• Clinical and Experimental Pediatrics
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• 제63권8호
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• pp.329-334
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• 2020

Background: Birth asphyxia is a leading cause of neonatal mortality. Ischemia-modified albumin (IMA) levels may have a predictive role in the identification and prevention of hypoxic disorders, as they increase in cases of ischemia of the liver, heart, brain, bowel, and kidney. Purpose: This study aimed to assess the value of IMA levels as a diagnostic marker for neonatal hypoxic-ischemic encephalopathy (HIE). Methods: Sixty newborns who fulfilled 3 or more of the clinical and biochemical criteria and developed HIE as defined by Levene staging were included in our study as the asphyxia group. Neonates with congenital malformation, systemic infection, intrauterine growth retardation, low-birth weight, cardiac or hemolytic disease, family history of neurological diseases, congenital or perinatal infections, preeclampsia, diabetes, and renal diseases were excluded from the study. Sixty healthy neonates matched for gestational age and with no maternal history of illness, established respiration at birth, and an Apgar score ≥7 at 1 and 5 minutes were included as the control group. IMA was determined by double-antibody enzyme-linked immunosorbent assay of a cord blood sample collected within 30 minutes after birth. Results: Cord blood IMA levels were higher in asphyxiated newborns than in controls (250.83±36.07 pmol/mL vs. 120.24±38.9 pmol/mL). Comparison of IMA levels by HIE stage revealed a highly significant difference among them (207.3±26.65, 259.28±11.68, 294.99±4.41 pmol/mL for mild, moderate, and severe, respectively). At a cutoff of 197.6 pmol/mL, the sensitivity was 84.5%, specificity was 86%, positive predictive value was 82.8%, negative predictive value was 88.3%, and area under the curve was 0.963 (P<0.001). Conclusion: IMA levels can be a reliable marker for the early diagnosis of neonatal HIE and can be a predictor of injury severity.

• Korean Circulation Journal
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• 제53권6호
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• pp.387-403
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• 2023

Background and Objectives: Myocardial ischemia and reperfusion injury (MIRI) has high morbidity and mortality worldwide. We aimed to explore the role of long noncoding RNA lysyl oxidase like 1 antisense RNA 1 (LOXL1-AS1) in cardiomyocyte pyroptosis. Methods: Hypoxia/reoxygenation (H/R) injury was constructed in human cardiomyocyte (HCM). The level of LOXL1-AS1, miR-761, phosphatase and tensin homolog (PTEN) and pyroptosis-related proteins was monitored by quantitative real-time polymerase chain reaction or western blot. Flow cytometry examined the pyroptosis level. Lactate dehydrogenase (LDH), creatine kinase-MB and cardiac troponin I levels were detected by test kits. Enzyme-linked immunosorbent assay measured the release of inflammatory cytokines. Dual-luciferase assay validated the binding relationship among LOXL1-AS1, miR-761, and PTEN. Finally, ischemia/reperfusion (I/R) animal model was constructed. Hematoxylin and eosin staining assessed morphological changes of myocardial tissue. NOD-like receptor pyrin domain-containing protein 3 (NLRP3) and casepase-1 expression was determined by immunohistochemistry. Results: After H/R treatment, LOXL1-AS1 and PTEN were highly expressed but miR-761 level was suppressed. LOXL1-AS1 inhibition or miR-761 overexpression increased cell viability, blocked the release of LDH and inflammatory cytokines (interleukin [IL]-1β, IL-18), inhibited pyroptosis level, and downregulated pyroptosis-related proteins (ASC, cleaved caspase-1, gasdermin D-N, NLRP3, IL-1β, and IL-18) levels in HCMs. LOXL1-AS1 sponged miR-761 to up-regulate PTEN. Knockdown of miR-761 reversed the effect of LOXL1-AS1 down regulation on H/R induced HCM pyroptosis. LOXL1-AS1 aggravated the MIRI by regulating miR-761/PTEN axis in vivo. Conclusions: LOXL1-AS1 targeted miR-761 to regulate PTEN expression, then enhance cardiomyocyte pyroptosis, providing a new alternative target for the treatment of MIRI.

