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Despite recent advancements, challenges persist in determining the optimal stenting strategy for LM bifurcation disease. Hence, this systematic review aims to compare single provisional and systematic dual stenting for managing LM bifurcation disease. A systematic search was performed until January 14, 2024. For the effect measure, risk ratios (RRs) was calculated. This study included 22 studies with 10776 participants. The all-cause mortality and cardiovascular mortality revealed comparable outcomes between provisional and dual-systematic stenting (RR 1.13, CI95 %: 0.87-1.47, p 0.36, I2 59 %; RR 1.16, CI95 %: 0.73-1.84, p 0.63, I2 80 %). In addition, MACE, MI, TLR, TVR, and in stent thrombosis also showed similar findings. Subgroup analysis revealed that cohort studies was the source of heterogeneity in all-cause mortality, stent thrombosis, and TLR. This meta-analysis suggests comparable outcomes between provisional and dual-systematic stenting in managing LM bifurcation disease. Further study is needed to validate the outcomes of novel techniques.
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Doença da Artéria Coronariana , Intervenção Coronária Percutânea , Stents , Humanos , Doença da Artéria Coronariana/cirurgia , Doença da Artéria Coronariana/terapia , Intervenção Coronária Percutânea/métodos , Stents Farmacológicos , Resultado do TratamentoRESUMO
BACKGROUND: Several studies have shown that adipose-derived mesenchymal stem cells (AMSCs) can differentiate into mesenchymal lineages, including cardiac cell types, but complete differentiation into cardiomyocytes is challenging. Unfortunately, the optimal method to maximize AMSCs differentiation has not yet been established. Platelet-rich plasma (PRP), which contains rich growth factors, is believed to stimulate stem cell proliferation and differentiation in the context of cardiac tissue regeneration. OBJECTIVE: This study aimed to analyze the effect of PRP administration to enhance the differentiation of AMSCs into cardiomyocytes. METHODS: This study used a randomized post-test-only controlled group design. AMSCs were isolated from adipose tissues and cultured for 4 passages. The samples were divided into 3 groups, a negative control group (α-MEM), a positive control group (differentiation medium), and a treatment group (PRP). The assessment of GATA-4 expression was conducted using flow cytometry on day-5. The assessment of troponin expression was conducted using immunocytochemistry on day- 10. Data analysis was conducted using T-test and One-Way ANOVA. RESULTS: Flowcytometry of GATA-4 expression revealed a significant improvement in PRP group compared to negative and positive control group (67.04 ± 4.49 vs. 58.15 ± 1.23 p < 0.05; 67.04 ± 4.49 vs. 52.96 ± 2.02 p < 0.05). This was supported by the results of immunocytochemistry on troponin expression, which revealed significant improvement in the PRP group compared to negative and positive controls (38.13 ± 5.2 vs. 10.73 ± 2.39 p < 0.05; 38.13 ± 5.2 vs. 26.00 ± 0.4 p < 0.05). CONCLUSION: PRP administration in the AMSCs culture could significantly improve the differentiation of AMSCs into cardiomyocytes measured by GATA-4 and troponin expressions. This was concordant with our hypothesis, which stated that there was an effect of PRP administration on AMSCs differentiation into cardiomyocytes.
