• Proceedings of the Korean Society for Bioinformatics Conference
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• 2004.11a
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• pp.57-63
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• 2004

본 연구에서는 3차원 심근조직에서의 회귀성파동에 대한 수치적 해석결과를 제시한다. 심근 조직에서의 회귀성파동은 심실세동(ventricular fibrillation)의 원인으로 지목되고 있으며 심근세포 이온채널 또는 전기전도시스템 등과 같은 여러 가지 요소들이 관련된 복합적 현상으로 생각되고 있다. 지금까지 이에 관한 많은 연구가 전기생리학적 모델을 이용하여 이루어진바 있으며, 주로 동물 심근세포모델에 기반으로 균일한 2차원 또는 3차원 모델에서의 전기전도 현상 해석을 한 바 있다. 그러나 실제 심장조직의 경우, 두께를 가진 3차원적 형상을 지니고 있으며 층을 따라서 전기생리학적으로 상이한 특성을 가진 세포들로 구성된다. 즉 심근은 층을 가로질러 Epi-cardiac, mid-cardiac, endo-cardiac cell들로 구성되며 각기 다른 APD(action potential duration)을 가지고 있다. 따라서 본 연구에서는 이러한 세가지 종류의 인체 심근세포모델을 사용한 3차원 심근조직에서의 활동전위 전도현상에 대한 결과를 제시한다. 이를 위하여 기존의 인체 3가지 종류의 심근세포 모델을 구현하여 그 타당성을 검토한다. 그리고 이를 바탕으로 3차원 조직모델을 구현하는데, simplified bidomain방법을 사용하였다. 3차원 공간상에서 심근세포에 의한 활동전위 전달현상을 해석하기 위하여 유한요소법을 도입한다. 최종적으로는 3가지의 심근세포층을 가진 3차원 심근조직을 구성하고, 여기에 회귀성 파동을 유도한다. 그리고 단일층으로 이루어진 3차원조직에서의 결과와 비교 분석하여 다세포층에 의한 불균일 효과를 분석하였다.

• 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.

• The Korean Journal of Nuclear Medicine
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• v.32 no.3
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• pp.259-265
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• 1998

Purpose: We studied early rest/24 hour delay T1-201 perfusion SPECT for prediction of wall motion improvement after reperfusion in patients with acute myocardial infarction. Materials and Methods: Among 17 patients (male/female= 11/6, age: $59{\pm}13$) with acute myocardial infarction, 15 patients were treated with percutaneous transcoronary angioplasty (direct:2, delay: 11) and intravenous urokinase (2). Spontaneous resolution occurred in infarct-related arteries of 2 patients. We confirmed TIMI 3 flow of infarct-related artery after reperfusion in all patients with coronary angiography. We performed rest T1-201 perfusion SPECT less then 6 hours after reperfusion and delay T1-201 perfusion SPECT next day. T1-201 uptake was visually graded as 4 point score from normal (0) to severe defect (3). Rest T1-201 uptake ${\le}2$ or combination of rest T1-201 uptake ${\le}2$ or late reversibility were considered to be viable. Myocardial wall motion was graded as 5 point score from normal (1) to dyskinesia (5). Myocardial wall motion was considered to be improved when a segment showed an improvement ${\ge} 1$ grade in follow up echo compared with the baseline values. Results: Among 98 segments with wall motion abnormality, the severity of myocardial wall motion decrease was as follow: mild hypokinesia: 18/98 (18%), severe hypokinesia: 28/98 (29%), akinesia: 51/98 (52%), dyskinesia: 1/98 (1%). The wall motion improved in 85%. Redistribution (13%), and reverse redistribution (4%) were observed in 24 hour delay SPECT. Positive predictive value (PPV) and negative predictive value (NPV) of combination of late reversibility and rest T1-201 uptake were 99%, and 54%. PPV and NPV of rest T1-201 uptake were 100% and 52% respectively. Predictive values of combination of rest T1-201 uptake and late reversibility were not significantly different compared with predictive values of rest T1-201 uptake only. Conclusion: We conclude that early T1-201 perfusion SPECT predict myocardial wall motion improvement with excellent positive but relatively low negative predictive values in patients with acute myocardial infarction after reperfusion.

• 건강소식
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• v.36 no.2
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• pp.26-27
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• 2012

매스컴을 통해 유명인의 갑작스러운 죽음에 대한 소식을 접하곤 한다. 교통사고, 자살 등 여러 원인 가운데 급성 심근경색이 원인이 되는 경우도 있다. 최근 인기그룹 2PM의 준수 아버지가 심근경색으로 사망했고 몇해 전 그룹 거북이의 리더 터틀맨 임성훈 씨도 급성 심근경색으로 사망해 팬들을 안타깝게 했다. 급성 심근경색은 현대인 급사의 가장 많은 질환의 하나이다.

