• 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.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.82-82
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• 1993

허혈-재관류손상 심근세포의 DNA에서 8-hydroxydeoxyguanosine (8-OHdG) 생성을 검토하였다. 흰쥐 적출심장의 Langendorff 관류 표본에서 대동맥 차단에 의한 60분 허혈후 산소가 포화된 Kredb-Henseleit용액으로 30분간 재관류 하므로서 허혈-재관류 손상을 유도하였다. 재관류 후 심근세포에서 DNA를 추출하고 HPLC(EC detector)를 이용하여 8-OHdG를 측정하였다. 실험결과 허혈-재관류 심근세포의 DNA에서 8-OHdG 함량이 증가하였으며 이는 $O_2$ 제거물질인 superoxide dismutase와 OH 제거물질인 mannitol에 의하여 방지되었다. Xanthine oxidase외 경쟁적 길항약인 allopurinol도 8-OHdG 생성을 억제하였으며 단백분해효소 억제제인 phenylsulfonylfluoride 그리고 관류액에서 칼슘의 제거 또한 허혈-재관류 심근 DNA의 생성을 방지하였다. 이상의 결과 허혈심근의 재관류시 8-OHdG 생성이 증가하며 이는 재관류 손상과 같은 산화성 심근손상을 평가하는 좋은 Index가 될 수 있을 것으로 여겨진다.

• Journal of Chest Surgery
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• v.30 no.11
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• pp.1083-1091
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• 1997

This study was purposed to assess the result of coronary artery bypass graft surgery by analyzing and comparing the pre and postoperative myocardial perfusion state quantitatively by using myocardial SPECT. Twenty patients who received coronary artery bypass graft surgery since 1993 underwent both preoperative and postoperative myocardial SPECT and the result were analyzed. The mean age was 56.4$\pm$9.0 years, and the patients were composed of thirteen males and seven females. For quantitative analysis, we used polar maps of SPECT generated by Cedars-Sin i Medical Center program and we calculated perfusion scores, ischemic myocardial area ratios and reperfusion scores from polar maps. Preoperative mean stressfrest perfusion score was 7.3$\pm$ 1.117.7$\pm$ 1.0 and postoperative score was 8.1 $\pm$ 1 118.3$\pm$ 1.1. Preoperative mean stress ischemic myocardial area ratio was 0.32$\pm$0.2 and postoperative ratio was 0.15 $\pm$0.1. Postoperative mean perfusion score was significantly increased but, on the other hand, mean ischemic myocardial area ratio was significantly decreased as compared with preoperative values(p<0.01). Preoperative mean perfusion score of patients with postoperative roper(usion score more than 1.5 was significantly higher(p<0.01) than that of patients with postoperative reperfusion score less than 1.5. Preoperative perfusion scores of coronary artery territories that had fixed perfusion defect at myocardial SPECT were significantly low(4.3 $\pm$0.514.6$\pm$0.6, stresslrest), nevertheless it proved quantitatively that there was improvement in myocardial perfusion after surgery by showing improved perfusion scores postoperatively. In conclusion, myocardial SPECT is useful method for quantitative analysis of the myocardial perfusion state after coronary artery bypass grafting surgery.

• Tuberculosis and Respiratory Diseases
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• v.46 no.5
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• pp.645-653
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• 1999