• Clinical and Experimental Pediatrics
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• 제53권6호
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• pp.680-687
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• 2010

Patients with congenital heart diseases (CHD) are confronted with early- and late-onset complications, such as conduction disorders, arrhythmias, myocardial dysfunction, altered coronary flow, and ischemia, throughout their lifetime despite successful hemodynamic and/or anatomical correction. Rhythm disturbance is a well-known and increasingly frequent cause of morbidity and mortality in patients with CHD. Predisposing factors to rhythm disturbances include underlying cardiac defects, hemodynamic changes as part of the natural history, surgical repair and related scarring, and residual hemodynamic abnormalities. Acquired factors such as aging, hypertension, diabetes, obesity, and others may also contribute to arrhythmogenesis in CHD. The first step in evaluating arrhythmias in CHD is to understand the complex anatomy and to find predisposing factors and hemodynamic abnormalities. A practical stepwise approach can lead to diagnosis and prompt appropriate interventions. Electrophysiological assessment and management should be done with integrated care of the underlying heart defects and hemodynamic abnormalities. Catheter ablation and arrhythmia surgery have been increasingly applied, showing increasing success rates with technological advancement despite complicated arrhythmia circuits in complex anatomy and the difficulty of access. Correction of residual hemodynamic abnormalities may be critical in the treatment of arrhythmia in patients with CHD.

• Journal of Chest Surgery
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• 제27권3호
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• pp.187-190
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• 1994

Between March, 1989, and August, 1993, 10 patients underwent aortocoronary bypass surgery concomittant with cardiac valve replacement. They were 6 men and 4 women, the age ranging from 47 to 64. 7 patients underwent single valve replacement and 2 patients underwent double valve replacement, Another one patient underwent only CABG one year after valve replacement and he had no evidence of prosthetic valve failure. Total number of graft vessels were.15,14 were saphenous venous grafts and 1 was internal mammary artery graft. Dyspnea on exertion was frequent symptom and was found in all patients. 8 patients presented stable angina, only 1 patient presented postinfarct angina and another 1 patient presented no angina symptom. The graft was placed prior to valve replacement and periods of myocardial ischemia were kept at a minimum by maintaining coronary perfusion throughout operation. Postoperative course was uneventful and there was no hospital mortality, as was supported by many reports, it is our opinion that simultaneous valve replacement and aortotomy bypass graft does not increase the risk of cardiac valve replacement substantially.

• 대한수의학회지
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• 제41권4호
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• pp.467-475
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• 2001

Cardiac arrest, hypoxia, shock or seizure has been known to induce cerebral ischemia. This study was designed to investigate the effect of ischemia on hippocampal pyramidal layer induced by transient bilateral occlusion of the common carotid arteries. Mature Mongolian gerbils were sacrificed at days 2, 4, and 7 after carotid occlusion for 10 minutes. Sham-operated gerbils of control group were subjected to the same protocol except for carotid occlusion. During operation for ischemia, body temperature was maintained $37{\pm}0.5^{\circ}C$ in all gerbils. Paraffin-embedded brain tissue blocks were cut into coronal slices and stained with H-E stain or immunostain by TUNEL method. Neurons with the oval and prominent nucleus and without the eosinophilic cytoplasm in the subfield of hippocamapal pyramidal layer were calculated as to be viable neurons. Their chromatins were condensed or clumped. Their nuclei appeared multiangular or irregularly shrinked. The width of the pyramidal layer was reduced due to the loss of nuclei. At day 2 after reperfusion, some neurons in the CA1 subfield were slightly eosinophilic. But most neurons in the CA2 subfield were strongly eosinophilic. At day 4 day, most neurons in the CA1 subfield were severely damaged and at day 7 day, only a few survived neurons were observed. Survived neurons per longitudinal 1mm sector in the CA1, CA2, CA3, and CA4 subfields of pyramidal layer were investigated. At day 2, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 104.5/mm (54.3%), 51.0/mm (33.8%), 105.5/mm (85.6%), and 124.3/mm (93.5%) compared to the nonischemic control group, respectively. At day 4, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfields were 3.2/mm (1.7%), 51.5/mm(34.2%), 95.3/mm (77.4%), and 112.5/mm (84.6%), respectively. At day 7, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 0.8/mm (0.4%), 5.7/mm(3.8%), 9.8/mm (8.0%), and 5.0/mm (3.7%), respectively. The mean numbers of apoptotic positive neurons in the CA1 subfield at day 2, 4, and 7 after reperfusion were 67.8/mm, 153.2/mm and 123.7/mm, respectively. These results suggest that the transient cerebral ischemia cause severe damages in most neurons at day 7 and that the prosminent apoptotic positive neurons in hippocampal pyramidal layer are the delayed neuronal death induced by ischemia.