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Células-Tronco Mesenquimais , Plasma Rico em Plaquetas , Humanos , Miócitos Cardíacos , Diferenciação Celular , Tecido Adiposo/metabolismo , Células-Tronco Mesenquimais/metabolismoRESUMO
Background: Polytetrafluoroethylene (PTFE) patch is commonly used during surgical closure for atrial septal defect (ASD) and ventricular septal defect (VSD). However, this patch has several limitations such as its inability to grow or remodel, especially in children and young adults. To tackle these limitations, we have tried to use fibronectin and human adipose-derived mesenchymal stem cells (hAMSCs) in the PTFE patch. Objective: To understand the impact of fibronectin to enhance hAMSCs cell-to-cell adherence and cell-to-patch surface attachment into PTFE patches used in the surgical closure of ASD or VSD. Materials and Methods: The hAMSCs were plated and fixated with 15 mL methanol and cluster of differentiation (CD) 90+, CD105+, and CD45 - antibodies were labeled with fluorescein isothiocyanate, rinsed with phosphate-buffered saline, and analyzed under a fluorescence microscope. Fibronectin solution (0.1%) was used to soak patch scaffolds for approximately 2-h duration and then dried for 20 min in the treatment group. The samples were examined with a scanning electron microscope (SEM). Results: SEM examination showed incomplete attachment of the cells even after 10 days in the control group at 1.14 ± 1.13. In contrast, the treatment group showed more cells attached to the patch surface at 31.25 ± 13.28 (P ≤ 0.0001). The observation at 5 days was 17.67 ± 20.21, at 7 days was 12.11 ± 10.94, and at 10 days was 18.83 ± 23.25. There was no significant statistical difference in mean cell per view among each treatment group (P = 0.802). Conclusion: Our work demonstrates that fibronectin has a positive impact on hAMSC attachment seeded onto the PTFE patch. These properties, in combination with their developmental plasticity, have generated tremendous interest in regenerative medicine.
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BACKGROUND: Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Acute coronary syndrome is a manifestation of CVD. In Indonesia, limited studies have been conducted on genetics as a potential risk factor for acute coronary syndrome (ACS). Consequently, this study aimed to examine the effect of the methylenetetrahydrofolate reductase (MTHFR) A1298C gene polymorphism on the incidence of ACS. METHOD: The study employed a case-control design. Outpatients from the cardiology and internal medicine clinics at the University of Airlangga (UNAIR) Hospital in Surabaya, Indonesia, constituted the study population. The case group comprised 60 patients with a history of ACS, while the control group consisted of 30 patients without a history of cardiovascular complaints. MTHFR A12980C gene polymorphism examination was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR RFLP) method at the Tropical Disease Center UNAIR Laboratory. RESULTS: Among the ACS group, 29 (48.1%), 13 (21.7%), and 18 (30%) of the individuals had AA, AC, and CC genotype patterns, respectively. In the control group, 16 individuals had AA (53.3%), 6 AC (20%), and 8 CC (26.7%). The C allele variant was identified in 41% of the ACS group and 37% of the control group. The odds ratio (OR) for the incidence of ACS was 1.195 (95% confidence interval [CI]; 0.381-3.752), 1.241 (95% CI; 0.481-3.486), and 1.222 (95% CI; 0.381-3.752). Chi-square analysis revealed no association between MTHFR A1298C gene polymorphism and the incidence of ACS (P > 0.05). CONCLUSIONS: MTHFR A1298C gene polymorphism did not significantly affect ACS incidence.
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Coronary heart disease (CHD) is a leading cause of death globally, while its current management is limited to reducing the myocardial infarction area without actually replacing dead cardiomyocytes. Direct cell reprogramming is a method of cellular cardiomyoplasty which aims for myocardial tissue regeneration, and CD34+ cells are one of the potential sources due to their shared embryonic origin with cardiomyocytes. However, the isolation and culture of non-adherent CD34+ cells is crucial to obtain adequate cells for high-efficiency genetic modification. This study aimed to investigate the optimal method for isolation and culture of CD34+ peripheral blood cells using certain culture media. A peripheral blood sample was obtained from a healthy subject and underwent pre-enrichment, isolation, and expansion. The culture was subsequently observed for their viability, adherence, and confluence. Day 0 observation of the culture showed a healthy CD34+ cell with a round cell shape, without any adherent cells present yet. Day 4 of observation showed that CD34+ cells within the blood plasma medium became adherent, indicated by their transformations into spindle or oval morphologies. Meanwhile, CD34+ cells in vitronectin and fibronectin media showed no adherent cells and many of them died. Day 7 observation revealed more adherent CD34+ cells in blood plasma medium, and which had 75% of confluence. In conclusion, the CD34+ cells that were isolated using a combination of density and magnetic methods may be viable and adequately adhere in culture using blood plasma medium, but not in cultures using fibronectin and vitronectin.
