• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.332-340
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• 2022

Background: Cardiac dysfunction patients have long been considered at high risk of reintubation. However, it is based on past studies in which only conventional oxygen therapy was applied after extubation. We investigated association between cardiac dysfunction and reintubation rate in situation where high-flow nasal cannula (HFNC) was widely used during post-extubation period. Methods: We conducted a retrospective observational cohort study of patients treated with HFNC after planned extubation in medical intensive care unit of single tertiary center. Patients were divided into normal function group (ejection fraction [EF] ≥45%) and cardiac dysfunction group (EF <45%). The primary outcome was reintubation rate within 72 hours following extubation. Results: Of 270 patients, 35 (13%) had cardiac dysfunction. Baseline characteristics were similar in both groups. There were no differences in the changes in vital signs between the two groups during the first 12 hours after extubation except diastolic blood pressure. The reintubation rates were 20% and 17% for cardiac dysfunction group and normal function group, respectively (p=0.637). In a multivariate Cox regression analysis, cardiac dysfunction was not associated with an increased risk of reintubation within 72 hours following extubation (hazard ratio, 1.56; p=0.292). Conclusion: Cardiac dysfunction was not associated with increased reintubation rate within 72 hours when HFNC is immediately applied after planned extubation.

• The Korean Journal of Nuclear Medicine
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• v.38 no.5
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• pp.331-337
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• 2004

Cardiac neurotransmission imaging allows in vivo assessment of presynaptic reuptake, neurotransmitter storage and postsynaptic receptors. Among the various neurotransmitter, I-123 MIBG is most available and relatively well-established. Metaiodobenzylguanidine (MIBG) is an analogue of the false neurotransmitter guanethidine. It is taken up to adrenergic neurons by uptake-1 mechanism as same as norepinephrine. As tagged with I-123, it can be used to image sympathetic function in various organs including heart with planar or SPECT techniques. I-123 MIBG imaging has a unique advantage to evaluate myocardial neuronal activity in which the heart has no significant structural abnormality or even no functional derangement measured with other conventional examination. In patients with cardiomyopathy and heart failure, this imaging has most sensitive technique to predict prognosis and treatment response of betablocker or ACE inhibitor. In diabetic patients, it allow very early detection of autonomic neuropathy. In patients with dangerous arrhythmia such as ventricular tachycardia or fibrillation, MIBG imaging may be only an abnormal result among various exams. In patients with ischemic heart disease, sympathetic derangement may be used as the method of risk stratification. In heart transplanted patients, sympathetic reinnervation is well evaluated. Adriamycin-induced cardiotoxicity is detected earlier than ventricular dysfunction with sympathetic dysfunction. Neurodegenerative disorder such as Parkinson's disease or dementia with Lewy bodies has also cardiac sympathetic dysfunction. Noninvasive assessment of cardiac sympathetic nerve activity with I-123 MIBG imaging nay be improve understanding of the pathophysiology of cardiac disease and make a contribution to predict survival and therapy efficacy.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.363-370
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• 2016

Cardiovascular disease is the most common cause of death in diabetic patients. Hyperglycemia is the primary characteristic of diabetes and is associated with many complications. The role of hyperglycemia in the dysfunction of human cardiac progenitor cells that can regenerate damaged cardiac tissue has been investigated, but the exact mechanism underlying this association is not clear. Thus, we examined whether hyperglycemia could regulate mitochondrial dynamics and lead to cardiac progenitor cell dysfunction, and whether blocking glucose uptake could rescue this dysfunction. High glucose in cardiac progenitor cells results in reduced cell viability and decreased expression of cell cycle-related molecules, including CDK2 and cyclin E. A tube formation assay revealed that hyperglycemia led to a significant decrease in the tube-forming ability of cardiac progenitor cells. Fluorescent labeling of cardiac progenitor cell mitochondria revealed that hyperglycemia alters mitochondrial dynamics and increases expression of fission-related proteins, including Fis1 and Drp1. Moreover, we showed that specific blockage of GLUT1 improved cell viability, tube formation, and regulation of mitochondrial dynamics in cardiac progenitor cells. To our knowledge, this study is the first to demonstrate that high glucose leads to cardiac progenitor cell dysfunction through an increase in mitochondrial fission, and that a GLUT1 blocker can rescue cardiac progenitor cell dysfunction and downregulation of mitochondrial fission. Combined therapy with cardiac progenitor cells and a GLUT1 blocker may provide a novel strategy for cardiac progenitor cell therapy in cardiovascular disease patients with diabetes.

• Journal of Chest Surgery
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• v.46 no.4
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• pp.289-292
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• 2013

Through the use of a dual chamber (DDD) pacemaker, we achieved a cardiac resynchronization effect in a 51-year-old female patient who was transferred to our hospital from another hospital for an operation for three-vessel coronary artery disease. Her electrocardiogram showed a left bundle branch block (LBBB) and a prolonged QRS interval of 166 milliseconds. Severe left ventricle (LV) dysfunction was diagnosed via echocardiography. Coronary artery bypass grafting (CABG) was then performed. In order to accelerate left atrial activation and reduce the conduction defect, DDD pacing using right atrial and left and right ventricular pacing wires was initiated postoperatively. The cardiac output was measured immediately, and one and twelve hours after arrival in the intensive care unit. The cardiac output changed from 2.8, 2.4, and 3.6 L/min without pacing to 3.5, 3.4, and 3.5 L/min on initiation of pacing. The biventricular synchronization using DDD pacing was turned off 18 hours after surgery. She was transferred to a general ward with a cardiac output of 3.9 L/min. In patients with coronary artery disease, severe LV dysfunction, and LBBB, cardiac resynchronization therapy can be achieved through DDD pacing after CABG.

