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정상 관상동맥조영술시 cardiac troponin I 상승의 원인
배우형,전국진,오준혁,이동원,안병재,김성호,이준상,김무영,이현국,고우석,박용현,김준,김준홍,홍택종,신영우 대한내과학회 2005 대한내과학회지 Vol.69 No.5
Background : Cardiac troponin I (cTnI) is most recently described and has nearly absolute myocardial tissue specificity, as well as high sensitivity. But an increased value for cTnI that indicates myocardial injury is not always synonym of myocardial infarction or ischemia due to coronary artery disease. Methods : Retrospective follow-up study for whom underwent coronary angiography for suspected coronary artery disease was done if they had an elevated cTnI value and angiographically normal or minimal disease. Results : 33 patients were qualified. Cut-off value for elevated cTnI was 0.06 ng/mL. Increased cTnI values were attributed to severe congestive heart failure in 7 patients, variant angina in 7 patients, myocarditis in 5 patients, pericarditis in 1 patient, severe myocardial bridge in 1 patient, rhabdomyolysis in 1 patient and cerebral infarction in 1 patient. Tachycardia was precipitating cause in 4 patients (sinus tachycardia, paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation and sustained ventricular tachycardia for each), two of whom had hemodynamic compromise. 2 of 33 patients had no identifiable cause for a rise in cTnI value. There was no acute myocardial infarction at 42±34 weeks follow-up. Conclusions : Although cTnI is a sensitive and specific marker of myocardial injury, an elevation of cTnI value may have a cause other than myocardial infarction or ischemia and may occur without significant angiographic coronary artery disease 목적 : Cardiac troponin I (cTnI)는 심근 조직에 절대적으로 높은 예민도와 특이도를 보인다. 그러나 심근 손상을 의미하는 cTnI 증가가 항상 관상동맥질환으로 인한 심근경색이나 허혈을 의미한다고 볼 수는 없다. 이에 저자들은 cTnI가 증가되어 있으면서, 관상동맥조영술에서 정상이거나 미소병변을 보이는 경우 그 유발 원인을 알아보고자 하였다. 방법 : 2002년 3월부터 2004년 2월까지 부산대학교병원을 내원한, cTnI가 상승하였으나 관상동맥조영술에서 정상소견 또는 복잡 병변이나 혈전이 관찰되지 않고 50% 미만의 협착소견인 미소병변을 보이는 33명의 환자들을 대상으로 후향적 추적조사를 시행하였다. 결과 : 유발 원인으로는 중증 심부전이 7명, 변이형 협심증이 7명, 심근염이 5명이었다. 빈맥이 유발 원인인 경우가 4명이었는데, 각각 동성 빈맥, 상심실성 빈맥, 발작성 심방세동 그리고 지속성 심실빈맥이었으며, 이들 중 2명에서 혈역학적 장애를 보였다. 그 외에 심외막염이 1명, 중증 심근교가 1명, 횡문근융해증이 1명 그리고 뇌경색이 1명이었다. 대상 환자들을 42±34주 동안 추적관찰 하였는데, 급성 심근경색증이 발생한 경우는 없었다. 결론 : cTnI가 심근손상의 매우 예민하고 특이적인 지표이지만, cTnI 상승은 심근경색이나 허혈 이외의 다른 원인에 의해 일어날 수 있고, 관상동맥조영술에서 특이소견 없이 발생할 수 있으므로 이에 대한 고려가 필요하리라 사료된다.
정상 관상동맥조영술시 cardiac troponin 1 상승의 원인
배우형 ( Woo Hyung Bae ),전국진 ( Kook Jin Chun ),오준혁 ( Jun Hyok Oh ),이동원 ( Dong Won Lee ),안병재 ( Byung Jae Ahn ),김성호 ( Seong Ho Kim ),이준상 ( Joon Sang Lee ),김무영 ( Moo Young Kim ),이현국 ( Hyeon Gook Lee ),고우석 ( 대한내과학회 2005 대한내과학회지 Vol.69 No.5
목적 : Cardiac troponin I (cTnI)는 심근 조직에 절대적으로 높은 예민도와 특이도를 보인다. 그러나 심근 손상을 의미하는 cTnI 증가가 항상 관상동맥질환으로 인한 심근경색이나 허혈을 의미한다고 볼 수는 없다. 이에 저자들은 cTnI가 증가되어 있으면서, 관상동맥조영술에서 정상이거나 미소병변을 보이는 경우 그 유발 원인을 알아보고자 하였다. 방법 : 2002년 3월부터 2004년 2월까지 부산대학교병원을 내원한, cTnI가 상승하였으나 관상동맥조영술에서 정상소견 또는 복잡 병변이나 혈전이 관찰되지 않고 50% 미만의 협착소견인 미소병변을 보이는 33명의 환자들을 대상으로 후향적 추적조사를 시행하였다. 결과 : 유발 원인으로는 중증 심부전이 7명, 변이형 협심증이 7명, 심근염이 5명이었다. 빈맥이 유발 원인인 경우가 4명이었는데, 각각 동성 빈맥, 상심실성 빈맥, 발작성 심방세동 그리고 지속성 심실빈맥이었으며, 이들 중 2명에서 혈역학적 장애를 보였다. 그 외에 심외막염이 1명, 중증 심근교가 1명, 횡문근융해증이 1명 그리고 뇌경색이 1명이었다. 대상 환자들을 42±34주 동안 추적관찰 하였는데, 급성 심근경색증이 발생한 경우는 없었다. 결론 : cTnI가 심근손상의 매우 예민하고 특이적인 지표이지만, cTnI 상승은 심근경색이나 허혈 이외의 다른 원인에 의해 일어날 수 있고, 관상동맥조영술에서 특이소견 없이 발생할 수 있으므로 이에 대한 고려가 필요하리라 사료된다. Background : Cardiac troponin I (cTnI) is most recently described and has nearly absolute myocardial tissue specificity, as well as high sensitivity. But an increased value for cTnI that indicates myocardial injury is not always synonym of myocardial infarction or ischemia due to coronary artery disease. Methods : Retrospective follow-up study for whom underwent coronary angiography for suspected coronary artery disease was done if they had an elevated cTnI value and angiographically normal or minimal disease. Results : 33 patients were qualified. Cut-off value for elevated cTnI was 0.06ng/mL. Increased cTnI values were attributed to severe congestive heart failure in 7 patients, variant angina in 7 patients, myocarditis in 5 patients, pericarditis in 1 patient, severe myocardial bridge in 1 patient, rhabdomyolysis in 1 patient and cerebral infarction in 1 patient. Tachycardia was precipitating cause in 4 patients (sinus tachycardia, paroxysmal supraventricular tachycardia, paroxysmal atrial fibrillation and sustained ventricular tachycardia for each), two of whom had hemodynamic compromise. 