Association between NT-proBNP level and the number of stents with major advanced cardiovascular events (MACE) in patients with multivessel coronary artery disease treated with percutaneous coronary intervention: A prospective cohort study.

Complex revascularization strategies, particularly complete revascularization, are controversial in coronary artery disease (CAD), and data supporting routine revascularization in stable CAD is lacking. The importance of percutaneous coronary intervention (PCI) in CAD and N-terminal pro-brain natriuretic peptide (NT-proBNP), which has been studied as a predictor of major advanced cardiovascular events (MACE) in CAD patients, still requires further research. The aim of this study was to determine the association between NT-proBNP levels and the number of stents with MACE incidence in CAD cases. A prospective cohort study was conducted in both types of CAD (acute coronary syndrome (ACS) and chronic coronary syndrome (CCS)). The NT-proBNP levels were measured pre- and post-PCI using fluorescence immunoassay, while MACE was assessed three months post-PCI. The Student t-test was used to compare the levels of NT-proBNP between pre- and post-PCI and between those who had MACE and did not; both in patients treated with single or multiple stenting groups. A total of 32 CAD patients were recruited, consisting of 20 ACS cases and 12 CCS cases. NT-proBNP levels post-PCI increased significantly in both ACS and CCS patients compared to pre-PCI either among those treated with single and multiple stentings. MACE occurred in 4 (12.5%) out of a total of 32 patients, all of which occurred in ACS patients treated with multiple stentings. Those who had MACE had higher post-PCI NT-proBNP levels compared to those who did not have MACE (23,703.50 vs 11,600.17 pg/mL, p=0.013). This study highlights the association between elevated NT-proBNP levels and multiple stenting with the presence of MACE in CAD patients, particularly in ACS cases.

Cryptogenic stroke in a 5-year-old girl with patent foramen ovale: A rare case.

Stroke ranks among the prevalent factors contributing to child mortality. Cryptogenic stroke has been linked with patent foramen ovale (PFO), which has been suggested as a possible route for thrombus, gas bubble, or another particulate that comes through systemic venous circulation to the brain artery. Yet, the most effective approach for managing cryptogenic stroke involving a PFO remains uncertain. This case aims to report a PFO patient with complications of stroke. A 5-year-old girl was admitted to the emergency department at Dr. Zainoel Abidin Hospital, Banda Aceh, Indonesia, after experiencing numbness and weakness on her right side and a sudden onset of slurred speech three days before admission. Laboratory findings only showed leukocytosis, while coagulation tests were normal. Non-contrast brain CT revealed an occurrence of cerebral infarction in the left hemisphere. Transcranial Doppler showed no atherosclerosis in cerebral arteries, and carotid Doppler ultrasound results were reported normal. Transthoracic echocardiography showed a PFO with the right-to-left shunt. The patient was treated with an intravenous infusion of citicoline 250 mg twice daily, oral aspirin 80 mg daily, and oral mecobalamin 250 mg daily and was planned to undergo a PFO closure procedure. However, the patient's parents rejected the plan to perform a PFO closure procedure. PFO has the potential to be a contributing factor to cryptogenic stroke among children. PFO closure followed by antiplatelet therapy for a couple of months has been shown to outperform medical therapy alone. However, additional evaluation should be done to cautiously consider the PFO closure procedure in children.

Potential molecular mechanism underlying cardiac fibrosis in diabetes mellitus: a narrative review.

