This study aimed to evaluate the plasma concentration of NT-proBNP in dogs with different stages of heart failure by chronic mitral valve insufficiency (CMVI). Fifty small-breed dogs with CMVI and 7 healthy control dogs without cardiac disease and critical systemic diseases were included in the study population. As a preliminary study, we compared the plasma concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) and the echocardiographic parameters between dogs of the International Small Animal Cardiac Health Council (ISACHC) classes. Then, we evaluated the associations between NT-proBNP and echocardiographic parameters. Plasma NT-proBNP levels showed a significant difference among the ISACHC groups. In the comparison between echocardiographic parameters and NT-proBNP, NT-proBNP were found to be associated with left atrium/aorta (LA/AO), early diastolic transmitral flow (E) velocity, late diastolic transmitral flow (A) velocity, end diastolic volume index (EDVI). Our study found plasma NT-proBNP might be useful to predict the disease progression in dogs with CMVI.
Proceedings of the Korean Biophysical Society Conference
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2003.06a
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pp.46-46
/
2003
Salviae Miltiorrhizae Radix has been used for treatment of cardiovascular diseases in oriental medicine. To investigate the possible involvement of cardiac ion channel in this effect, we examined electrophysiological effects of the extract of Salviae Miltiorrhizae Radix on action potentials and ionic currents in rat ventricular myocytes. The extracts of Salviae Miltiorrhizae Radix were fractionated into nine fractions, and the effect of each fraction on action potential was tested. The fraction containing monomethyl lithospermic acid-A (LSA-A) induced a significant prolongation of action potential duration (APD). LSA-B which is a major component of Salviae Miltiorrhizae Radix, however, did not cause a significant effect. In voltage clamp experiments, the effects of LSA-A on K currents, Ca currents and Na currents were tested. Neither K currents nor L-type Ca currents were affected by LSA-A. On the contrary, LSA-A significantly slowed down the inactivation kinetics of the Na current with no effect on the fast component of the inactivation process. The amplitude of the peak current and the voltage-dependence of activation were not changed by LSA-A. The effect of LSA-A on Na current was abolished when high concentration of $Ca^{2+}$ buffer (10 mM BAPTA) was included in the pipette solution or when Ca2+ current was blocked by nicardipine (1 $\mu$M) in the bath solution.n.
Renal dysfunction is a common complication of open-heart surgery: a form of controlled hemorrhagic shock, and successful perioperative management of renal dysfunction depends on recognition of the risk factors and optimal management of factors influencing renal function, including cardiopulmonary bypass, and early detection of renal failure. Changes in renal functional parameters including Ccr, Cosm, CH2O, FENa, and RFI were observed prospectively in forty five patients operated on at Dept. of Thoracic and Cardiovascular Surgery, S.N.U.H., from April to June, 1985. They were 23 males and 22 females with 35 acquired and 10 congenital heart diseases and the mean age and body surface area of them were 38.010.3 years [22-63] and 1.5518 M2[1.151.92] respectively. Followings are the conclusion. 1. The Ccr, representative of renal function, is significantly improved from 90.231.3 ml/min/M2 preoperatively to 101.536.4 ml/min/M2 postoperative and day [P<0.05], and all patients were classified as postoperative renal functional class I of Abel, which representing adequate renal protection during our cardiopulmonary bypass. 2. The Cosm is significantly elevated at immediate postperfusion time and remained high at postoperative one day representing osmotic diuresis at that time, but CH2O shows no significant changes at immediate postperfusion period and is decreased significantly at postoperative one day, representing recovery of renal concentrating ability at that time with decreasing urine flow. 3. The absolute value and changing tendency in FENa and RFI during perioperative period shows no diagnostic reliability on these parameters, but those of CH2O appear to reveal future renal function more accurately than Ccr 4. The depth of hypothermia may be protective upon renal function against the ill effects of prolonged nonpulsatile cardiopulmonary bypass. 5. The depth of the hypothermia, pump time of more than 150 minutes, poor cardiac function, and intraoperative events such as embolism appear to be related with immediate postperfusion renal function. 6. Hemoglobinuria and hemolysis, poor preoperative renal function, history of cardiac surgery, and massive transfusion associated with bleeding appear not to be related with renal dysfunction.
