• Clinical and Experimental Pediatrics
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• v.64 no.5
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• pp.188-195
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• 2021

Acute fulminant myocarditis (AFM) occurs as an inflammatory response to an initial myocardial insult. Its rapid and deadly progression calls for prompt diagnosis with aggressive treatment measures. The demonstration of its excellent recovery potential has led to increasing use of mechanical circulatory support, especially extracorporeal membrane oxygenation (ECMO). Arrhythmias, organ failure, elevated cardiac biomarkers, and decreased ventricular function at presentation predict requirement for ECMO. In these patients, ECMO should be considered earlier as the clinical course of AFM can be unpredictable and can lead to rapid haemodynamic collapse. Key uncertainties that clinicians face when managing children with AFM such as timing of initiation of ECMO and left ventricular decompression need further investigation.

• Journal of Ginseng Research
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• v.45 no.3
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• pp.371-379
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• 2021

Mitochondrial dysfunction contributes to the pathogenesis and prognosis of many common disorders, including neurodegeneration, stroke, myocardial infarction, tumor, and metabolic diseases. Ginsenosides, the major bioactive constituents of Panax ginseng (P. ginseng), have been reported to play beneficial roles in the molecular pathophysiology of these diseases by targeting mitochondrial dysfunction. In this review, we first introduce the types of ginsenosides and basic mitochondrial functions. Then, recent findings are summarized on different ginsenosides targeting mitochondria and their key signaling pathways for the treatment of multiple diseases, including neurological disorders, cancer, heart disease, hyperglycemia, and inflammation are summarized. This review may explain the common targets of ginsenosides against multiple diseases and provide new insights into the underlying mechanisms, facilitating research on the clinical application of P. ginseng.

• The Korean Journal of Nuclear Medicine
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• v.37 no.6
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• pp.355-363
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• 2003

Purpose: Regional contractility can be calculated using the regional volume change of left ventricle measured by gated myocardial SPECT image and curve of central artery pressure obtained from radial artery pressure data. In this study, a program to obtain the regional contractility was developed, and reproducibility of regional contractility measurement was assessed. Materials and Methods: Seven patients(male:female=5:2, $58{\pm}11.9$ years) with coronary artery diseases underwent gated Tc-99m MIBI myocardial SPECT twice without delay between two scans. Regional volume change of left ventricle was estimated using CSA (Cardiac SPECT Analyzer) software developed in this study. Regional contractility was iteratively estimated from the time-elastance curve obtained using the time-pressure curve and regional time-volume curve. Reproducibility of regional contractility measurement assessed by comparing the contractility values measured twice from the same SPECT data and by comparing those measured from the pair of SPECT data obtained from a same patient. Results: Measured regional contractility was $3.36{\pm}3.38{mm}Hg/mL$ using 15-segment model, $3.16{\pm}2.25{mm}Hg/mL$ using 7-segment model, and $3.11{\pm}2.57{mm}Hg/mL$ using 5-segment model. The harmonic average of regional contractility value was almost identical to the global contractility. Correlation coefficient of regional contractility values measured twice from the same data was greater than 0.97 for all models, and two standard deviations of contractility difference on Bland Altman plot were 1.5%, 1.0%, and 0.9% for 15-, 7-, and 5-segment models, respectively. Correlation coefficient of regional contractility values measured from the pair of SPECT data obtained from a same patient was greater than 0.95 for all models, and two standard deviations on Bland Altman plot were 2.2%, 1.0%, and 1.2%. Conclusion: Regional contractility of left ventricle measured using developed software in this study was reproducible. Regional contractility of left ventricle will be a new useful index for myocardial function after analysis of the clinical data.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.321-330
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• 1994

The protective effect of 'ischemic preconditioning (PC)' on ischemia-reperfusion injury of heart has been reported in various animal species, but without known mechanisms in detail. In an attempt to investigate the cardioprotective mechanism of PC, we examined the effects of PC on the myocardial oxidative injuries and the oxygen free radical production in the ischemia-reperfusion model of isolated Langendorff preparations of rat hearts. PC was performed with three episodes of 5 min ischemia and 5 min reperfusion before the induction of prolonged ischemia (30 min)-reperfusion(20 min). PC prevented the depression of cardiac function (left ventricular pressure x heart rate) observed in the ischemic-reperfused heart, and reduced the release of lactate dehydrogenase during the reperfusion period. On electron microscopic pictures, myocardial ultrastructures were relatively well preserved in PC hearts as compared with non-PC ischemic-reperfused hearts. In PC hearts, lipid peroxidation of myocardial tissue as estimated from malondialdehyde production was markedly reduced. PC did not affect the activity of xanthine oxidase which is a major source of oxygen radicals in the ischemic rat hearts, but the myocardial content of hypoxanthine (a substrate for xanthine oxidase) was much lower in PC hearts. It is suggested from these results that PC brings about significant myocardial protection in ischemic-reperfused heart and this effect may be related to the suppression of oxygen free radical reactions.