BACKGROUND: Diabetes mellitus (DM) is among the most common risk factors for cardiovascular disease in the world with prevalence of more than 500 million population in 2021. Cardiac fibrosis with its complex process has been hypothesized as one of the mechanisms explaining development of heart failure in diabetic patients. Recently, the biomolecular mechanism of cardiac fibrosis in the hyperglycemia setting has been focusing around transforming growth factor ß-1 (TGFß-1) as a major factor. However, there is interplay role of several factors including microRNAs (miRNAs) which acts as a potential regulator of cardiac fibrosis connected with TGFß-1. In this review, we explored interplay role of several factors including microRNAs which acts as a potential regulator of cardiac fibrosis connected with TGFß-1 in diabetes mellitus. This narrative review included articles from the PubMed and Science Direct databases published in the last 10 years (2012-2022). MAIN TEXT: In diabetic patients, excessive activation of myofibroblasts occurs and triggers pro-collagen to convert into mature collagen to fill the cardiac interstitial space resulting in a pathological process of extracellular matrix remodeling. The balance between matrix metalloproteinase (MMP) and its inhibitor (tissue inhibitor of metalloproteinase, TIMP) is crucial in degradation of the extracellular matrix. Diabetes-related cardiac fibrosis is modulated by increasing level of TGF-ß1 mediated by cellular components, including cardiomyocyte and non-cardiomyocyte cells involving fibroblasts, vascular pericytes smooth muscle cells, endothelial cells, mast cells, macrophages, and dendritic cells. Several miRNAs such as miR-21, miR-9, miR-29, miR-30d, miR-144, miR-34a, miR-150, miR-320, and miR-378 are upregulated in diabetic cardiomyopathy. TGF-ß1, together with inflammatory cytokines, oxidative stress, combined sma and the mothers against decapentaplegic (smad) protein, mitogen-activated protein kinase (MAPK), and microRNAs, is interconnectedly involved in extracellular matrix production and fibrotic response. In this review, we explored interplay role of several factors including microRNAs which acts as a potential regulator of cardiac fibrosis connected with TGFß-1 in diabetes mellitus. CONCLUSIONS: Long-term hyperglycemia activates cardiac fibroblast via complex processes involving TGF-ß1, miRNA, inflammatory chemokines, oxidative stress, smad, or MAPK pathways. There is increasing evidence of miRNA's roles lately in modulating cardiac fibrosis.

Ascorbic Acid vs Calcitriol in Influencing Monocyte Chemoattractant Protein-1, Nitric Oxide, Superoxide Dismutase, as Markers of Endothelial Dysfunction: In Vivo Study in Atherosclerosis Rat Model.

Introduction: Ascorbic acid and calcitriol were frequently utilized in conjunction as therapy during the COVID-19 pandemic, and individuals with minor symptoms had notable improvements. There have been a few studies, often with conflicting findings, that examine the use of them for endothelium restoration and numerous clinical trial studies that failed to establish the efficacy. The aim of this study was to find the efficacy of ascorbic acid compared to calcitriol on the inflammatory markers monocyte chemoattractant protein-1 (MCP-1), nitric oxide (NO), and superoxide dismutase (SOD), as protective agents which play an important role in the early stages of atherosclerosis formation. This study was an experimental in vivo study. Methods: The total of 24 male Rattus norvegicus strain Wistar rats were divided into 4 groups, namely: control/normal group (N), atherosclerosis group (DL) given atherogenic diet, atherosclerosis group given atherogenic diet and ascorbic acid (DLC), and atherosclerosis group given atherogenic diet and calcitriol (DLD) treatment for 30 days. Results: Ascorbic acid and calcitriol treatment was significantly effective (P<0.05) in lowering expression of MCP-1 and increasing NO and SOD level. Calcitriol was superior to ascorbic acid in increasing SOD (P<0.05). There was no significant difference between ascorbic acid and calcitriol in decreasing MCP-1 and increasing NO (P>0.05). Discussion: Both treatments could reduce MCP-1, and increase NO and SOD by increasing antioxidants. In this study calcitriol was superior to ascorbic acid in increasing SOD, but not NO and decreasing MCP-1. According to the theory, it was found that calcitriol through nuclear factor erythroid 2-related factor 2 (Nrf2) causes a direct increase in the amount of SOD. Nrf2 is an emerging regulator of cellular resistance to oxidants. Conclusion: Ascorbic acid and calcitriol treatment was able to reduce MCP-1 and increase NO and SOD in atherosclerosis rat. Calcitriol was significantly superior in increasing SOD levels compared to ascorbic acid.