Introduction : Although myocardial ischemia tends to occur more frequently than can he documented in ventilated patients, it has not been well studied on the factors related to the occurrence of the ischemia. Methods : To investigate the related factors to ischemia development, a prospective study was done in 95 cases with consecutive 73 patients who had received mechanical ventilation(MV) in MICU. In addition to 24 h holter monitoring, echocardiogram, electrolytes, cardiac enzymes, hemodynamic, and gas exchange measurements were done within 24 h after initiation of MV in 69 cases. The measurements were repeated at weaning period in 26 cases. The ischemia was defined by the ST segment changes; up-sloping depression more than 1.5 mm or down-sloping or horizontal depression more than 1.0 mm from isoelectric baseline for 80 ms following J point. Results : Twelve patients(12.6% in 95 cases) developed ischemia in total. The incidence of ischemia development showed an increased tendency in the initial 24 hr after MV (15.9%) and in patients with left-sided heart failure found by echocardiogram (18.2%) compared with that of the weaning period (3.8%) and patients without heart failure (10.9%) (P=0.12, P=0.09, in each). There were no differences in APACHE III score, baseline ECG findings, electrolytes abnormalities, use of inotropics or bronchodilators, presence of sepsis or shock, mode of ventilation, and survival rate according to the development of ischemia. Maximal heart rates and mean arterial pressure also were not different between patients with ($137.2{\pm}30.9/min$, $82.5{\pm}15.9$ mm Hg) and without ischemia ($l29.5{\pm}29.7/min$, $83.8{\pm}17.6$ mm Hg). Conclusion : Although the incidence of myocardial ischemia was 12.6% in total, there were no clinically predictable factors to the development of ischemia during mechanical ventilation.

• Applied Microscopy
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• v.19 no.1
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• pp.1-18
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• 1989

It has been debated whether postischemic reperfusion is necessarily beneficial to salvage the myocardium after ischemic insult or not. Therefore, this study was undertaken to compare the ultrastructural changes as well as the distribution of $Ca^{2+}$ in the ventricular myocardial cells after transient ischemia and after postischemic reperfusion, and to suspect to what extent the postischemic reperfusion is beneficial. After 10 minutes of ischemia, the heart developed wide I bands, glycogen depletion, intramyofibrillar edema, mitochondrial swelling, clumping and migration of chromatin, ghosts of lipid droplets, disintegration of cell junctions, sarcolemmal disruption, and loss of $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria. In spite of reperfusion, in a large number of cells, the ultrastructure was more severely damaged, however, $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria restored. These results suggest that postischemic reperfusion may help the myocardial cells to restore their function to control $Ca^{2+}$ to a certain extent, but that it could aggravate the ischemic insult.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.15 no.10
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• pp.2223-2230
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• 2011

ECG is used to diagnose heart diseases such as myocardial ischemia, arrhythmia and myocardial infarction. Particularly, myocardial ischemia causes the shape change of the ST segment, this change is transient and may occur without symptoms. So it is important to detect the transient change of ST segment through long term monitoring. ST segment classification algorithm for making diagnosis myocardial ischemia is presented in this paper. The first step in the ST segment shape classification process is to detect R wave point and feature points based adaptive threshold and window. And then, the suggested algorithm detects the ST level change, To classify the ST segment shape, the suggested algorithm uses the slope values of the four points between the S and T wave. The ECG data in the European ST-T database were used to verify the performance of the developed algorithm. The best correct rate was 99.40% and the worst correct rate was 68.48%.

• Investigative Magnetic Resonance Imaging
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• v.6 no.1
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• pp.5-20
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• 2002

허혈성 심질환 환자의 평가도구로서 MRI의 역할이 확대된 데에는 소위 "one-stop shop"이라는 통합적 심장검사법의 개발이 계기가 되었다. 즉 한 번의 MRI 검사로서 심실벽운동을 평가하여 심근의 기능과 예비능을 측정하여 만성 심근경색을 평가할 수 있고, 심근의 관류를 평가할 수 있고, 관동맥의 혈류 예비능과 심근의 viability를 평가하고, 관동맥 조영술을 통해, 수술 후의 우회로 평가 및 관동맥의 협착 여부의 진단이 가능한 프로토콜이 MRI장비마다 각각 개발되어 보급되고 있다. 하드웨어와 소프트웨어의 개발과 지속적인 연구를 통해서 MRI는 허혈성 심질환의 진단적 검사로서 기존의 다른 검사들과 비교하여 높은 시간적, 공간적 해상력으로 정확한 구조와 기능의 평가를 제공할 수 있는 가장 유용한 검사가 될 것으로 사료된다 특히, MR 관동맥조영술, 심근관류검사, 심근 표지법, dobutamine 부하검사, viability 평가, plaque characterization, MR spectroscopy 분야에서 현재 활발히 연구가 진행되고 있으며 향후 임상적용이 확대될 것으로 예상된다.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.164-164
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• 1993

