Soo-Jin Kim;Mei Hua Li;Chung Il Noh;Seong-Ho Kim;Chang-Ha Lee;Ja-Kyoung Yoon
Korean Circulation Journal
/
v.53
no.6
/
pp.406-417
/
2023
Background and Objectives: Pathophysiological changes of right ventricle (RV) after repair of tetralogy of Fallot (TOF) are coupled with a highly compliant low-pressure pulmonary artery (PA) system. This study aimed to determine whether pulmonary vascular function was associated with RV parameters and exercise capacity, and its impact on RV remodeling after pulmonary valve replacement. Methods: In a total of 48 patients over 18 years of age with repaired TOF, pulmonary arterial elastance (Ea), RV volume data, and RV-PA coupling ratio were calculated and analyzed in relation to exercise capacity. Results: Patients with a low Ea showed a more severe pulmonary regurgitation volume index, greater RV end-diastolic volume index, and greater effective RV stroke volume (p=0.039, p=0.013, and p=0.011, respectively). Patients with a high Ea had lower exercise capacity than those with a low Ea (peak oxygen consumption [peak VO2] rate: 25.8±7.7 vs. 34.3±5.5 mL/kg/min, respectively, p=0.003), while peak VO2 was inversely correlated with Ea and mean PA pressure (p=0.004 and p=0.004, respectively). In the univariate analysis, a higher preoperative RV end-diastolic volume index and RV end-systolic volume index, left ventricular end-systolic volume index, and higher RV-PA coupling ratio were risk factors for suboptimal outcomes. Preoperative RV volume and RV-PA coupling ratio reflecting the adaptive PA system response are important factors in optimal postoperative results. Conclusions: We found that PA vascular dysfunction, presenting as elevated Ea in TOF, may contribute to exercise intolerance. However, Ea was inversely correlated with pulmonary regurgitation (PR) severity, which may prevent PR, RV dilatation, and left ventricular dilatation in the absence of significant pulmonary stenosis.
Purpose: We investigated the role of myocardial perfusion SPECT in prediction of ventricular dilatation and the role of revascularization including thrombolytic therapy and PTCA in prevention of ventricular dilatation after an acute myocardial infarction (AMI). Materials and Methods: We performed dipyridamole stress, 4 hour redistribution, and 24 hour reinjection Tl-201 SPECT in 16 patients with AMI two to nine days after attack. Perfusion and wall motion abnormalities were quantified by perfusion index (PI) and wall motion index (WMI). Left ventricular ejection fraction (LVEF), WMI and ventricular volume were measured within 1 week of AMI and after average of 6 months. According to serial changes of left ventricular end-diastolic volume (LVEDV), patients were divided into two groups. We compared WMI, PI and LVEF between the two groups. Relationships among degree of volume, stress-rest PI, WMI, CKMB, Q wave, LVEF and revascularization were analysed using multivariate analysis. Results: Only initial rest perfusion index was significantly different between the two groups (p<0.05). While initial LVEF, stress PI, CKMB, trial of revascularization procedure, presence of Q wave and WMI were not significantly different between the two groups. Eight of 16 patients (50%) showed LV dilatation on follow-up echocardiography. Three of 3 patients (100%) who did not undergo revascualrization procedure documented LV dilatation. And only 5 (38%) of the remaining 13 patients who underwent revascularization revealed LV dilatation. There was no difference in infarct location between the two groups. By multivariate linear regression analysis in patients only undergoing revascularization, rest perfusion index was the only significant factor. Conclusion: Myocardial perfusion SPECT performed prior to revascularization was useful in prediction of LV dilatation after an AMI. Rest perfusion index on myocardial perfusion plays as a significant predictor of left ventricular dilatation after AMI. And revascularization appears to be a valuable procedure in alleviating LV dilatation after AMI with or without viable myocardium in a limited number of patients studied retrospectively.
Ischemic mitral regurgitation (IMR) is the primary mitral valve (MV) pathology in the aftermath of myocardial infarction as a consequence of regional left ventricular (LV) remodeling. We investigated the effect of asymmetric papillary muscle (PM) displacement and annular dilation on IMR development. Virtual MV modeling was performed to create a normal human MV. Asymmetric PM displacement, asymmetric annular dilation, and the combination of these two pathologic characteristics were modeled. Dynamic finite element evaluation of MV function was performed across the complete cardiac cycle for the normal and three different IMR MV models. While the normal MV demonstrated complete leaflet coaptation, each pathologic MV model clearly revealed deteriorated leaflet coaptation and abnormal stress distributions. The pathologic MV model having both asymmetric PM displacement and annular dilation showed the worst leaflet malcoaptation. Simulation-based biomechanical evaluation of post-ischemic LV remodeling provides an excellent tool to better understand the pathophysiologic mechanism of IMR development.
