• Tuberculosis and Respiratory Diseases
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• v.81 no.3
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• pp.247-255
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• 2018

Background: Patients with acute respiratory failure secondary to tuberculous destroyed lung (TDL) have a poor prognosis. The aim of the present retrospective study was to develop a mortality prediction model for TDL patients who require mechanical ventilation. Methods: Data from consecutive TDL patients who had received mechanical ventilation at a single university-affiliated tertiary care hospital in Korea were reviewed. Binary logistic regression was used to identify factors predicting intensive care unit (ICU) mortality. A TDL on mechanical Ventilation (TDL-Vent) score was calculated by assigning points to variables according to ${\beta}$ coefficient values. Results: Data from 125 patients were reviewed. A total of 36 patients (29%) died during ICU admission. On the basis of multivariate analysis, the following factors were included in the TDL-Vent score: age ${\geq}65$ years, vasopressor use, and arterial partial pressure of oxygen/fraction of inspired oxygen ratio <180. In a second regression model, a modified score was then calculated by adding brain natriuretic peptide. For TDL-Vent scores 0 to 3, the 60-day mortality rates were 11%, 27%, 30%, and 77%, respectively (p<0.001). For modified TDL-Vent scores 0 to ${\geq}3$, the 60-day mortality rates were 0%, 21%, 33%, and 57%, respectively (p=0.001). For both the TDL-Vent score and the modified TDL-Vent score, the areas under the receiver operating characteristic curve were larger than that of other illness severity scores. Conclusion: The TDL-Vent model identifies TDL patients on mechanical ventilation with a high risk of mortality. Prospective validation studies in larger cohorts are now warranted.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.2301-2305
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• 2016

Background: The early detection of anthracycline- induced cardiotoxicity is very important since it might be useful in prevention of cardiac decompensation. This study was designed with the intent of assessing the usefulness of cardiac troponin T (cTnT) and NT- Pro BNP estimation in early prediction of anthracycline induced cardiotoxicity. Materials and Methods: In this prospective study histologically proven breast cancer patients who were scheduled to receive anthracycline containing combination chemotherapy as a part of multimodality treatment were enrolled. Baseline cardiac evaluation was performed by echocardiography (ECHO) and biomarkers like cardiac troponin T (cTnT) and N terminal- pro brain natriuretic peptide (NT- Pro BNP). All patients underwent cTnT and NT- Pro BNP estimation within 24 hours of each cycle of chemotherapy and were followed up after 6 months of initiation of chemotherapy. Any changes in follow up ECHO were compared to ECHO at baseline and cTnT and NT- Pro BNP levels after each cycle of anthracycline-based chemotherapy. Results: Initial data were obtained for 33 patients. Mean change in left ventricular diastolic diameter (LVDD) within 6 months was $0.154{\pm}0.433cms$ (p value=0.049). Seven out of 33 patients had an increase in biomarker cTnT levels (p value=0.5). A significant change in baseline and follow up LVDD was observed in patients with raised cTnT levels (p value=0.026) whereas no change was seen in ejection fraction (EF) and left atrial diameters (LAD) within 6 months of chemotherapy. NT- Pro BNP levels increased in significant number of patients (p value ${\leq}0.0001$) but no statistically significant change was observed in the ECHO parameters within 6 months. Conclusions: Functional monitoring is a poorly effective method in early estimation of anthracycline induced cardiac dysfunction. Estimation of biomarkers after chemotherapy may allow stratification of patients in various risk groups, thereby opening window for interventional strategies in order to prevent permanent damage to the myocardium.

• Journal of Chest Surgery
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• v.48 no.3
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• pp.164-173
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• 2015

Background: Hypertrophied myocardium is especially vulnerable to ischemic injury. This study aimed to compare the early and late clinical outcomes of three different methods of myocardial protection in patients with aortic stenosis. Methods: This retrospective study included 225 consecutive patients (mean age, 65{\pm}10 years; 123 males) with severe aortic stenosis who underwent aortic valve replacement. Patients were excluded if they had coronary artery disease, an ejection fraction <50%, more than mild aortic regurgitation, or endocarditis. The patients were divided into three groups: group A, which was treated with antegrade and retrograde cold blood cardioplegia; group B, which was treated with antegrade crystalloid cardioplegia using histidine-tryptophan-ketoglutarate (HTK) solution; and group C, treated with retrograde cold blood cardioplegia. Results: Group A contained 70 patients (31.1%), group B contained 74 patients (32.9%), and group C contained 81 patients (36%). The three groups showed significant differences with regard to the proportion of patients with a New York Heart Association functional classification ${\geq}III$ (p=0.035), N-terminal pro-brain natriuretic peptide levels (p=0.042), ejection fraction (p=0.035), left ventricular dimensions (p<0.001), left ventricular mass index (p<0.001), and right ventricular systolic pressure (p <0.001). Differences in cardiopulmonary bypass time (p=0.532) and aortic cross-clamp time (p=0.48) among the three groups were not statistically significant. During postoperative recovery, no significant differences were found regarding the use of inotropes (p=0.328), mechanical support (n=0), arrhythmias (atrial fibrillation, p=0.347; non-sustained ventricular tachycardia, p=0.1), and ventilator support time (p=0.162). No operative mortality occurred. Similarly, no significant differences were found in long-term outcomes. Conclusion: Although the three groups showed some significant differences with regard to patient characteristics, both antegrade crystalloid cardioplegia with HTK solution and retrograde cold blood cardioplegia led to early and late clinical results similar to those achieved with combined antegrade and retrograde cold blood cardioplegia.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.106-116
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• 2023