The number of patients with cardiovascular diseases who experience an out-of-hospital cardiac arrest (OHCA) are increasing among young adults as well as the aged population. An automated external defibrillator (AED) is vital in improving survival rates of OHCA victims. Survival rates of OHCA were shown to decline exponentially in time to defibrillation, yet studies in Korea are uncommon that captures the properties of their survival rates in examining optimal locations of AEDs. In this study, we worked on the maximal gradual coverage location problem (MGCLP) with exponential decay coverage function to decide on their optimal locations. The exponential decay coverage function mitigates the drawback of over-estimating survival rates of OHCA patients. It is expected that a more sophisticated facility location problem will be developed to identify the "emergent" characteristics of pedestrians who responds to the OHCA occurrence by incorporating random pedestrian locations and movement through simulation.
Choi, Hong Bae;Yun, Sangchul;Cho, Sung Woo;Lee, Min Hyuk;Lee, Jihyoun;Park, Suyeon
Korean Journal of Clinical Oncology
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v.14
no.2
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pp.102-107
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2018
Purpose: Cardiotoxicity is a serious late complication of breast cancer treatment. Individual treatment risk of specific drugs has been investigated. However, studies on the evaluation of the composite risk of chemotherapeutic agents are limited. Methods: We retrospectively analyzed the medical records of breast cancer patients who received adjuvant treatment and had available serial echocardiography results. Patients were assigned to subgroups based on chemotherapy containing anthracyclines (A), anthracyclines and taxanes (A+T), and radiotherapy (RT). The development of cardiac disease and serial ejection fraction (EF) were reviewed. EF decline up to 10% from baseline was considered grade 1 cardiotoxicity and EF decline >20% or absolute value <50% was considered grade 2 cardiotoxicity. The most recent medical records and echocardiography results over 1 year of chemotherapy completion were also reviewed. Late cardiotoxicity was defined as a lack of recovery of EF decline or aggravated EF decline from baseline. Results: In total, 123 patients were evaluated. A small reduction in EF was observed after chemotherapy in both chemotherapy groups. There were no significant differences between groups A and A+T in EF decline following chemotherapy. We could not find any differences in composite risk between the chemotherapy groups and the RT group during follow-up. Late cardiotoxicity was seen in 15.45% of patients. During follow-up, three patients were diagnosed with dilated cardiomyopathy. Conclusion: There was no significant composite risk elevation following adjuvant treatment of breast cancer. However, late cardiotoxicity was considerable and further research in this direction is necessary.
The aim of this review was to understand the effects of ${\beta}$-adrenergic stimulation on oxidative stress, structural remodeling, and functional alterations in the heart and cerebral artery. Diverse stimuli activate the sympathetic nervous system, leading to increased levels of catecholamines. Long-term overstimulation of the ${\beta}$-adrenergic receptor (${\beta}AR$) in response to catecholamines causes cardiovascular diseases, including cardiac hypertrophy, stroke, coronary artery disease, and heartfailure. Although catecholamines have identical sites of action in the heart and cerebral artery, the structural and functional modifications differentially activate intracellular signaling cascades. ${\beta}AR$-stimulation can increase oxidative stress in the heart and cerebral artery, but has also been shown to induce different cytoskeletal and functional modifications by modulating various components of the ${\beta}AR$ signal transduction pathways. Stimulation of ${\beta}AR$ leads to cardiac dysfunction due to an overload of intracellular $Ca^{2+}$ in cardiomyocytes. However, this stimulation induces vascular dysfunction through disruption of actin cytoskeleton in vascular smooth muscle cells. Many studies have shown that excessive concentrations of catecholamines during stressful conditions can produce coronary spasms or arrhythmias by inducing $Ca^{2+}$-handling abnormalities and impairing energy production in mitochondria, In this article, we highlight the different fates caused by excessive oxidative stress and disruptions in the cytoskeletal proteome network in the heart and the cerebral artery in responsed to prolonged ${\beta}AR$-stimulation.