• Journal of Dental Anesthesia and Pain Medicine
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• v.22 no.1
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• pp.11-18
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• 2022

Background: The vasoconstrictive effect of epinephrine in local anesthetics affects the heart, which leads to hesitation among dentists in injecting local anesthetics into patients with cardiovascular disease. Due to its vasoconstrictive effects, the present study investigated the effects of vasopressin administration on cardiac function in rats. Methods: Experiment 1 aimed to determine the vasopressin concentration that could affect cardiac function. An arterial catheter was inserted into the male Wistar rats. Next, 0.03, 0.3, and 3.0 U/mL arginine vasopressin (AVP) (0.03V, 0.3V, and 3.0V) was injected into the tongue, and the blood pressure was measured. The control group received normal saline only. In Experiment 2, following anesthesia infiltration, a pressure-volume catheter was placed in the left ventricle. Baseline values of end-systolic elastance, end-diastolic volume, end-systolic pressure, stroke work, stroke volume, and end-systolic elastance were recorded. Next, normal saline and 3.0V AVP were injected into the tongue to measure their effect on hemodynamic and cardiac function. Results: After 3.0V administration, systolic blood pressures at 10 and 15 min were higher than those of the control group; they increased at 10 min compared with those at baseline. The diastolic blood pressures at 5-15 min were higher than those of the control group; they increased at 5 and 10 min compared with those at baseline. The preload decreased at 5 and 10 min compared to that at baseline. However, the afterload increased from 5 to 15 min compared with that of the control group; it increased at 10 min compared with that at baseline. Stroke volume decreased at 10 and 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Stroke work decreased from 5 to 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Conclusion: Our results showed that 3.0 U/mL concentration of vasopressin resulted in increased blood pressure, decreased stroke volume and stoke work, decreased preload and increased afterload, without any effect on myocardial contractility.

• Journal of Chest Surgery
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• v.29 no.8
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• pp.807-815
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• 1996

The protective effect of'ischemic preconditioning'on ischemid-reperfusion injury of heart has been reported in various animal species. but without known mechAnism in detail, In An attempt to investigate the cardioprotective mechanism of ischemic preconditioning, we examined the effects of nitric oxide(UO) synthesis in preconditioned heart of rat The isolated hearts perfused by Langendorfr's method were ex- posed to 30min global ischemia followed by 30min reperfusion with oxygenated Krebs-Henseleit(K-H) sol- ution. Ischemic preconditioning was performed with three episodes of Sm n ischemia and Smin repeyfusion before the induction of prolong ischemia(30min)-reperfusion(30min). Ischemic preconditioning prevented the depression of cardiac function(left ventricular pressure .K heart rate) observed in the ischemia- reperfusion hearts and reduced the release of lactate dehydrogenase during the reperfusion period. On electromicroscopic pictures, myocardial ultrastructures wore relatively well preserved in isthemic preconditioned hearts. N6_nitro-L-arginine methyl ester(L-NAME) an inhibitor of L-arginine citric oxide pathway, was infused at a rate O.Smllmin In a dose of 10mg kg-1 before the initial ischemic preconditioning. neither the protection of cardiac function nor the reduction of LDH releAse in ischemic preconditioning hearts was altered in the presence of added L-NAME On ultrastructural finding, the preservation of morphology in ischemic preconditioning heart was not change by the pretreatment of L-UAME. The failure of the WO synthesis inhibitor to reduce t e effect of ischemic preconditioning may be related to be species specific in that NO may allot be the trigger for ischemic preconditioning in rats.

• Clinical and Experimental Pediatrics
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• v.49 no.11
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• pp.1202-1210
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• 2006

Purpose : A quantitative and easily measured Doppler index of combined systolic and diastolic ventricular myocardial performance (Tei index) was recently proposed as a potentially useful predictor of global myocardial performance. However, presence of heart rate fluctuation makes it unreliable. Therefore, the modified Tei index was introduced by using tissue Doppler imaging (TDI) which enables measuring contraction and relaxation velocities from myocardium simultaneously. The purpose of this study was to investigate the effectiveness of the modified Tei index in the evaluation of global cardiac function. Methods : Forty eight patients in the acute phase of Kawasaki disease (KD) were studied. These patients were divided into two groups according to the modified Tei index. TDI and conventional echocardiography were performed. Systolic velocity, systolic displacement, E' velocity, E' displacement, A' velocity and A' displacement were measured at the base, mid-septum and the apex of the interventricular septum. Ejection fraction (EF), Tei index and modified Tei index were estimated. Results : Modified Tei index correlated negatively with systolic displacement, E' displacement and A' displacement at the base. Modified Tei index correlated positively with ESR and CRP. EF and Tei index were normal in KD patients. Conclusion : Modified Tei index is a safe, feasible and sensitive index for evaluating global ventricular functions in spite of normal EF and Tei index in KD.