2 of 33 patients had no identifiable cause for a rise in cTnI value. There was no acute myocardial infarction at 42±34 weeks follow-up. Conclusions : Although cTnI is a sensitive and specific marker of myocardial injury, an elevation of cTnI value may have a cause other than myocardial infarction or ischemia and may occur without significant angiographic coronary artery disease.(Korean J Med 69:487-492, 2005)
고혈압 환자에서 좌심실비대가 심실성 부정맥 발생에 미치는 영향
배우형(Woo Hyung Bae),이현국(Hyeon Gook Lee),박융인(Yoong In Park),박용현(Yong Hyun Park),오현명(Hyun Myung Oah),임종훈(Jong Hoon Lim),안병재(Byung Jae An),김성호(Seong Ho Kim),전국진(Kook Jin Chun),홍택종(Taek Jong Hong),신영우(Yung 대한내과학회 1999 대한내과학회지 Vol.56 No.4
N/A Objectives:Left ventricular hypertrophy(LVH) increases the risk of sudden death in hypertensive patients and this is known due to ventricular arrhythmias. Thus, author studied the relationship between LVH as a hypertensive target organ damage and ventricular arrhythmias. Methods:24-hour ambulatory electrocardiographic monitoring, measurement of microalbumin in 24-hour urine and fundoscopic examination were performed on 100 hypertensives (50 patients without LVH and 50 patients with LVH on EKG) who admitted Pusan National University Hospital. Results:In patients with LVH, ventricular extrasystoles occurred more frequently than without LVH(p<0.05) and ventricular couplet and ventricular tachycardia were more common but statistically not different. Microalbuminuria and hypertensive retinopathy were more severe in patients with LVH than without LVH(p<0.05 and p<0.01, respectively). Conclusion:Of the ventricular arrhythmias, ventricular extrasystole but not ventricular couplet and ventricular tachycardia occurred more frequently in patients with LVH than without LVH. Thus, prospective study with long-term follow up should be done to establish the relationship between hypertensive LVH and cardiovascular mortality, especially sudden death. And, further study should be done to make the relationship between reduction in LVH with antihypertensive therapy and reduction in LVH-associated ventricular arrhythmias.
허혈성 심질환 환자에서 Sirolimus 용출성 스텐트 삽입술시 과확장의 안전성과 효과
이승은,배우형,김남식,윤성한,이한철,김준,김준홍,전국진,홍택종,신영우 대한노인병학회 2008 Annals of geriatric medicine and research Vol.12 No.1
Background: We have no information about the safety and effectiveness when we perform overdilating a sirolimuseluting stent (SES) with high pressure. In some specific animal model, the study reported overdilatation of SES with high pressure resulted in increase of restenosis. The aim of this study was to evaluate the safety and effectiveness of overdilatation of SES with high pressure. Methods: 97 patients underwent PCI using SES between August 2003 and July 2005 were divided into two group(high pressure group, low pressure group), stents were implanted with high pressure (>18 atm) and low pressure (<12 atm). We compared between the two group of safety of stents, major adverse cardiac events (MACE), rate of restenosis, late loss. Results: In high pressure group, there are more type C lesion (51% vs 38%, p<0.01). There were no significant differences between the two groups regarding MACE (12.8% vs 17.2%, p=0.78), in-stent restenosis rate (2.6 % vs 5.2%, p=0.65). There are small increasing of late loss in high pressure group, but no statistically significant difference (0.30 vs 0.15, p=0.05). Conclusion: Implantation of SES overdilated with high pressure is able to be performed safely to obtain wider inner lumen of stents.