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Coronary stent infection (CSI) is the rarest complication associated with the percutaneous coronary intervention, occurring in less than 0.1% of cases. So far, all reported instances are limited to case reports. CSI presents itself in various, often confusing, ways in clinical settings. Therefore, the current systematic review summarizes reports of CSI's clinical presentations, causative pathogens, diagnoses and treatments. This systematic review considered three online databases, using reference lists as an additional source. All case reports or case series with stent infection in the coronary artery were included - however, reviews or commentaries, articles not published in English, and articles mentioning a history of hemodialysis or any surgery were excluded. Thirty-two studies on 34 CSI patients were included in the final qualitative analysis. CSI predominantly affected males of a wide range of ages. The most common symptoms were chest pain and fever with various onsets. Interestingly, CSI usually occurred during the first stent implantation. Cultures and coronary angiography were the most common methods used to diagnose CSI. Furthermore, drug-eluting stents had a higher risk of infection than bare-metal stents. Aneurysms were the most frequent abnormalities observed in infected stents. The bacteria that most often caused CSI were Staphylococcus aureus and Pseudomonas aeroginosa. More than 90% of the reports mentioned using various antibiotics, and 74% mentioned carrying out surgery. Finally, a mortality rate of 26.47% among CSI patients was calculated.
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Reestenose Coronária , Stents Farmacológicos , Intervenção Coronária Percutânea , Angiografia Coronária , Feminino , Humanos , Masculino , Intervenção Coronária Percutânea/efeitos adversos , Stents , Resultado do TratamentoRESUMO
Thymoma is the most common primary anterior mediastinum mass with various clinical manifestations, and one of the manifestations is pericardial effusion. While pericardial effusion in thymoma is usually serous, it can become purulent when an infection occurs in a nearby organ, albeit rare. In this report, we present a rare case of a 27-year-old woman who had purulent pericarditis secondary to an advanced thymoma. The patient came to the emergency department with the chief complaints of worsening chest discomfort, non-productive cough, and fever in the past 2 weeks. The patient was diagnosed with thymoma 5 months prior. Based on the examinations, it was discovered that the patient had pericarditis. After the pericardiocentesis was performed and the fluid was examined, the patient was diagnosed with purulent pericarditis secondary to thymoma. The patient was then treated with intravenous antibiotic and pericardial drain. Unfortunately, the patient's condition deteriorated, and the patient died on the fifth day of hospitalization. This case highlights an infrequent but potentially life-threatening complication of thymoma. In addition, thymic pathologies should be included as a rare etiology in the differential diagnosis of purulent pericardial effusion.
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Background. Cigarette smoking could induce endothelial dysfunction and the increase of circulating markers of inflammation by activation of monocytes. This can lead to increased intima media thickness (IMT) of entire blood vessels and result in acceleration of the atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. The aim of this study is to explore the link between cigarette smoking and its effect on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1). Methods. An experimental study with a post-test only controlled group design was used. We used 18 Wistar rats ( Rattus norvegicus) randomly subdivided into two groups: group K (-) were not exposed to tobacco smoke, whereas group K (+) were exposed to smoke equivalent of more than 40 cigarettes for 28 days daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT. Results . Our results indicate that tobacco smoke can enhance the expression of VCAM-1 on rat cardiac vascular endothelial cells, resulting in a decreased expression of e-NOS level and increase of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT ( r 2 = 0.584, ß = -0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT ( r 2 = 0.197, p = 0.065). Conclusion. Low e-NOS level and high VCAM-1 level observed after cigarette smoke exposure which may increase aortic IMT.