Background: Pirarubicin (THP) is an anthracycline antibiotic used to treat various malignancies in humans. The clinical usefulness of THP is unfortunately limited by its dose-related cardiotoxicity. Ginsenoside F1 (GF1) is a metabolite formed when the ginsenosides Re and Rg1 are hydrolyzed. However, the protective effects and underlying mechanisms of GF1 on THP-induced cardiotoxicity remain unclear. Methods: We investigated the anti-apoptotic and anti-oxidative stress effects of GF1 on an in vitro model, using H9c2 cells stimulated by THP, plus trigonelline or AKT inhibitor imidazoquinoxaline (IMQ), as well as an in vivo model using THP-induced cardiotoxicity in rats. Using an enzyme-linked immunosorbent test, the levels of malondialdehyde (MDA), brain natriuretic peptide (BNP), creatine kinase (CK-MB), cardiac troponin (c-TnT), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione (GSH) were determined. Nuclear factor (erythroid-derived2)-like 2 (Nrf2) and the expression of Nrf2 target genes, including heme oxygenase-1 (HO-1), glutathione-S-transferase (Gst), glutamate-cysteine ligase modifier subunit (GCLM), and expression levels of AKT/Bcl-2 signaling pathway proteins were detected using Western blot analysis. Results: THP-induced myocardial histopathological damage, electrocardiogram (ECG) abnormalities, and cardiac dysfunction were reduced in vivo by GF1. GF1 also decreased MDA, BNP, CK-MB, c-TnT, and LDH levels in the serum, while raising SOD and GSH levels. GF1 boosted Nrf2 nuclear translocation and Nrf2 target gene expression, including HO-1, Gst, and GCLM. Furthermore, GF1 regulated apoptosis by activating AKT/Bcl-2 signaling pathways. Employing Nrf2 inhibitor trigonelline and AKT inhibitor IMQ revealed that GF1 lacked antioxidant and anti-apoptotic effects. Conclusion: In conclusion, GF1 was found to alleviate THP-induced cardiotoxicity via modulating Nrf2 and AKT/Bcl-2 signaling pathways, ultimately alleviating myocardial oxidative stress and apoptosis.

• Korean Journal of Clinical Laboratory Science
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• v.54 no.4
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• pp.256-264
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• 2022

Ischemic stroke is caused by an occlusion by a thrombus or embolus in a cerebral artery, preventing oxygenated blood from reaching the brain and causing the necrosis of nerve cells. This paper summarizes the serum candidate markers associated with cardiovascular disease and atrial fibrillation (AF) disease that enable an early diagnosis of ischemic stroke studied thus far and compares the odds ratio (OR) of each marker. This study examined the effect size of these serum candidate markers using meta-analysis techniques. The academic database search screening for articles containing the keywords "cardiovascular disease," "atrial fibrillation," "ischemic stroke," and "serum marker" was limited to results for patients with ischemic stroke. The most derived markers in this study were N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), D-dimer, C-reactive protein (CRP), and glial fibrillary acidic protein (GFAP), the rest being investigated individually. In conclusion, NT-pro-BNP appears to be very useful for the early diagnosis of ischemic stroke. Primarily, it is a marker of AF, and more AF markers will be uncovered and studied in the future.

• Journal of Veterinary Clinics
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• v.40 no.2
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• pp.130-134
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• 2023