• Journal of Preventive Medicine and Public Health
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• v.31 no.2 s.61
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• pp.183-198
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• 1998

In order to determine the prevalence rate and find out the sexual difference of abnormal electrocardiographic findings manifested by computerized EKG, which is equipped with auto-analyzing function, a total of 2,083 electrocardiograms that were taken from population over 20 years-old from October 1996 to February 1997 were studied according to their age, gender and blood pressure. 1. Using the electrocardiography with auto-analyzing function, 33 kinds of abnormal findings were manifested. The prevalence rate of abnormal findings was 52.8% in male and 43.7% in female. Among them, the most common finding was sinus brady-cardia found in 17.6% of male and 15.4% of female. Left ventricular hypertrophy by voltage criteria, minimal voltage of left ventricular hypertrophy, left axis deviation and atrial fibrillation were more common in male than in female statistically. Both of nospecific T wave and ST segment abnormality were more common in female than in male statistically. 2. Thirty-three kinds of abnormal findings were manifested. They revealed one abnormal finding alone or combined with some other ones making 128 kinds of abnormal finding. The most common abnormal finiding that manifested alone was right axis deviation (100%), then myocardial ischemia (95.7%) the next. The most common abnormal finding that complexed with other abnormal findings were left anterior fascicular block(percentage of single manifestation, 26.2%) and nonspecific T wave abnormality(percentage of single manifestation; 32.9%). Also, combination of sinus bradycardia and minimal voltage of left ventricular hypertrophy, and combination of sinus bradycardia and left ventricular hypertrophy were included in 25th sequences of abnormal findings. 3. The prevalence rate of abnormal electrocardiographic findings were higher in older group, hypertensive group, and the group of higher systolic or diastolic pressure in both sexes. 4. Abnormal findings that commonly manifested with sinus bradycardia were voltage criteria or minimal voltage of left ventricular hypertrophy(38.6%): sinus arrhythmia(10.5%): nonspecific T wave or ST segment abnormality(18.4%) and first degree AV block(7.2%) in descending order. 5. The most common site which manifested myocardial ischemia was posterior and inferior wall with equal percentage of 23.4%. And then anterior wall(19.1%), and antero-lateral wall and septum with equal percentage of 10.6% was noted in descending order.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.3
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• pp.209-217
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• 2024

In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague-Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.

• Korean Journal of Radiology
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• v.22 no.3
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• pp.324-333
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• 2021

Objective: The clinical course of an individual patient with heart failure is unpredictable with left ventricle ejection fraction (LVEF) only. We aimed to evaluate the prognostic value of cardiac magnetic resonance (CMR)-derived myocardial fibrosis extent and to determine the cutoff value for event-free survival in patients with non-ischemic cardiomyopathy (NICM) who had severely reduced LVEF. Materials and Methods: Our prospective cohort study included 78 NICM patients with significantly reduced LV systolic function (LVEF < 35%). CMR images were analyzed for the presence and extent of late gadolinium enhancement (LGE). The primary outcome was major adverse cardiac events (MACEs), defined as a composite of cardiac death, heart transplantation, implantable cardioverter-defibrillator discharge for major arrhythmia, and hospitalization for congestive heart failure within 5 years after enrollment. Results: A total of 80.8% (n = 63) of enrolled patients had LGE, with the median LVEF of 25.4% (19.8-32.4%). The extent of myocardial scarring was significantly higher in patients who experienced MACE than in those without any cardiac events (22.0 [5.5-46.1] %LV vs. 6.7 [0-17.1] %LV, respectively, p = 0.008). During follow-up, 51.4% of patients with LGE ≥ 12.0 %LV experienced MACE, along with 20.9% of those with LGE ≤ 12.0 %LV (log-rank p = 0.001). According to multivariate analysis, LGE extent more than 12.0 %LV was independently associated with MACE (adjusted hazard ratio, 6.71; 95% confidence interval, 2.54-17.74; p < 0.001). Conclusion: In NICM patients with significantly reduced LV systolic function, the extent of LGE is a strong predictor for long-term adverse cardiac outcomes. Event-free survival was well discriminated with an LGE cutoff value of 12.0 %LV in these patients.