dependent kinase inhibitors (CDKIs: p21, p53, and p16), and senescence-associated secretory phenotype (SASP). Results: A total of 20 studies met the inclusion criteria. SIRT1 activators, including dapagliflozin, rhHAPLN1, ginsenoside Rb1, resveratrol, and others, demonstrated significant reductions in SA-β-gal expression, oxidative stress, and inflammatory cytokines (IL-6, IL-1β, and CCL2). Additionally, SIRT1 activation was associated with downregulation of CDKIs and enhanced nitric oxide (NO) bioavailability, contributing to improved endothelial function. Conclusion: SIRT1 activators exhibit potential in delaying endothelial senescence by suppressing senescence markers and inflammatory mediators, thereby preserving endothelial integrity. Future studies should focus on clinical validation to explore their therapeutic applications in endothelial senescence and cardiovascular disease prevention

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