A 6-year-old female Maltese (body weight, 3.1 kg) without clinical signs was referred for further evaluation of the cause of cardiac murmur. Thoracic radiography revealed right-sided cardiomegaly. Echocardiography showed marked hypertrophic remodeling of the right ventricular free wall and an anomalous muscular bundle and fibrous nodule near the subinfundibular portion of the right ventricular outflow tract (RVOT), indicating a double-chambered right ventricle (DCRV). The turbulent flow from the anomalous muscular bundle to the main pulmonary artery was 4.6 m/sec, in addition to the tricuspid valvular regurgitation of 4.4 m/sec and main pulmonary artery flow of 1.1 m/sec. The dog is receiving atenolol (0.5 mg/kg) to minimize the deleterious cardiac effects of the high afterload, even though she remains asymptomatic. This report describes a case of DCRV, a rare congenital heart disease in dogs in South Korea.
Ranjini Srinivasan;Jennifer A. Faerber;Grace DeCost;Xuemei Zhang;Michael DiLorenzo;Elizabeth Goldmuntz;Mark Fogel;Laura Mercer-Rosa
Journal of Cardiovascular Imaging
/
v.30
no.1
/
pp.50-58
/
2022
BACKGROUND: Little is known regarding right ventricular (RV) remodeling immediately after Tetralogy of Fallot (TOF) repair. We sought to describe myocardial deformation by cardiac magnetic resonance imaging (CMR) after TOF repair and investigate associations between these parameters and early post-operative outcomes. METHODS: Fifteen infants underwent CMR without sedation as part of a prospective pilot study after undergoing complete TOF repair, prior to hospital discharge. RV deformation (strain) was measured using tissue tracking, in addition to RV ejection fraction (EF), volumes, and pulmonary regurgitant fraction. Pearson correlation coefficients were used to determine associations between both strain and CMR measures/clinical outcomes. RESULTS: Most patients were male (11/15, 73%), with median age at TOF repair 53 days (interquartile range, 13,131). Most patients had pulmonary stenosis (vs. atresia) (11/15, 73%) and 7 (47%) received a transannular patch as part of their repair. RV function was overall preserved with mean RV EF of 62% (standard deviation [SD], 9.8). Peak radial and longitudinal strain were overall diminished (mean ± SD, 33.80 ± 18.30% and -15.50 ± 6.40%, respectively). Longer hospital length of stay after TOF repair was associated with worse RV peak radial ventricular strain (correlation coefficient (r), -0.54; p = 0.04). Greater pulmonary regurgitant fraction was associated with shorter time to peak radial RV strain (r = -0.55, p = 0.03). CONCLUSIONS: In this small study, our findings suggest presence of early decrease in RV strain after TOF repair and its association with hospital stay when changes in EF and RV size are not yet apparent.
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.
Objective: This study aimed to develop and validate models using radiomics features on a native T1 map from cardiac magnetic resonance (CMR) to predict left ventricular reverse remodeling (LVRR) in patients with nonischemic dilated cardiomyopathy (NIDCM). Materials and Methods: Data from 274 patients with NIDCM who underwent CMR imaging with T1 mapping at Severance Hospital between April 2012 and December 2018 were retrospectively reviewed. Radiomic features were extracted from the native T1 maps. LVRR was determined using echocardiography performed ≥ 180 days after the CMR. The radiomics score was generated using the least absolute shrinkage and selection operator logistic regression models. Clinical, clinical + late gadolinium enhancement (LGE), clinical + radiomics, and clinical + LGE + radiomics models were built using a logistic regression method to predict LVRR. For internal validation of the result, bootstrap validation with 1000 resampling iterations was performed, and the optimism-corrected area under the receiver operating characteristic curve (AUC) with 95% confidence interval (CI) was computed. Model performance was compared using AUC with the DeLong test and bootstrap. Results: Among 274 patients, 123 (44.9%) were classified as LVRR-positive and 151 (55.1%) as LVRR-negative. The optimism-corrected AUC of the radiomics model in internal validation with bootstrapping was 0.753 (95% CI, 0.698-0.813). The clinical + radiomics model revealed a higher optimism-corrected AUC than that of the clinical + LGE model (0.794 vs. 0.716; difference, 0.078 [99% CI, 0.003-0.151]). The clinical + LGE + radiomics model significantly improved the prediction of LVRR compared with the clinical + LGE model (optimism-corrected AUC of 0.811 vs. 0.716; difference, 0.095 [99% CI, 0.022-0.139]). Conclusion: The radiomic characteristics extracted from a non-enhanced T1 map may improve the prediction of LVRR and offer added value over traditional LGE in patients with NIDCM. Additional external validation research is required.
