• Journal of Cardiovascular Imaging
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• v.30 no.3
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• pp.153-168
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• 2022

Recent studies have shown that sodium/glucose cotransporter 2 (SGLT2) inhibitors might exert favourable changes on cardiac parameters as observed on cardiovascular imaging. We conducted a systematic review and meta-analysis to determine the effects of SGLT2 inhibitors on cardiac imaging parameters. Four electronic databases (PubMed, Embase, Cochrane, Scopus) were searched for studies in which the effects of SGLT2 inhibitors on cardiac imaging parameters were examined. Studies in which a population was administered SGLT2 inhibitors and analysed by echocardiography and/or cardiac magnetic resonance (CMR) imaging were included. Random-effects pair-wise meta-analysis models were utilized to summarize the studies. A total of 11 randomized controlled trials was included with a combined cohort of 910 patients. Comparing patients receiving SGLT2 inhibitors with subjects receiving placebo, the mean change in CMR-measured left ventricular mass (LVM) was -3.87 g (95% confidence interval [CI], -7.77 to 0.04), that in left ventricular end-systolic volume (LVESV) was -5.96 mL (95% CI, -10.52 to -1.41) for combined LVESV outcomes, that in left atrial volume index (LAVi) was -1.78 mL/m² (95% CI, -3.01 to -0.55) for combined LAVi outcomes, and that in echocardiography-measured E/e' was -0.73 (95% CI, -1.43 to -0.03). Between-group differences were not observed in LVM and LVESV after indexation. The only between-group difference that persisted was for LAVi. Treatment with SGLT2 inhibitors resulted in reduction in LAVi and E/e' on imaging, indicating they might have an effect on outcomes associated with LV diastolic function.

• Journal of Chest Surgery
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• v.32 no.5
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• pp.422-427
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• 1999

Background: Tachycardia induced heart failure model would be the model of choice for the dilated cardiomyopathy. This more closely resembles the clinical syndrome and does not require major surgical trauma, myocardial ischemia and pharmacological or toxic depression of cardiac function. When heart failure is progressive, application of new surgical procedures to the faling heart is highly risky. It has been shown that recovery trajectory from heart failure is a new method in decreasing animal mortality. The purpose is to establish the control datas for recovery trajectory in the canine heart failure model. Material and Method: 21 mongrel dogs were studied at 4 stages(baseline, at the heart failure, 4 and 8 weeks after recovery). Heart failure was induced during 4 weeks of continuous rapid pacing using a pacemaker. Eight weeks of trajectory of recovery period was allowed. Indices of left ventricular function and dimension were measured every 2 weeks and the hemodynamics were measured by use of Swan-Ganz catheterization and thermodilution method every 4 weeks. Values were expressed as mean${\pm}$standard deviation. Result: 4(20%) dogs died due to heart failure. Left ventricular end-diastolic volume at the 4 stages were 40.8${\pm}$7.4, 82.1${\pm}$21.1, 59.9${\pm}$7.7 and 46.5${\pm}$6.5ml. Left ventricular end-systolic volume showed the same trend. Ejection fractions were 50.6${\pm}$4.1, 17.5${\pm}$5.8, 36.3${\pm}$7.3, and 41.5${\pm}$2.4%. Blood pressure and heart rate showed no significant changes. Pressures of central vein, right ventricle, pulmonary artery, and pulmonary capillary wedge showed significant increase during the heart failure period, normalizing at the end of recovery period. Stroke volumes were 21.5${\pm}$8.2, 12.3${\pm}$3.5, 17.9${\pm}$4.6, and 15.5${\pm}$3.4ml. Blood norepinephrine level was 133.3${\pm}$60.0pg/dL at the baseline and 479.4${\pm}$327.3pg/dL at the heart failure stage(p=0.008). Conclusion: Development of tachycardia induced heart failure model is of high priority due to ready availability and reasonable amenability to measurements. Recovery trajectory after cessation of tachycardia showed reduction of cardiac dilatation and heart function. Application of new surgical procedures during the recovery period could decrease animal mortality.

• Journal of Chest Surgery
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• v.36 no.4
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• pp.242-254
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• 2003

Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of 25℃ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups. All hearts were perfused at 37℃ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained. Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37℃, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4℃) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at 25℃, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minutes (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37℃ normothermic ischemia and 30 minutes of reperfusion (n=6). Group 4 served as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, improving the LVSP, LVEDP, RPP, and LVdp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.