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Fumar Cigarros , Poluição por Fumaça de Tabaco , Ratos , Animais , Molécula 1 de Adesão de Célula Vascular/metabolismo , Óxido Nítrico Sintase Tipo III , Espessura Intima-Media Carotídea , Poluição por Fumaça de Tabaco/efeitos adversos , Células Endoteliais , Ratos Wistar , Nicotiana/efeitos adversos , Nicotiana/metabolismoRESUMO
Background: Contributing factors for improved survival of human adipocytes mesenchymal stem cells (h-AMSCs) cultured through hypoxia preconditioning, in example apoptosis inhibition involving BCL2 and HSP27 expression, trigger signal expression (VEGF), SCF expression, OCT-4 expression, and CD44+ expression. The objective if this study was to explain the mechanism and role of hypoxic preconditioning and the optimal duration of hypoxic preconditioning exposure to improve survival of h-AMSCs. Methods: An experimental laboratory explorative study ( in vitro) with hypoxic preconditioning in h-AMSCs cultures. This research was conducted through four stages. First, isolation of h-AMSCs culture from adipose tissue of patients. Second, the characterization of h-AMSCs from adipose tissue by phenotype (flowcytometry) through CD44+, CD90+ and CD45-expression before being pre-conditioned for hypoxic treatment. Third, the hypoxic preconditioning in h-AMSCs culture ( in vitro) was performed with an oxygen concentration of 1% for 24, 48 and 72 hours. Fourth, observation of survival from h-AMSCs culture was tested on the role of CD44+, VEGF, SCF, OCT-4, BCL2, HSP27 with Flowcytometry and apoptotic inhibition by Tunnel Assay method. Results: The result of regression test showed that time difference had an effect on VEGF expression ( p<0.001; ß=-0.482) and hypoxia condition also influenced VEGF expression ( p<0.001; ß=0.774). The result of path analysis showed that SCF had effect on OCT-4 expression ( p<0.001; ß=0.985). The regression test results showed that time effects on HSP27 expression ( p<0.001; ß=0.398) and hypoxia precondition also affects HSP27 expression ( p<0.001; ß=0.847). Pathway analysis showed that BCL2 expression inhibited apoptosis ( p=0.030; ß=-0.442) and HSP27 expression also inhibited apoptosis ( p<0,001; ß=-0.487). Conclusion: Hypoxic preconditioning of h-AMSC culture has proven to increase the expression of VEGF, SCF, OCT-4, and BCL2 and HSP27. This study demonstrated and explained the existence of a new mechanism of increased h-AMSC survival in cultures with hypoxic preconditioning (O2 1%) via VEGF, SCF, OCT-4, BCL2, and HSP 27.
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BACKGROUND: Wellens' syndrome is known to be associated with left anterior descending artery occlusion that could lead to an extensive anterior wall myocardial infarction. Thus, emergency cardiac catheterization is needed. However, during coronavirus disease 2019 (COVID-19) pandemic, it is recommended for hemodynamically stable acute coronary syndrome patients with COVID-19 infection to be treated conservatively in an isolated hospital ward. CASE PRESENTATION: We report an 85-year-old patient with chief complaints of typical, squeezing chest pain in the past 4 h. The patient had a high fever, dyspnea, sore throat, and fatigue for 3 days. He had previously come into contact with COVID-19 positive relatives. The patient was hemodynamically stable and pulmonary auscultation revealed coarse rales in the entire lung. Electrocardiography (ECG) evaluation during the pain episode showed non-specific ST-T changes in lead V2-V5. After sublingual nitrate was administered, ECG evaluation during the pain-free period revealed a biphasic T wave inversion in lead V2 and V3. Laboratory workup showed elevated cardiac marker and leucopenia with neutrophilia and lymphopenia. Rapid immunochromatographic test and initial severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reverse transcription-polymerase chain reaction (RT-PCR) evaluation from nasopharyngeal swab showed negative results. However, radiographic evaluations suggest the diagnosis of COVID-19 infection. While waiting for the second RT-PCR evaluation, the patient was diagnosed with Wellens' syndrome with suspected COVID-19 infection. The patient was treated conservatively according to national guidelines and scheduled for elective cardiac catheterization. On the third day, the patient felt better and insisted on being discharged home. Ten days after discharged, the patient died of myocardial infarction. CONCLUSION: Emergency cardiac catheterization should be done for patient with Wellens' syndrome, regardless of the COVID-19 infection status.