• Journal of Chest Surgery
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• v.57 no.1
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• pp.70-78
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• 2024

Background: This study investigated the outcomes of biventricular repair using right ventricle to pulmonary artery (RV-PA) conduit placement in patients aged <1 year. Methods: Patients aged <1 year who underwent biventricular repair using an RV-PA conduit between 2011 and 2020 were included in this study. The outcomes of interest were death from any cause, conduit reintervention, and conduit dysfunction (peak velocity of ≥3.5 m/sec or moderate or severe regurgitation). Results: In total, 141 patients were enrolled. The median age at initial conduit implantation was 6 months. The median conduit diameter z-score was 1.3. The overall 5-year survival rate was 89.6%. In the multivariable analysis, younger age (p=0.006) and longer cardiopulmonary bypass time (p=0.001) were risk factors for overall mortality. During follow-up, 61 patients required conduit reintervention, and conduit dysfunction occurred in 68 patients. The 5-year freedom from conduit reintervention and dysfunction rates were 52.9% and 45.9%, respectively. In the multivariable analysis, a smaller conduit z-score (p<0.001) was a shared risk factor for both conduit reintervention and dysfunction. Analysis of variance demonstrated a nonlinear relationship between the conduit z-score and conduit reintervention or dysfunction. The hazard ratio was lowest in patients with a conduit z-score of 1.3 for reintervention and a conduit z-score of 1.4 for dysfunction. Conclusion: RV-PA conduit placement can be safely performed in infants. A significant number of patients required conduit reintervention and had conduit dysfunction. A slightly oversized conduit with a z-score of 1.3 may reduce the risk of conduit reintervention or dysfunction.

• YAKHAK HOEJI
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• v.45 no.3
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• pp.276-281
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• 2001

The present study was conducted to evaluate the effect of KST221085, a newly synthesized antidiabetic agent, on the hearts from streptozotocin (STZ)-induced diabetic rats. In isolated diabetic hearts, left ventricular developed pressure (LVDP), heart rate (HR) and coronary flow rate (CFR) were decreased compared to normal control, indicating cardiovascular dysfunction in diabetic heart. The treatment with 10 $\mu$M KST221085 remarkably improved the diabetes-induced contractile impairment, without any influence on HR. Reduced coronary flow in diabetic heart was also significantly increased by treatment with 10 $\mu$M KST221085. In isolated aorta from diabetic rat, treatment with 10 $\mu$M KST221085 increased endothelium-dependent relaxation, suggesting that KST221085 can improve the impaired endothelial function in diabetic aorta. Our results suggest that KST221085 treatment can improve the cardiovascular dysfunction in STZ-induced diabetic rats.

• Biomolecules & Therapeutics
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• v.30 no.5
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• pp.399-408
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• 2022

Diabetic cardiomyopathy (DCM) is described as abnormalities of myocardial structure and function in diabetic patients without other well-established cardiovascular factors. Although multiple pathological mechanisms involving in this unique myocardial disorder, mitochondrial dysfunction may play an important role in its development of DCM. Recently, considerable progresses have suggested that mitochondrial biogenesis is a tightly controlled process initiating mitochondrial generation and maintaining mitochondrial function, appears to be associated with DCM. Nonetheless, an outlook on the mechanisms and clinical relevance of dysfunction in mitochondrial biogenesis among patients with DCM is not completely understood. In this review, hence, we will summarize the role of mitochondrial biogenesis dysfunction in the development of DCM, especially the molecular underlying mechanism concerning the signaling pathways beyond the stimulation and inhibition of mitochondrial biogenesis. Additionally, the evaluations and potential therapeutic strategies regarding mitochondrial biogenesis dysfunction in DCM is also presented.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.144-154
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• 2023