• Journal of Chest Surgery
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• v.36 no.5
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• pp.242-254
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• 2003

Background: Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of $25^{\circ}C$ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups All hearts were perfused at 37$^{\circ}C$ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained, Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37$^{\circ}C$, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4$^{\circ}C$) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at $25^{\circ}C$, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minuts (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37$^{\circ}C$ normothermic ischemia and 30 minutes of reperfusion (n=6) Group 4 soloed as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, Improving the LVSP, LVEDP, RPP, and LV dp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.

• Journal of Chest Surgery
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• v.39 no.1 s.258
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• pp.18-27
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• 2006

Background: Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly, but is one of the most common causes of myocardial ischemia which would result in high mortality within the first year of life. This is our early result of the surgical management for these patients. Material and Method: From June 1989 to July 2003, 6 patients with ALCAPA and one patient with ARCAPA (Anomalous origin of the Right coronary artery from the pulmonary artery) underwent surgical repair. We have reviewed the all medical records, electrocardiogram, chest X-ray and echocardiography retrospectively. Result: Three of the patients were boys and four were girls. The median age at the operation was 5.4 months (Range: 3$\∼$33 months). The average body weight of at the operation was 6.7 kg (Range: 3.7$\∼$11.3 kg). A mean follow up period was 18 months. Only 3 patients were initially diagnosed as ALCAPA. And 3 patients had moderate mitral regurgitation. Immediate coronary artery reimplantation on diagnosis with the aim of restoring a two-coronary system circulation was done. The average bypass time was 114$\pm$37 minutes, and the average aortic cross clamping time was 55$\pm$22 minutes. The average stay of intensive care unit was 5$\pm$3 days, the mean mechanical ventilator time was 38$\pm$45 hours and the hospital stay after operation was 12$\pm$5 days. There were significant improvements in electrocardiogram and chest X-ray of the all patients except one late death patient. The ventricular function showed almost normal recovery after operation; the EF (Ejection Fraction) increased from 41.2$\pm$ 10.3$\%$ to 60.5$\pm$ 15.8$\%$ within 1 month and to 59.8$\pm$13.9$\%$ within 1 year after operation, the SF (Shortening Fraction) increased from 23.6$\pm$4.7$\%$ to 38.6$\pm$8.4$\%$ within 1 month and to 37.4$\pm$7.9$\%$ within 1 year after operation, LVEDDI (Left Ventricular End-diastolic Dimension Index) decreased from 100.8$\pm$25.6 mm/$m^{2}$ to 90.3$\pm$ 19.2 mm/$m^{2}$ within f month and to 79.3$\pm$ 15.8 mm/$m^{2}$ within 1 year after operation. Concomitant mitral repair was done in two patients with anterior mitral leaflet prolapse. In every patient, mitral valve showed less than mild regurgitation during follow up. One late death occurred in which patient Dor procedure was applied 10 months after initial operation due to the dilated cardiomyopathy Conclusion: In the management of this rare and could be fatal Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA), early suspicion and correct diagnosis is of most important. But, after diagnosis, immediate restoration of 2 coronary systems could result in good outcome.

• Journal of Chest Surgery
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• v.30 no.4
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• pp.383-389
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• 1997

From March, 1992 to March, 1996, a total of 279 patients underwent coronary bypass surgery at the Sejong General Hospital, Puchon. We selected 22 patients with severe left ventricular(LV) dysfunction from them. The criteria were the presence of global or segmental abnormalities of left ventricular contraction and LV ejection fraction(EF) less than 35% based on biplane LV angiography by planimetry method. The mean age of 17 male and 5 female patients was 60$\pm$5.6years(range:47~73 years). All had the anginas, which were Canadian class II in 6, class 111 in 12 and class IV in 4. All patients except one had the history of previous myocardial infarction more than once. Seven of them had the symptoms and signs of congestive heart failure, such as dyspnea on excertion and increased pulmonary vascular markings. Their mean LVEF was 29.4$\pm$4 5%(range : 18~35%) and mean LV end-diastolic pressure was 18.7 $\pm$8. 2mmHg(range:10~42mmHg). 21 patients had 3 vessel-disease and 1 had 2 vessel-disease. Complete revascularization was tried with the use of 16 internal mammary arteries and 60 sapheuous veins and 3 radial arteries grafts. The mean number of distal anastomosis was 3.5$\pm$ 1.1. Concomitantly, one mitral valvuloplasty and annuloplasty was performed in the patient with moderate mitral regurtigation. The hospital mortality was 4.5%. During the follow-up, there were 3 late deaths. Of 18 survivors, 2 patients were lost in follow-up 24 and 27 month respectively after operation and the remaining 16 patients have bcen followed up with an average of 30.4 $\pm$ 13.4 months.15 patients had improvement with respect to angina but 8 patients still have the continuing or progressing heart failure. The 1-year, 2-year and 3-year actuarial survival rate was 85.2, 69.1, 46.1%, respectively. This study indicates that coronary artery bypass sur ery can be performed in the patients with severe LV dysfunction at acceptable risk but does not greatly contribute to the improvement of congestive heart failure.