• Journal of Sasang Constitutional Medicine
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• v.13 no.1
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• pp.70-78
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• 2001

ADR유발성 심근독성에 대한 심근세포의 손상기전을 규명하기 위해 ADR의 독성을 MTT정량, NR정량, LDH활성도 및 심박동을 측정하였다. 배양된 심근세포에서 청심연자탕 전탕액의 심근세포 보호효과는 LDH활성도 측정과 심박동 측정을 통해 관찰할 수 있었다. 이 실험을 통해 다음과 같은 결과를 얻을 수 있었다. 1. ADR은 배양심근세포에서 세포의 생존능력을 떨어뜨렸고, LDH의 활성도를 높였으며, 심박동수를 감소시켰다. 2. 청심연자탕 전탕액은 배양심근세포에서 ADR에 의해 증가된 LDH 활성도를 유의하게 감소시켰다. 3. 청심연자탕 전탕액은 배양심근세포에서 ADR에 의해 감소된 심박동을 유의하게 증가시켰다. 이상의 결과를 통해 ADR은 신생 마우스에서 적출해낸 배양 심근세포에서 독성효과를 나타냈음을 알 수 있었으며, 청심연자탕 전탕액은 ADR에 의해 유발된 심근세포독성에 매우 효과적으로 방어효과를 나타냄을 알 수 있었다.

• Proceeding of EDISON Challenge
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• 2017.03a
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• pp.653-655
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• 2017

심근섬유증은 심장에서 전도 장애를 일으키며 심부전증상을 발생시킨다. 심근섬유증으로 인한 심장박동현상의 변화를 확인하기 위해 시뮬레이션 연구를 진행하였다. 심실의 유한요소 모델을 설계하고 무작위로 전도 블록을 생성하여 심근섬유증을 적용하고 그 비율을 조절하였다. 심근섬유증의 비율에 따라 전기생리학적 시뮬레이션을 진행하고 그 결과를 바탕으로 기계 수축 시뮬레이션을 진행하여 심실의 수축 변화를 확인하였다. 심근섬유증의 비율이 증가할수록 좌심실의 압력이 감소하고 박출되는 혈액량과 박출계수, 심장박동의 효율이 감소하였다.

• 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.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.109-117
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• 1989

The changes in adenosine triphosphate (ATP), creatine phosphate (CP) and lactic acid (LA) contents of guinea pig hearts were studied during the cardioplegia and recovery phase. 1) ATP and CP contents in cardiac ventricular tissue were decreased during the cardioplegia, regardless of $Ca^{2+}$ concentration in the cardioplegic solutions, and CP contents were recovered with the reperfusion of normal Tyrode solution faster than those of ATP. And there were no significant differences in the recovery of CP contents with different concentration of $Ca^{2+}$ in the cardioplegic solutions tested, while the recovery of ATP contents was faster with 15 mM $K^{+}$, 0.1 mM $Ca^{2+}$ cardioplegic solutions. 2) LA contents were increased during the cardioplegia and decreased with the reperfusion of normal Tyrode solution. 3) The more recovery time (up to 3 hrs), the more CP contents were recovered with the reperfusion of normal Tyrode solution faster than those of ATP. And LA contents were decreased as the duration of recovery time. These results suggest that $Ca^{2+}$ and $K^{+}$ concentration in the cardioplegic solution is one of the major factors influencing the recovery of cardiac tissue from the cardioplegia.

• The Korean Journal of Nuclear Medicine
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• v.31 no.1
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• pp.43-49
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• 1997

We studied to investigate the predictive values of gated SPECT for the improvement of wall motion after bypass surgery. As we compared postoperative SPECT with preoperative ones, we defined viability as wall motion improvement. We peformed rest T1-201/s1ress Tc-99m-MIBI gated SPECT in 25 patients before and 3 months after bypass surgery. Myocardial wall motion was graded as normal, hypokinesia, akinesia, and dyskinesia by pair-wise visual analysis of gated pre and postoperative SPECT's on the same monitor screen. Myocardial wall thickening was determined good or poor Among 92 segments with wall motion abnormalities before operation, 69 (75%) improved and 23 did not. Before operation, we could find segments with good systolic thickening in 64 segments among total 92. Thickening of the remaining 28 was poor. Wall motion improved postoperatively in 45 segments (70%) among 64 with good thickening. Twenty four(86%) among 28 segments with poor thickening had also improved. We grouped segments into mild(hypokinetic) and severe(akinetic/dyskinetic) ones. Among 33 segments with severe motion abnormalities, 14 had good thickening and 19 did not. Nine(60%) improved out of 14 segments having severe abnormality with good thickening However, 16(84%) segments out of 19 haying severe abnormality with poor thickening also improved. Neither degree of perfusion decrease nor severity of wall motion abnormalities could explain the high rate of false negatives. In conclusion, as we defined viability as wall motion improvement by comparing pre and postoperative SPECT, systolic thickening observed by gated Tc-99m-MIBI SPECT in myocardial segments with wall motion abnormalities predicted wall motion improvement after bypass surgery. However, poor thickening could not be referred as evidence of nonviable myocardium both in mild and severe contractile dysfunction, so that we might need stimulation study such as dobutamine echocardiography or dobutamine gated SPECT.