• Korean Journal of Radiology
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• 제22권12호
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• pp.1964-1973
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• 2021

Objective: To investigate the diagnostic performance of CT fractional flow reserve (CT-FFR) for myocardial bridging-related ischemia using dynamic CT myocardial perfusion imaging (CT-MPI) as a reference standard. Materials and Methods: Dynamic CT-MPI and coronary CT angiography (CCTA) data obtained from 498 symptomatic patients were retrospectively reviewed. Seventy-five patients (mean age ± standard deviation, 62.7 ± 13.2 years; 48 males) who showed myocardial bridging in the left anterior descending artery without concomitant obstructive stenosis on the imaging were included. The change in CT-FFR across myocardial bridging (ΔCT-FFR, defined as the difference in CT-FFR values between the proximal and distal ends of the myocardial bridging) in different cardiac phases, as well as other anatomical parameters, were measured to evaluate their performance for diagnosing myocardial bridging-related myocardial ischemia using dynamic CT-MPI as the reference standard (myocardial blood flow < 100 mL/100 mL/min or myocardial blood flow ratio ≤ 0.8). Results: ΔCT-FFR_systolic (ΔCT-FFR calculated in the best systolic phase) was higher in patients with vs. without myocardial bridging-related myocardial ischemia (median [interquartile range], 0.12 [0.08-0.17] vs. 0.04 [0.01-0.07], p < 0.001), while CT-FFR_systolic (CT-FFR distal to the myocardial bridging calculated in the best systolic phase) was lower (0.85 [0.81-0.89] vs. 0.91 [0.88-0.96], p = 0.043). In contrast, ΔCT-FFR_diastolic (ΔCT-FFR calculated in the best diastolic phase) and CT-FFR_diastolic (CT-FFR distal to the myocardial bridging calculated in the best diastolic phase) did not differ significantly. Receiver operating characteristic curve analysis showed that ΔCT-FFR_systolic had largest area under the curve (0.822; 95% confidence interval, 0.717-0.901) for identifying myocardial bridging-related ischemia. ΔCT-FFR_systolic had the highest sensitivity (91.7%) and negative predictive value (NPV) (97.8%). ΔCT-FFR_diastolic had the highest specificity (85.7%) for diagnosing myocardial bridging-related ischemia. The positive predictive values of all CT-related parameters were low. Conclusion: ΔCT-FFR_systolic reliably excluded myocardial bridging-related ischemia with high sensitivity and NPV. Myocardial bridging showing positive CT-FFR results requires further evaluation.

• 한국산학기술학회:학술대회논문집
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• 한국산학기술학회 2011년도 추계학술논문집 1부
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• pp.170-173
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• 2011

Therapeutic hypothermia(TH) improves neurological outcomes and reduces mortality among survivors of out-of-hospital cardiac arrest. Animal and human studies have shown that TH results in improved salvage of the myocardium, reduced infarct size, reduced left ventricular remodeling and better long-term left ventricular function in settings of regional myocardial ischemia. This study is to investigate the effect of TH on post-resuscitation myocardial dysfunction and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction (MI). Thoracotomies were performed in 10 Male Sprague-Dawley rats weighing 450-550 g. MI was induced by ligation of the left anterior descending coronary artery (LAD). Ninety min after LAD ligation, ventricular fibrillation induction and subsequent cardiopulmonary resuscitation was performed before defibrillation attempts. Animals were randomized to two groups: a) Acute MI-Normothermia b) Acute MI-Hypothermia ($32^{\circ}C$ for 4 h). Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured echocardiographically together with duration of survival. Ejection fraction, cardiac output and myocardial performance index were $54.74{\pm}9.16$, $89.00{\pm}8.89$, $1.30{\pm}0.09$ respectively and significantly better in the TH group than those of the normothermic group at the first 4 h after resuscitation($32.20{\pm}1.85$,$41.60{\pm}8.62$,$1.77{\pm}0.19$)(p=0.00). The survival time of the hypothermic group ($31.8{\pm}14.8$ h) was greater than that of the normothermic group($12.3{\pm}6.5$ h, p<0.05). This study suggested that TH attenuated post resuscitation myocardial dysfunction in acute MI and would be a potential strategy in post resuscitation care.