• Clinical and Experimental Pediatrics
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• v.57 no.5
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• pp.232-239
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• 2014

Purpose: Mitochondrial disease (MD) and Duchenne muscular dystrophy (DMD) are often associated with cardiomyopathy, but the myocardial variability has not been isolated to a specific characteristic. We evaluated the left ventricular (LV) mass by echocardiography to identify the general distribution and functional changes of the myocardium in patients with MD or DMD. Methods: We retrospectively evaluated the echocardiographic data of 90 children with MD and 42 with DMD. Using two-dimensional echocardiography, including time-motion (M) mode and Doppler measurements, we estimated the LV mass, ratio of early to late mitral filling velocities (E/A), ratio of early mitral filling velocity to early diastolic mitral annular velocity (E/Ea), stroke volume, and cardiac output. A "z score" was generated using the lambda-mu-sigma method to standardize the LV mass with respect to body size. Results: The LV mass-for-height z scores were significantly below normal in children with MD ($-1.02{\pm}1.52$, P<0.001) or DMD ($-0.82{\pm}1.61$, P =0.002), as were the LV mass-for-lean body-mass z scores. The body mass index (BMI)-for-age z scores were far below normal and were directly proportional to the LV mass-for-height z scores in both patients with MD (R =0.377, P<0.001) and those with DMD (R =0.330, P=0.033). The LV mass-for-height z score correlated positively with the stroke volume index (R =0.462, P<0.001) and cardiac index (R =0.358, P<0.001). Conclusion: LV myocardial atrophy is present in patients with MD and those with DMD and may be closely associated with low BMI. The insufficient LV mass for body size might indicate deterioration of systolic function in these patients.

• The Korean Journal of Nuclear Medicine
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• v.26 no.1
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• pp.58-64
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• 1992

We performed exercise radionuclide ventriculography to evaluate left ventricular (LV) function in 35 patients with pure mitral stenosis (MS). There were 6 males and 29 females ranging from 21 to 63 years of age (mean $37{\pm}10$ years). We also studied 8 healthy men as control group (mean age $27{\pm}5$ years). Each patients was evaluated at rest and during maximal exercise on an isokinetic bicycle ergometer. Peak filling rate (PFR), peak ejection rate (PER), ejection fracion (EF), end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and cardiac output (CO) were determined by the radionuclide technique. The results were summarized as follows: 1) LV systolic dysfunction and reduced PFR were noted in patients with MS. 2) EDV as well as SV decreased with exercise in patients with MS. 3) No significant increase in EF during exercise compared to rest value was observed because it was caused by reduced EDV and SV during exercise in patients with MS. 4) CO increased with exercise was significantly lower than normal in patients with MS. 5) Patients with MS were divided into two groups according to whether SF increased more than 5% druing exercise compared to resting state or decreased. Significant difference were found between these two groups. Patients with a fall in EF with exercise were older, had larger left atrial size, and had lesser decreased in ESV during exercise.

• Journal of Chest Surgery
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• v.37 no.1
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• pp.19-26
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• 2004