Myocarditis was previously attributed to an epidemic viral infection. Additional harmful reagents, in addition to viruses, play a role in its etiology. Coronavirus disease 2019 (COVID-19) vaccine-induced myocarditis has recently been described, drawing attention to vaccine-induced myocarditis in children and adolescents. Its pathology is based on a series of complex immune responses, including initial innate immune responses in response to viral entry, adaptive immune responses leading to the development of antigen-specific antibodies, and autoimmune responses to cellular injury caused by cardiomyocyte rupture that releases antigens. Chronic inflammation and fibrosis in the myocardium eventually result in cardiac failure. Recent advancements in molecular biology have remarkably increased our understanding of myocarditis. In particular, microRNAs (miRNAs) are a hot topic in terms of the role of new biomarkers and the pathophysiology of myocarditis. Myocarditis has been linked with microRNA-221/222 (miR-221/222), miR-155, miR-10a*, and miR-590. Despite the lack of clinical trials of miRNA intervention in myocarditis yet, multiple clinical trials of miRNAs in other cardiac diseases have been aggressively conducted to help pave the way for future research, which is bolstered by the success of recently U.S. Food and Drug Administration-approved small-RNA medications. This review presents basic information and recent research that focuses on myocarditis and related miRNAs as a potential novel biomarker and the therapeutics.
Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngII induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngII-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenI, collagen III and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngII. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngII induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.
Background: Ginsenoside Rg2 (Rg2) has a variety of pharmacological activities and provides benefits during inflammation, cancer, and other diseases. However, there are no reports about the relationship between Rg2 and atherosclerosis. Methods: We used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) to detect the cell viability of Rg2 in vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs). The expression of inflammatory factors in HUVECs and the expression of phenotypic transformation-related marker in VSMCs were detected at mRNA levels. Western blot method was used to detect the expression of inflammation pathways and the expression of phenotypic transformation at the protein levels. The rat carotid balloon injury model was performed to explore the effect of Rg2 on inflammation and phenotypic transformation in vivo. Results: Rg2 decreased the expression of inflammatory factors induced by lipopolysaccharide in HUVECs-without affecting cell viability. These events depend on the blocking regulation of NF-κB and p-ERK signaling pathway. In VSMCs, Rg2 can inhibit the proliferation, migration, and phenotypic transformation of VSMCs induced by platelet derived growth factor-BB (PDGF-BB)-which may contribute to its anti-atherosclerotic role. In rats with carotid balloon injury, Rg2 can reduce intimal proliferation after injury, regulate the inflammatory pathway to reduce inflammatory response, and also suppress the phenotypic transformation of VSMCs. Conclusion: These results suggest that Rg2 can exert its anti-atherosclerotic effect at the cellular level and animal level, which provides a more sufficient basis for ginseng as a functional dietary regulator.
Hyeonjun Kim;Seunghyeon Cho;Inho Jung;Sunjin Jung;Won-Ju Park
Annals of Occupational and Environmental Medicine
/
v.35
/
pp.34.1-34.8
/
2023
Background: Hydrogen sulfide is a toxic substance that humans can be exposed to occupationally, and cases of hydrogen sulfide poisoning of workers in industrial sites are commonly reported. However, there have been no cases of poisoning of the public due to an unauthorized discharge of wastewater, so it is important to describe this incident. Case presentation: In a small village in Jeollanam-do, Republic of Korea, accounts of a terrible stench had been reported. A 26-year-old man who lived and worked in a foul-smelling area was taken to the emergency room with a headache, dizziness, nausea, and repeated syncope. A subsequent police and Ministry of Environment investigation determined that the cause of the stench was the unauthorized discharge of 9 tons of wastewater containing hydrogen sulfide through a stormwater pipe while the villagers were sleeping. The patient had no previous medical history or experience of symptoms. Leukocytes and cardiac markers were elevated, an electrocardiogram indicated biatrial enlargement, left ventricular hypertrophy, and corrected QT interval prolongation. Myocardial hypertrophy was detected on a chest computed tomography scan, and hypertrophic cardiomyopathy was confirmed on echocardiography. After hospitalization, cardiac marker concentrations declined, symptoms improved, and the patient was discharged after 7 days of hospitalization. There was no recurrence of symptoms after discharge. Conclusions: We suspect that previously unrecognized heart disease manifested or was aggravated in this patient due to exposure to hydrogen sulfide. Attention should be paid to the possibility of unauthorized discharge of hydrogen sulfide, etc., in occasional local incidents and damage to public health. In the event of such an accident, it is necessary to have government guidelines in place to investigate health impact and follow-up clinical management of exposed residents.
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