• 대한한의학방제학회지
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• 제31권3호
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• pp.157-169
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• 2023

Gracilaria Verrucosa (GV), a seaweed used in traditional Korean medicine, was studied for its effects on MI-induced heart failure in rats. MI is caused by a blocked coronary artery, leading to severe cardiac dysfunction. The study used a rat model to assess cardiac changes over time and evaluate the impact of GV on heart failure. Ischemia was induced through LAD ligation surgery, and the extent of ischemic area was measured as a prognostic factor. GV extract administration significantly improved cardiac morphology and reduced cardiac weight compared to the MI group. GV treatment also improved cardiac function, as evidenced by positive effects on chamber dilation during MI-induced heart failure. Parameters such as ejection fraction (EF) and fractional shortening (FS) were measured. The MI group showed decreased EF and FS compared to the sham group, while these parameters improved in the GV group. GV treatment also reduced levels of LDH, CPK, and CK-MB in the serum, indicating reduced myocardial damage. Histological analysis revealed that GV treatment attenuated cardiac hypertrophy and fibrosis, with reduced collagen deposition in the myocardium. Immunohistochemistry analysis showed suppressed expression of TGF-β1 and collagen 1, involved in fibrosis. In conclusion, GV showed potential in improving cardiac function in a rat model of MI-induced heart failure. It alleviated myocardial damage, attenuated cardiac hypertrophy and fibrosis, and suppressed fibrotic markers. Further studies are needed to explore its clinical efficacy and underlying mechanisms in cardiac diseases beyond animal models.

• Clinical and Experimental Pediatrics
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• 제58권1호
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• pp.37-40
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• 2015

The presence of a single coronary artery is a rare congenital anomaly; such patients often present with severe myocardial ischemia. We experienced the case of a 13-year-old girl with the right coronary artery originating from the left circumflex artery. She visited our Emergency Department owing to severe chest pain; her cardiac enzyme levels were elevated, but her initial electrocardiogram (ECG) was normal. Echocardiography showed normal anatomy and normal regional wall motion. When she presented with recurrent chest pain on admission, the ECG showed significant ST-segment elevation in the left precordial leads and inferior leads with ST-segment depression in aVR lead, suggesting myocardial ischemia, and her cardiac enzyme levels were also elevated. We performed coronary angiography that showed a single right coronary artery originating from the left circumflex artery without stenosis. We confirmed the presence of a single coronary artery using coronary computed tomography. In addition, the treadmill test that was performed showed normal results. She was discharged from the hospital without any medications but with a recommendation of a regular followup.

• Journal of Microbiology and Biotechnology
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• 제27권3호
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• pp.584-590
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• 2017

Ginkgo biloba extract (EGb 761) has been widely used clinically to reduce myocardial ischemia reperfusion injury (MIRI). Microvascular endothelial cells (MVECs) may be a proper cellular model in vitro for the effect and mechanism study against MIRI. However, the protective effect of EGb 761 on MVECs resisting hypoxia/reoxygenation (H/R) injury is little reported. In this study, H/R-injured MVECs were treated with EGb 761, and then the cell viability, apoptosis, ROS production, SOD activity, caspase-3 activity, and protein level of ATM, ${\gamma}$-H2AX, p53, and Bax were measured. ATM siRNA was transfected to study the changes of protein in the ATM pathway. EGb 761 presented protective effect on H/R-injured MVECs, with decreasing cell death, apoptosis, and ROS, and elevated SOD activity. Next, EGb 761 could inhibit H/R-induced ATM, ${\gamma}$-H2AX, p53, and Bax in a dose-dependent manner. Moreover, ATM siRNA also could inhibit H/R-induced ATM, ${\gamma}$-H2AX, p53, and Bax. Overall, these findings verify that EGb 761 protects cardiac MVECs from H/R injury, and for the first time, illustrate the influence on the ATM pathway and apoptosis by EGb 761 via dampening ROS.