Background: The aims of this study are to verify the result of the surgical treatment of ALCAPA and to identify the postoperative changes of left ventricular dimensions and mitral regurgitation (MR), Material and Method: Fifteen patients operated on since 1985 were included in the study. The patients operated on before 1998 (n=9) showed heterogeneous properties with various surgical strategies and cardiopulmonary bypass techniques. However, six patients were operated on with the established surgical strategy since 1998; 1) Dual perfusion and dual cardioplegic solution delivery through ascending aorta and main pulmonary artery, 2) Coronary transfer by rolled-conduit made of pulmonary artery wall flap, and 3) Additional mitral valvular procedure was not peformed. Result: Median age of the study group was 6 months (1 month to 34 years). The operative methods were left subclavian artery to left coronary artery anastomosis in 1, simple ligation in 2, Takeuchi operation in 2, and coronary reimplantation in 10 patients. The mean follow up period was 5.5<5.8 years (2 months 14 years), There were one early death (6.7%) and one late death. Overall 5-year survival rate was 85.6$\pm$9.6%. The Z-value of left ventricular end-diastolic and end-systolic dimensions were 6.4$\pm$3.0 and 5.1 $\pm$3.6 preoperatively, and decreased to 1.7$\pm$ 1.9 and 0.8$\pm$ 1.6 in 3 months (p<0.05). Significant preoperative MR was identified in 6 patients (40%) and all the patients showed immediate improvement of MR within f month postoperatively. There were 3 cases of reoperation due to coronary anastomosis site stenosis and recurrence of MR. However, there was no mortality nor late reoperation in the patients operated on after 1998. Conclusion: The surgical treatment of ALCAPA showed favorable survival and early recovery of ventricular dimensions and mitral valvular function. Although long-term reintervention was required in some cases of earlier period, all the cases after 1998 showed excellent surgical outcome without long-term problem.

• Journal of Chest Surgery
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• v.32 no.7
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• pp.603-612
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• 1999

Background : It has been documented that brief repetitive periods of ischemia and reperfusion (ischemic preconditioning, IP) enhances the recovery of post-ischemic contractile function and reduces infarct size after a longer period of ischemia. Many mechanisms have been proposed to explain this process. Recent studies have suggested that transient increase in the intracellular calcium may have triggered the activation of protein kinase C(PKC); however, there are still many controversies. Accordingly, the author performed the present study to test the hypothesis that preconditioning with high concentration of calcium before sustained subsequent ischemia(calcium preconditioning) mimics IP by PKC activation. Material and Method : The isolated hearts from the New Zealand White rabbits(1.5∼2.0 kg body weight) Method: The isolated hearts from the New Zealand White rabbits(1.5∼2.0 kg body weight) were perfused with Tyrode solution by Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to 45-minute global ischemia followed by a 120-minute reperfusion with IP(IP group, n=13) or without IP(ischemic control, n=10). IP was induced by single episode of 5-minute global ischemia and 10-minute reperfusion. In the Ca2+ preconditioned group, perfusate containing 10(n=10) or 20 mM(n=11) CaCl2 was perfused for 10 minutes after 5-minute ischemia followed by a 45-minute global ischemia and a 120-minute reperfusion. Baseline PKC was measured after 50-minute perfusion without any treatment(n=5). Left ventricular function including developed pressure(LVDP), dP/dt, heart rate, left ventricular end-diastolic pressure(LVEDP) and coronary flow(CF) was measured. Myo car ial cytosolic and membrane PKC activities were measured by 32P-${\gamma}$-ATP incorporation into PKC-specific pepetide. The infarct size was determined using the TTC (tetrazolium salt) staining and planimetry. Data were analyzed using one-way analysis of variance(ANOVA) variance(ANOVA) and Tukey's post-hoc test. Result: IP increased the functional recovery including LVDP, dP/dt and CF(p<0.05) and lowered the ascending range of LVEDP(p<0.05); it also reduced the infarct size from 38% to 20%(p<0.05). In both of the Ca2+ preconditioned group, functional recovery was not significantly different in comparison with the ischemic control, however, the infarct size was reduced to 19∼23%(p<0.05). In comparison with the baseline(7.31 0.31 nmol/g tissue), the activities of the cytosolic PKC tended to decrease in both the IP and Ca2+ preconditioned groups, particularly in the 10 mM Ca2+ preconditioned group(4.19 0.39 nmol/g tissue, p<0.01); the activity of membrane PKC was significantly increased in both IP and 10 mM Ca2+ preconditioned group (p<0.05; 1.84 0.21, 4.00 0.14, and 4.02 0.70 nmol/g tissue in the baseline, IP, and 10 mM Ca2+ preconditioned group, respectively). However, the activity of both PKC fractions were not significantly different between the baseline and the ischemic control. Conclusion: These results indicate that in isolated Langendorff-perfused rabbit heart model, calcium preconditioning with high concentration of calcium does not improve post-ischemic functional recovery. However, it does have an effect of limiting(reducing) the infart size by ischemic preconditioning, and this cardioprotective effect, at least in part, may have resulted from the activation of PKC by calcium which acts as a messenger(or trigger) to activate membrane PKC.