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시술 전 아미노필린 투여가 회전형 죽상반절제술시 서맥성 부정맥의 발생과 혈역학 변화에 미치는 영향
차광수 ( Cha Gwang Su ),김무현 ( Kim Mu Hyeon ),김영대 ( Kim Yeong Dae ),김진우 ( Kim Jin U ),김신재 ( Kim Sin Jae ),김종성 ( Kim Jong Seong ) 대한내과학회 2003 대한내과학회지 Vol.64 No.6
목적 : 우관상동맥 또는 우위성 좌회선동맥에서의 회전형 죽상반절제술은 서맥성 부정맥을 초래할 수 있어 예방적 심박조율기의 설치를 필요로 한다. 아데노신은 허혈 또는 저산소증때 세포에서 유리되며 관상동맥 혈류장애와 연관되는 서맥성 부정맥을 매개한다. 아데노신 수용체 길항제인 아미노필린은 저산소증때 유발되는 서맥성부정맥을 예방한다고 알려진다. 이 연구의 목적은 시술 전 아미노필린 투여가 회전형 죽상반절제술시 서맥성 부정맥의 발생과 혈역학 변화에 미치는 영향 Background : Rotational atherectomy or rotablation in right coronary artery (RCA) or dominant left circumflex artery (LCX) can cause bradyarrhythmias and requires the placement of prophylactic pacemaker. Adenosine is released endogenously by ischemic or h
돼지 관상동맥 스텐트 재협착 모델에서 Carvedilol 부착 Biodiv Ysio(TM) 스텐트의 신생내막 증식 억제 효과
김원 ( Kim Won ),정명호 ( Jeong Myeong Ho ),차광수 ( Cha Gwang Su ),이승현 ( Lee Seung Hyeon ),홍영준 ( Hong Yeong Jun ),김주한 ( Kim Ju Han ),안영근 ( An Yeong Geun ),박옥영 ( Park Og Yeong ),김무현 ( Kim Mu Hyeon ),조정관 ( Jo 대한내과학회 2004 대한내과학회지 Vol.66 No.1
목적 : Carvedilol은 알파 및 베타수용체 차단제로서 혈관 평활근 세포의 이동과 증식을 억제하며, 동물실험에서 신생내막의 증식을 효과적으로 억제하였다. 저자 등은 돼지 관상동맥 스텐트 재협착 모형을 이용하여 carvedilol 부착 스텐트의 스텐트 내 신생내막 증식 억제와 스텐트 재협착의 예방에 대한 효과를 알아보고자 하였다. 방법 : 실험용 동물은 25~35 kg의 암돼지를 aspirin과 ticlopidine으로 전처치하고, 확립된 방법을 이 Background : Carvedilol is a beta- and alpha-receptor blocker, a direct inhibitor of smooth muscle cell proliferation and migration, and produces a significant suppression of neointimal hyperplasia in rat carotid injury model. We tested whether carvedilol
방실결절회귀성 빈맥의 유발에 관여하는 심전기생리학적 인자에 관한 연구
조정관(Jeong Gwan Cho),신순철(Soon Chul Shin),류제영(Jay Young Rhew),배열(Youl Bae),김준우(Jun Woo Kim),김성희(Sung Hee Kim),김주한(Ju Han Kim),서정평(Jeong Pyeong Seo),박종철(Jong Chul Park),차광수(Gwang Su Cha),박주형,정명호(Myung Ho 대한내과학회 1997 대한내과학회지 Vol.52 No.6
N/A Objectives: Although a subtle balance between conduction time of the antgrade slow pathway and refractory period of the retrograde fast pathway is known to play the most critical role in the induction of AV nodal reentrant tachycardia(AVNRT), other electrophysiologic factors such as concealed conduction in to the fast pathway have been suggested to be responsible. The present study was performed to determine the electrophysiologic factors responsible for the induction of AVNRT. Methods: Total 34 subjects undergoing electrophysiologic study(EPS) including 9 normal subjects(SAVNP), 7 subjects with dual AV nodal pathways(DAVNP) but no inducible AVNBT, and 18 inducible AVNRT patients were included in this study. EPS was performed using the conventional technique. To evaluate the presence of concealed conduction into the fast AV nodal pathway(FP) and its effects on the effective refractory period(ERP) of the FP (FP-ERP) to a subsequent impulse, single(A2) and double atrial extrastimuli(A2A3) were given. FP-ERP of conducted A2 [FP-ERP-A2(+)] was measured with a second atrial extrastimulus(A3) following a first atrial extrastimulus(A2), which was delivered at a coupling interval 20-30ms longer than FP-ERP. ERPs of non-conducted A2 [FP-ERP-A(-)] was measured with A3 following A2 at coupling intervals 20 ms shorter than FP-ERP. Concealed conduction was considered to be present when A1A3 interval of A3 blocked at the FP with a longest A2A3 interval was longer than FP-ERP. Concealment index(CI)-1 and CI-2 were calculated by dividing FP-ERP-A2(-) by FP-ERP-A2(+) and FP-ERP, respectively. In addition, relationship between antegrade slow pathway conduction time(A2H2) and retrograde fast pathway conduction time(HA), retrograde AV conduction system block cycle length(VA-BCL), and retrograde AV conduction system EBP(VA-ERP) was evaluated by a regression analysis. Results: Concealed conduction was present in all the subjects. CI-1 was 0.63±0.04 and CI-2, 0.79±0.04 in SAVNP and 0.67±0.11, 0.68±0.07 respectively, in AVNRT patients in whom the antegrade slow pathway(SP) was ablated with catheter ablation, showing no significant difference in CI between 2 groups. At the time of induction of AVNRT with A2, A2H2. was significantly correlated with FP-ERP and FP-CT(r=OA43, p=0.04; r=0.507, p=0,02, respectively). By multivariate regression analysis, it was derived that A2H2 should be greater than 0.79 FP-ERP+1.57 FP-CT-0.44 HA-190(ms) (r=0.71, p< 0.05). Conclusion: Induction of typical AVNRT with A2 is determined by conduction time of the slow pathway, refractory period and conduction velocity of the fast pathway, and concealed conduction into the fast pathway.