• Journal of Chest Surgery
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• v.49 no.1
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• pp.42-45
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• 2016

Thrombosis at the left ventricular outflow tract occurs without any detectable heart disease or predisposing factors only extremely rarely. A 48-year-old male visited Konkuk University Medical Center with loss of consciousness one month prior to presentation. Before he visited our hospital, he had been diagnosed with a cardiac tumor, which was located between the left atrium and posterior aortic root, and which was adjacent to both the aortic and mitral valves. Cardiac transplantation was recommended at the other hospital because of the high risk of cardiac dysfunction induced by both aortic and mitral valvular dysfunction after surgical resection. Based on preoperative transthoracic echocardiography, cardiac computed tomography, cardiac magnetic resonance imaging, and intraoperative transesophageal echocardiography, we considered it to be a benign tumor. Complete resection was achieved and the pathology confirmed organizing thrombus. We report a case of organizing thrombus mimicking a cardiac tumor, which was located at the mitral-aortic intervalvular fibrosa of the left ventricular outflow tract without any heart disease.

• Journal of Chest Surgery
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• v.27 no.5
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• pp.339-344
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• 1994

Sinus node dysfunction is common after orthotopic heart transplantation.Electrophysiologic studies have documented a high incidence [46% to 50%] of impaired sinus node automaticity and sinoatrial conduction in the early posttransplantation period. Sinus node dysfunction persists in over 20 % of patients and leads to prolonged bradyarrythmias, including sinus or nodal bradycardia and sinus arrest.The purpose of this paper was to observe sinus node dysfunction after orthotopic heart transplantation. Ten cardiac recipient dogs were monitored continuously after orthotopic transplantations between unrelated adult mongrel dogs. Crystalloid cardioplegic solution [Choongwoi Cardioplegia

• 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.

• Journal of Chest Surgery
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• v.25 no.11
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• pp.1261-1263
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• 1992

Primary cardiac fibroma of the left ventricular myocardium is a rare tumor of the heart which is usually located within the anterior wall and /or septum of the left ventricle and is the second most common cardiac tumor in infant and children. Although the tumor is benign histologically, it may cause severe cardiac dysfunction and sudden death. A 30-day-old neonate with a huge intramural fibroma involving the posterolateral wall of the left ventricle underwent it`s partial resection under extracorporeal circulation on April 1992.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.43-50
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• 2004

Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. Amrinone, a specific inhibitor of phosphodiesterase 3, has an antioxidant activity against PMNs. Therefore, we hypothesized that amrinone could attenuate PMNs-Induced cardiac dysfunction by suppression of reactive oxygen species (ROS) produced fby PMNs. In the present study, we examined the effects of amrinone on isolated ischemic (20 min) and reperfused (45 min) rat hearts perfused with PMNs. Amrinone at $25\;{\mu}M$, given to hearts during the first 5 min of reperfusion, significantly improved coronary flow, left ventricular developed pressure (P<0.001), and the maximal rate of development of left ventricular developed pressure (P<0.001), compared with ischemic/reperfused hearts perfused with PMNs in the absence of amrinone. In addition, amrinone significantly reduced myeloperoxidase activity by 50.8%, indicating decreased PMNs infiltration (p< 0.001). Superoxide radical and hydrogen peroxide production were also significantly reduced in fMLP- and PMA-stimulated PMNs pretreated with amrinone. Hydroxyl radical was scavenged by amrinone. fMLP-induced elevation of $[Ca^{2+}]_i$ was also inhibited by amrinone. These results provide evidence that amrinone can significantly attenuate PMN-induced cardiac contractile dysfunction in the ischemic/reperfused rat heart via attenuation of PMNs infiltration into the myocardium and suppression of ROS release by PMNs.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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• pp.437-442
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• 2009

A non-steroidal anti-inflammatory drug (NSAID) has many adverse effects including cardiovascular (CV) risk. Diclofenac among the nonselective NSAIDs has the highest CV risk such as congestive heart failure, which resulted commonly from the impaired cardiac pumping due to a disrupted excitationcontraction (E-C) coupling. We investigated the effects of diclofenac on the L-type calcium channels which are essential to the E-C coupling at the level of single ventricular myocytes isolated from neonatal rat heart, using the whole-cell voltage-clamp technique. Only diclofenac of three NSAIDs, including naproxen and ibuprofen, significantly reduced inward whole cell currents. At concentrations higher than $3\;{\mu}M$, diclofenac inhibited reversibly the $Na^+$ current and did irreversibly the L-type $Ca^{2+}$ channels-mediated inward current $(IC_{50}=12.89\pm0.43\;{\mu}M)$ in a dose-dependent manner. However, nifedipine, a well-known L-type channel blocker, effectively inhibited the L-type $Ca^{2+}$ currents but not the $Na^+$ current. Our finding may explain that diclofenac causes the CV risk by the inhibition of L-type $Ca^{2+}$ channel, leading to the impairment of E-C coupling in cardiac myocytes.