Role of forkhead box protein 2 (FOXP2) in oral-motor abilities of preterm infants: A brief literature review.

Preterm infants, born before the 37-week gestation period, have limited storage for nutrients at birth and are vulnerable to poor feeding, severe nutritional deficits and growth retardation. The immature gastrointestinal system leads preterm infants to experience a delay in initiating enteral nutrition. Inappropriate feeding can cause acute and long-term morbidity, prolonged hospitalization and increased treatment cost. Generally, preterm infants that are born after 32 weeks of gestation without severe comorbidities do not have dysphagia and should start oral feeding soon after birth. Preterm infants should have well-developed sucking-swallowing-breathing coordination by 32-34 weeks of gestational age. However, some infants take days or weeks to master the skill. The oral feeding development involves forkhead box protein 2 (FOXP2)-expressing neurons that are found in the deep layers of the cortex, basal ganglia, parts of the thalamus and Purkinje cells of the cerebellum. In mammals, these areas belong to the brain network circuits working for motor coordination in learning and acquiring sensorimotor skills. This review aimed to describe the role of FOXP2 in oral-motor skills in preterm infants, including oral feeding, sucking-swallowing-breathing coordination and language development. The oral-motor skills development could be an early predictor for language delay in premature infants, representing a vulnerable group susceptible to such delays.

Risk factors of MDR-TB and impacts of COVID-19 pandemic on escalating of MDR-TB incidence in lower-middle-income countries: A scoping review.

The coronavirus disease 2019 (COVID-19) pandemic is affecting tuberculosis (TB) treatment in many ways that might lead to increasing the prevalence of multi-drugs-resistance tuberculosis (MDR-TB), especially in lower-middle-income-countries (LMICs). This scoping review aimed to identify the risk factors of MDR-TB and to determine the impacts of the COVID-19 pandemic on MDR-TB prevalence in LMICs. This study was reported according to the preferred reporting items for systematic reviews and meta-analyses extension for scoping reviews (PRISMA-ScR) guideline. The relevant keywords were used to search studies in three databases (PubMed, ScienceDirect and SpringerLink) to identify the related articles. The English-written articles published from January 2012 to December 2022 that explored risk factors or causes of MDR-TB in LMICs were included. Out of 1,542 identified articles, 17 retrospective, prospective, case-control and cross-sectional studies from ten LMICs met were included in this scoping review. Twenty-one risk factors were discovered, with prior TB treatment (relapsed cases), diabetes, living area, living condition, smoking and low socioeconomic status were the main factors in developing MDR-TB during COVID-19 pandemic. The pandemic increased the MDR-TB prevalence through drug resistance transmission inside households, the distance between home and healthcare facilities and low socioeconomic status. This scoping review demonstrates how the COVID-19 pandemic has affected the rising incidence of MDR-TB in LMICs.

Study of NT-proBNP and Hs-Troponin I biomarkers for early detection of children's heart function of proteinenergy malnutrition.

The Protein Energy Malnutrition (PEM) is the condition of a lack of carbohydrate and protein stores in the body that trigger chronic failure nutrient intake and body maintenance function caused to impact the heart functions. The NT-pro-BNP and Hs- Troponin I proteins were found as the indicator of cardiac dysfunction. The sixty subjects of PEM, analyzed by standard of Indonesia Healt Ministry as well as nutritional status. The blood electrolytes examined by laboratory assay and the levels of Hs-Troponin 1 and NT-Pro-BNP were analyzed by Immune-Chromatography method. Assessing of the ventricular mass with the seeing the peak of the diastolic flow rate of left ventricular that estimated by the curve of the receiver operating characteristic and the area under the curve (P<0.05). The result has shown that the PEM decreased in the left ventricular mass for impaired heart function and systolic disorder. The Hs- Troponin I (90.9%) has better sensitivity than NT-pro-BNP (85.5%) if the merger of those markers possesses the lowest sensitivity (81.8%). These proteins have good biomarkers in heart function, mainly in cases where PEM is present.