Background: As the major pathophysiological feature of obstructive sleep apnea (OSA), chronic intermittent hypoxia (CIH) is vital for the occurrence of cardiovascular complications. The activation of calpain-1 mediates the production of endothelial reactive oxygen species (ROS) and impairs nitric oxide (NO) bioavailability, resulting in vascular endothelial dysfunction (VED). Ginsenoside Rg1 is thought to against endothelial cell dysfunction, but the potential mechanism of CIH-induced VED remains unclear. Methods: C57BL/6 mice and human coronary artery endothelial cells (HCAECs) were exposed to CIH following knockout or overexpression of calpain-1. The effect of ginsenoside Rg1 on VED, oxidative stress, mitochondrial dysfunction, and the expression levels of calpain-1, PP2A and p-eNOS were detected both in vivo and in vitro. Results: CIH promoted VED, oxidative stress and mitochondrial dysfunction accompanied by enhanced levels of calpain-1 and PP2A and reduced levels of p-eNOS in mice and cellular levels. Ginsenoside Rg1, calpain-1 knockout, OKA, NAC and TEMPOL treatment protected against CIH-induced VED, oxidative stress and mitochondrial dysfunction, which is likely concomitant with the downregulated protein expression of calpain-1 and PP2A and the upregulation of p-eNOS in mice and cellular levels. Calpain-1 overexpression increased the expression of PP2A, reduced the level of p-eNOS, and accelerated the occurrence and development of VED, oxidative stress and mitochondrial dysfunction in HCAECs exposed to CIH. Moreover, scavengers of O₂^·-, H₂O₂, complex I or mitoKATP abolished CIH-induced impairment in endothelial-dependent relaxation. Conclusion: Ginsenoside Rg1 may alleviate CIH-induced vascular endothelial dysfunction by suppressing the formation of mitochondrial reactive oxygen species through the calpain-1 pathway.

• Journal of Chest Surgery
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• v.52 no.1
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• pp.16-24
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• 2019

Background: Optimal graft selection for coronary artery bypass grafting (CABG) in patients with severe left ventricular (LV) dysfunction remains debatable. We report an analysis of our experiences of isolated CABG in patients with severe LV dysfunction and the impact of graft strategy on long-term outcomes. Methods: We analyzed 209 patients with severe LV dysfunction (ejection fraction [EF] <30%) who underwent primary isolated CABG. Of these, 169 were revascularized with a bilateral internal thoracic arterial (ITA) graft (BITA group) and 40 were revascularized with a single ITA graft (SITA group). The mean follow-up duration was $22{\pm}32$ months. Results: There were 18 early deaths (8.6%). Overall survival at 5 years was 66.7%. The rate of freedom from cardiac-related death at 5 years was 74.1%, and was significantly higher in patients who underwent off-pump CABG (p=0.005) and in the BITA group (p=0.023). Multivariate analysis demonstrated that old age (hazard ratio [HR], 2.548; 95% confidence interval [CI], 1.134-5.762; p=0.024), off-pump CABG (HR, 0.245; 95% CI, 0.090-0.661; p=0.006), and BITA grafts (HR, 0.333; 95% CI, 0.146-0.757; p=0.009) were correlated with cardiac mortality. Conclusion: CABG in patients with severe LV dysfunction (EF <30%) showed reasonable long-term outcomes. The rate of freedom from cardiac-related death was significantly higher in patients who underwent off-pump CABG and in the BITA group. Off-pump BITA grafting strategies can be accepted as a viable primary option in patients with severe LV dysfunction if performed by an experienced surgeon.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.2
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• pp.95-102
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• 2019

Endoplasmic reticulum (ER) stress is mediated by disturbance of $Ca^{2+}$ homeostasis. The store-operated calcium (SOC) channel is the primary $Ca^{2+}$ channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on $Ca^{2+}$ influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular $Ca^{2+}$ in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.

• Journal of Chest Surgery
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• v.48 no.6
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• pp.407-410
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• 2015

A two-month-old infant presented with coarctation of the aorta, severe left ventricular dysfunction, and moderate to severe mitral regurgitation. Through median sternotomy, the aortic arch was repaired under cardiopulmonary bypass and regional cerebral perfusion. The patient was postoperatively supported with a left ventricular assist device for five days. Left ventricular function gradually improved, eventually recovering with the concomitant regression of mitral regurgitation. Prompt surgical repair of coarctation of the aorta is indicated for patients with severe left ventricular dysfunction. A central approach for surgical repair with a back-up left ventricular assist device is a safe and effective treatment strategy for these patients.