A 12-year-old Standard Poodle presented with intermittent weakness and occasional dyspnea at the Veterinary Medicine Teaching Hospital of Kangwon National University. A grade of 4 out of 6 systolic murmur with an irregular tachycardic rhythm was auscultated on both sides of the chest. Systolic blood pressure was 140 mmHg. Panting was noticed in the hospital, but there was no crackle sound. Blood analysis revealed mild increases in liver panel levels (alanine aminotransferase 149 [reference interval, 19-70] U/L; and alkaline phosphatase, 185 [reference interval, 15-127] U/L) and severe increases in cardiac biomarker levels (n-terminal pro-brain natriuretic peptide, 4169 [reference interval, 50-900] pmol/L; and cardiac troponin I, 0.22 [reference interval, 0.03-0.12] ng/mL). On electrocardiography, irregularly irregular supraventricular tachycardic rhythm with an f-wave and no distinct p-wave was observed. Generalized cardiomegaly with an enlarged right atrium and left ventricle was confirmed on thoracic radiography. Moreover, hepatomegaly and an enlarged caudal vena cava were observed. Echocardiographic evaluation revealed a fibromuscular diaphragm in the right ventricle. Because of the obstructive lesion in the right ventricle, the right atrium and ventricle were enlarged (right atrial area index, 38.82 cm²/m² [reference interval, 4.2-10.2 cm²/m²]; right ventricle end-diastolic area index, 14.152 cm²/m² [reference interval, 4.9-10.92 cm²/m²]). Accordingly, the patient was diagnosed with double-chambered right ventricle (DCRV). Pimobendan, furosemide, enalapril, diltiazem, and S-adenosylmethionine (SAMe) were prescribed, and all symptoms were relieved. DCRV is a right-sided congenital heart defect resembling pulmonic valve stenosis. If symptoms are not severe, medical therapy can be facilitated without surgery or the balloon dilation.

• The Korean journal of internal medicine
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• v.39 no.3
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• pp.488-500
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• 2024

Background/Aims: Roxadustat, an oral medication for treating renal anemia, is a hypoxia-inducible factor prolyl hydroxylase inhibitor used for regulating iron metabolism and promoting erythropoiesis. To investigate the efficacy and safety of roxadustat in patients undergoing peritoneal dialysis (PD) with erythropoietin hyporesponsiveness. Methods: Single-center, retrospective study, 81 PD patients (with erythropoietin hyporesponsiveness) were divided into the roxadustat group (n = 61) and erythropoiesis-stimulating agents (ESAs) group (n = 20). Hemoglobin (Hb), total cholesterol, intact parathyroid hormone (iPTH), brain natriuretic peptide (BNP), related indicators of cardiac function and high-sensitivity C-reactive protein (hs-CRP) were collected. Additionally, adverse events were also recorded. The follow-up period was 16 weeks. Results: The two groups exhibited similar baseline demographic and clinical characteristics. At baseline, the roxadustat group had a mean Hb level of 89.8 ± 18.9 g/L, while the ESAs group had a mean Hb level of 95.2 ± 16.0 g/L. By week 16, the Hb levels had increased to 118 ± 19.8 g/L (p < 0.05) in the roxadustat group and 101 ± 19.3 g/L (p > 0.05) in the ESAs group. The efficacy of roxadustat in improving anemia was not influenced by baseline levels of hs-CRP and iPTH. Cholesterol was decreased in the roxadustat group without statin use. An increase in left ventricular ejection fraction and stabilization of BNP were observed in the roxadustat group. Conclusions: For PD patients with erythropoietin hyporesponsiveness, roxadustat can significantly improve renal anemia. The efficacy of roxadustat in improving renal anemia was not affected by baseline levels of hs-CRP0 and iPTH.

• Pediatric Infection and Vaccine
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• v.23 no.1
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• pp.25-30
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• 2016

Purpose: We undertook this study to investigate discrepancies in C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) values, and variations following intravenous immunoglobulin (IVIG) therapy in Kawasaki disease (KD). Methods: A total of 123 KD patients were retrospectively enrolled. Patients were treated with IVIG 2 g/kg at 2 to 9 days after disease onset. We obtained white blood cell (WBC) count, percentage of neutrophils (% neutrophils), CRP, ESR, and N-terminal pro-brain natriuretic peptide (NT-proBNP) values before and 48 to 72 hours after IVIG treatment. Discrepancy was defined as $CRP{\geq}10mg/dL$ and ESR <50 mm/hr (Group 1), or CRP <10 mg/dL and $ESR{\geq}50mm/hr$ (Group 2). Results: Thirty-six of 123 subjects (29.2%) had a discrepancy: 25 (20.3%) in Group 1 and 11 (8.9%) in Group 2. In Group 1, 15 patients (60%) had fever for <5 days (early presenter) and 10 (40%) had fever for ${\geq}5days$ (late presenter). There were six early presenters (55%) and five late presenters (45%) in Group 2. Late presenters had higher ESR than early presenters ($34.3{\pm}21.0mm/hr$ vs. $26.3{\pm}19.3mm/hr$, P=0.029). After IVIG treatment, elevated WBC count, % neutrophils, CRP, and NT-proBNP levels normalized. In contrast, ESR increased from $37.4{\pm}21.9mm/hr$ to $48.0{\pm}22.7mm/hr$ (n=36, P=0.051). Conclusions: A discrepancy may be related to the duration of fever. Due to discrepancies in CRP and ESR values in acute KD, both should be measured to assess the degree of inflammatory activity before IVIG treatment. After IVIG treatment, the ESR should not be used as a marker of response to therapy in KD.