Objective: The occurrence of intramyocardial hemorrhage (IMH) and microvascular obstruction (MVO) in myocardial infarction (MI), known as severe ischemia/reperfusion injury (IRI), has been associated with adverse remodeling. APT102, a soluble human recombinant ecto-nucleoside triphosphate diphosphohydrolase-1, can hydrolyze extracellular nucleotides to attenuate their prothrombotic and proinflammatory effects. The purpose of this study was to temporally evaluate the therapeutic effect of APT102 on IRI in rats and to elucidate the evolution of IRI in the acute stage using cardiovascular magnetic resonance imaging (CMRI). Materials and Methods: Fifty-four rats with MI, induced by ligation of the origin of the left anterior descending coronary artery for 60 minutes, were randomly divided into the APT102 (n = 27) or control (n = 27) group. Intravenous infusion of APT102 (0.3 mg/kg) or placebo was administered 15 minutes before reperfusion, and then 24 hours, 48 hours, 72 hours, and on day 4 after reperfusion. CMRI was performed at 24 hours, 48 hours, 72 hours, and on day 5 post-reperfusion using a 7T system and the hearts were collected for histopathological examination. Cardiac function was quantified using cine imaging and IMH/edema using T2 mapping, and infarct/MVO using late gadolinium enhancement. Results: The extent of infarction (p < 0.001), edema (p < 0.001), IMH (p = 0.013), and MVO (p = 0.049) was less severe in the APT102 group than in the control group. IMH size at 48 hours was significantly greater than that at 24 hours, 72 hours, and 5 days after reperfusion (all p < 0.001). The left ventricular ejection fraction (LVEF) was significantly greater in the APT102 group than in the control group (p = 0.006). There was a negative correlation between LVEF and IMH (r = -0.294, p = 0.010) and a positive correlation between IMH and MVO (r = 0.392, p < 0.001). Conclusion: APT102 can significantly alleviate damage to the ischemic myocardium and microvasculature. IMH size peaked at 48 hours post reperfusion and IMH is a downstream consequence of MVO. IMH may be a potential therapeutic target to prevent adverse remodeling in MI.
We evaluated the efficacy of Dor procedure in patients with ischemic left ventricular dysfunction. Material and Method: Between April 1998 and December 2002, 45 patients underwent the Dor procedure con-comitant with coronary artery bypass grafting (CABG). Left ventricular ejection fraction (LVEF) and left ventricular end-diastolic/end-systolic volumes (LVEDV/LVESV) were measured by echocardiography, myocardial SPECT, and cardiac catheterization and angiography performed at the sequence of preoperative, early postoperative, and one year postoperative stage. Result: Cardiopulmonary bypass and aortic clamp times were mean 141$\pm$64, 69$\pm$24 minutes, respectively. Intraaortic balloon pump (IABP) therapy was required in 19 patients (42%; 7 preoperatively, 9 intraoperatively, 3 postoperatively). Operative mortality rate was 2.2% (1/45). Postoperative morbidities were low cardiac output syndrome (12), atrial fibrillation (5), acute renal failure (4), and postoperative bleeding (4). Functional class (NYHA) was improved from classes 2.8 to 1.1 (p < 0,01). When we compared between the preoperative and early postoperative values, LVEF was improved from 32$\pm$9% to 52$\pm$11% (p<0.01). The asynergy portion decreased from 57$\pm$12% to 22$\pm$9%, and LVEDV/LVESV indexes improved from 125$\pm$39 mL/$m^2$, 85$\pm$30 mL/$m^2$ to 66$\pm$23 mL/$m^2$, 32$\pm$16 mL/$m^2$ (p<0.01). Although these changes in volumes were relatively preserved at postoperative one year, the left ventricular volumes showed a tendency to increase. Conclusion: After the Dor procedure for ischemic left ventricular dysfunction, LVEF improvement and left ventricular volume reduction were maintained till postoperative one year. The tendency for left ventricular volume to increase at postoperative one year suggested the requirement of strict medical management.
Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) ($576{\mu}g/kg/day$) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor ($AT_2R$) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as $TNF-{\alpha}$, MCP-1, $IL-1{\beta}$, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via $AT_2R$.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.