Nicorandil의 심근허혈 감소효과를 평가하고운동부하 201-Thallium 심근허혈 감소효과의 임상적 판정에 적용 가능성 여부를 알아보고자 하였다. 대상 및 방법: 위약투여 후 시행한운동부하 201-thallium-SPECT 상에서 가역적 thallium 결손을 보였던 49명의 노작성 협심증 환자들을 대상으로 하여 7일후 nicorandil을 10mg (group 1:n=19)혹은 20mg (group 2: n=20) 1회 경구투여한후 다시 운동부하201- thallium-SPECT를 시행하여 비교 분석하였다. 다답차운동 부하의 최대 운동량에 도달시 201-thallium을 정주하여 1분간 운동을 지속시킨후 부하영상을 얻고 안정 4시간후 재촬영하여 thallium결손 범위를 비교하여 심근허혈 범위를 정하였다.

• Journal of Chest Surgery
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• v.37 no.2
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• pp.119-130
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• 2004

Decrease in cardiac function after open heart surgery is due to an ischemia induced myocardial damage during surgery, and ischemic preconditioning, a condition in which the myocardial damage does not accumulate after repeated episodes of ischemia but protects itself from damage after prolonged ischemia due to myocytes tolerating the ischemia, is known to diminish myocardial damage, which also helps the recovery of myocardium after reperfusion, and decreases incidences of arrythmia. Our study is performed to display the ischemic preconditioning and show the myocardial protective effect by applying cardioplegic solution to the heart removed from rat. Material and Method: Sprague-Dawley male rats were used, They were fixed on a modified isolated working heart model after cannulation. The reperfusion process was according to non-working and working heart methods and the working method was executed for 20 minutes in which the heart rate, aortic pressure, aortic flow and coronary flow were measured and recorded. The control group is the group which the extracted heart was fixed on the isolated working heart model, recovered by reperfusion 60 minutes after infusion and preserved in the cardioplegic solution 20 minutes after the working heart perfusion and aortic cross clamp, The thesis groups were divided into group I, which ischemic hearts that were hypoxia induced were perfused by cardioplegic solution and preserved for 60 minutes; group II, the cardioplegic solution was infused 45 seconds (II-1), 1 minutes (II-2), 3 minutes (II-3), after the ischemia induction, 20 minutes after working heart perfusion and aortic cross clamp; and group III, hearts were executed on working heart perfusion for 20 minutes and aortic cross clamp was performed for 45 seconds (III-1), 1minute (III-2), 3 minutes (III-3), reperfused for 2 minutes to recover the heart, and then aortic cross clamping was repeated for reperfusion, all the groups were compared based on hemodynamic performance after reperfusion of the heart after preservation for 60 minutes. Result: The recovery time until spontaneous heart beat was longer in groups I, II-3, III-2 and III-3 to control group (p<0.01). Group III-1 (p<0.05) had better results in terms of recovery in number of heart rates compared to control group, and recovered better compared to II-1 (p<0.05). The recovery of aortic blood pressure favored group III-1 (p<0.05) and had better outcomes compared with II-1 (p<0.01). Group III-1 also showed best results in terms of cardiac output (p<0.05) and group III-2 was better compared to II-2 (p<0.05). Group I (p<0.01) and II-3 (p<0.05) showed more cardiac edema than control group. Conclusion: When the effects of other organs are dismissed, protecting the heart by infusion of cardioplegic solution after enforcing ischemia for a short period of time before the onset of abnormal heart beats for preconditioning has a better recovery effect in the cardioplegic group with preconditioning compared to the cardioplegic solution itself. we believe that further study is needed to find a more effective method of preconditioning.