• Annals of Geriatric Medicine and Research
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• v.22 no.4
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• pp.176-183
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• 2018

Background: Although the frequency and intensity of headaches decrease in older adults, headaches in this population are still an important neurological disorder. The purpose of this study was to investigate the associations of headache characteristics in older adults with the development of cardiovascular disease and cognitive dysfunction. Methods: We prospectively enrolled 125 older (${\geq}65$ years old) patients with headache who were making their first visit to outpatient clinics and who had no prior history of cognitive dysfunction from 11 hospitals in Korea between August 2014 and February 2015. We investigated the occurrence of newly developed/or recurrent headache, cardiovascular disease, cognitive dysfunction, and poor functional outcomes. Results: The mean age of all included patients was 72.6 years, 68.8% were women, and 43 (34.4%) had newly developed/or recurrent headache during follow-up. During a median follow-up of 31 months (interquartile range, 28-34 months), 21 participants (16.8%) experienced cardiovascular disease, and 26 (20.8%) developed cognitive dysfunction. Upon multivariate analysis and after adjusting for sex, age, and other factors, presence of newly developed/or recurrent headache was found to be associated with cardiovascular disease (hazard ratio [HR], 4.03; 95% confidence interval [CI], 1.28-12.61; p=0.017) and frequency of headache for the recent 3 months was related with cognitive dysfunction (HR, 1.05; 95% CI, 1.00-1.09; p=0.017) and poor functional outcomes (HR, 1.06; 95% CI, 1.01-1.11; p=0.011). Conclusion: Our study demonstrated that there is an increased risk of cardiovascular disease, cognitive dysfunction, and poor functional outcomes in older patients with frequent, newly developed, or recurrent headache.

• YAKHAK HOEJI
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• v.45 no.6
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• pp.739-745
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• 2001

Of all pesticides, carbamates are known to be most common, since alternatives such as organophosphates have long lifetime and are extremely toxic to produce a delayed neurotoxic effect. Although a number of studies about toxicity of carbofuran, a most widely used carbamate, have been reported, its cardiovascular toxicity has not yet been studied. In the present study, we investigated its cardiovascular toxic effect in anesthetized rat in vivo and in isolated Langendorff rat heart, In anesthetized rat model, carbofuran (10 mg/kg) significantly reduced heart rate, and transiently increased blood pressure. In isolated rat heart, carbofuran (10${\mu}{\textrm}{m}$) caused a significant depression in the left ventricular developed pressure (LVDP), indicating contractile dysfunction by carbofuran. Carbofuran (10${\mu}{\textrm}{m}$) also decreased coronary flow rate (CFR) in isolated heart, indicating carbofuran-induced coronary dysfunction. These results suggest that carbofuran can cause cardiac dysfunction in rat in vivo and vitro.

• Journal of Chest Surgery
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• v.49 no.5
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• pp.350-355
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• 2016

Background: Mitral stenosis (MS) remains one of the important heart diseases. There are many factors that influence the clinical outcomes, and little is known about how left ventricular (LV) dysfunction clinically affects the prognosis of the patient with MS after mitral valve replacement (MVR). We reviewed our clinical experiences of MVR in patients with MS who had LV dysfunction. Methods: Between January 1991 and January 2013, 110 patients with MS who underwent MVR were analyzed and divided into two groups according to ejection fraction (EF). Group 1 ($EF{\leq}45%$) included 13 patients and group 2 (EF>45%) included 97 patients. Results: Thromboembolism occurred in 8 patients after MVR (group 1: n=3, 23.1%; group 2: n=5, 5.2%) and its incidence was significantly higher in group 1 than in group 2 (p=0.014). There were 3 deaths each in groups 1 and 2 during follow-up. The overall rate of cardiac-related death in group 1 was significantly higher than in group 2 (group 1: n=3, 23.1%; group 2: n=3, 3.1%; p=0.007). The cumulative survival rate at 1 and 15 years was 83.9% and 69.9% in group 1 and 97.9% and 96.3% in group 2 (p=0.004). The Cox regression analysis revealed that survival was significantly associated with postoperative stroke (p=0.011, odds ratio=10.304). Conclusion: This study identified postoperative stroke as an adverse prognostic factor in patients with MS after MVR, and a s more prevalent in patients with LV dysfunction. Postoperative stroke should be reduced to improve clinical outcomes for patients. Preventive care should be made in multiple ways, such as management of LV dysfunction, atrial fibrillation, and anticoagulation.