Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.052
M. Henry, M. Esmaeilzadeh., A. Christie, E. Lam, J. Wheately, C. Fackoury, C. Slorach, W. Hui, E. Somerset, S. Fan, P. Nathan, L. Mertens
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): CIHR Anthracyclines, which are commonly used in cancer treatment can induce myocardial damage, result in heart failure during treatment and have cardiac effects even decades after treatment. Monitoring of cardiotoxicity during treatment is largely based on the use of echocardiographic functional markers like ejection fraction and more recently myocardial strain imaging. Some studies have also looked at the utility of biomarkers like troponin and BNP. The utility of this surveillance strategy remains controversial as larger prospective studies are lacking. The aim of this study was to prospectively describe the impact of anthracycline treatment on echocardiographic functional parameters and cardiac biomarkers (high sensitivity troponin T and NT-Pro BNP) during the treatment period and twelve months after completion of treatment. In the current study we wanted to look at whether monitoring parameters during treatment were predictive of left ventricular function 12 months after treatment. This was a prospective multi-centre nested case-control study of 256 children diagnosed with cancer requiring anthracycline therapy. Baseline functional echocardiographic parameters and cardiac biomarkers were obtained prior to starting anthracycline therapy, during the treatment protocol, and 12 months after treatment completion. Patients were assigned to one of two comparison groups based on the fractional shortening at the12-month echocardiogram: patients in group 1 had normal fractional shortening, (FS ³ 28%) while patients in group 2 had reduced fractional shortening (FS < 28%). A total of 917 echoes were performed, 376 of these occurred during the treatment period. FS was reduced in 27 (7%) of echoes obtained during the treatment period with 22 patients developing new onset dysfunction. Twelve months after treatment completion 232 patients had normal FS (Group 1), while 24 patients showed reduced FS (Group 2). Both groups had normal systolic function and cardiac biomarkers at baseline, however patients in group 2 were older at diagnosis (13.2 years (11.8-16) vs 6.5 years (3.4-13.2), p = 0.003) and received a higher cumulative anthracycline dose (200 mg/m2 (143-318) vs 125 mg/m2 (75-200), p= 0.005). One third (8/24) of patients in group 2 had at least 1 abnormal echo during the treatment period compared to 7% (16/232) in the normal group P < 0.001. The proportion of patients with at least one abnormal biomarker during this period however, was similar between groups. Conclusion(s) Patients receiving higher accumulative anthracycline doses and those with abnormal FS during the treatment period are at higher risk of having reduced cardiac function 12 months after treatment. High sensitivity troponin and NT-Pro BNP levels during the treatment period fail to discriminate patients at risk of developing early reduced systolic function. The re
{"title":"Early surveillance of anthracycline induced cardiotoxicity in children using echocardiography and biomarkers: A prospective study","authors":"M. Henry, M. Esmaeilzadeh., A. Christie, E. Lam, J. Wheately, C. Fackoury, C. Slorach, W. Hui, E. Somerset, S. Fan, P. Nathan, L. Mertens","doi":"10.1093/EHJCI/JEAA356.052","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.052","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: Public grant(s) – National budget only. Main funding source(s): CIHR\u0000 \u0000 \u0000 \u0000 Anthracyclines, which are commonly used in cancer treatment can induce myocardial damage, result in heart failure during treatment and have cardiac effects even decades after treatment. Monitoring of cardiotoxicity during treatment is largely based on the use of echocardiographic functional markers like ejection fraction and more recently myocardial strain imaging. Some studies have also looked at the utility of biomarkers like troponin and BNP. The utility of this surveillance strategy remains controversial as larger prospective studies are lacking.\u0000 \u0000 \u0000 \u0000 The aim of this study was to prospectively describe the impact of anthracycline treatment on echocardiographic functional parameters and cardiac biomarkers (high sensitivity troponin T and NT-Pro BNP) during the treatment period and twelve months after completion of treatment. In the current study we wanted to look at whether monitoring parameters during treatment were predictive of left ventricular function 12 months after treatment.\u0000 \u0000 \u0000 \u0000 This was a prospective multi-centre nested case-control study of 256 children diagnosed with cancer requiring anthracycline therapy. Baseline functional echocardiographic parameters and cardiac biomarkers were obtained prior to starting anthracycline therapy, during the treatment protocol, and 12 months after treatment completion. Patients were assigned to one of two comparison groups based on the fractional shortening at the12-month echocardiogram: patients in group 1 had normal fractional shortening, (FS ³ 28%) while patients in group 2 had reduced fractional shortening (FS < 28%).\u0000 \u0000 \u0000 \u0000 A total of 917 echoes were performed, 376 of these occurred during the treatment period. FS was reduced in 27 (7%) of echoes obtained during the treatment period with 22 patients developing new onset dysfunction. Twelve months after treatment completion 232 patients had normal FS (Group 1), while 24 patients showed reduced FS (Group 2). Both groups had normal systolic function and cardiac biomarkers at baseline, however patients in group 2 were older at diagnosis (13.2 years (11.8-16) vs 6.5 years (3.4-13.2), p = 0.003) and received a higher cumulative anthracycline dose (200 mg/m2 (143-318) vs 125 mg/m2 (75-200), p= 0.005). One third (8/24) of patients in group 2 had at least 1 abnormal echo during the treatment period compared to 7% (16/232) in the normal group P < 0.001. The proportion of patients with at least one abnormal biomarker during this period however, was similar between groups.\u0000 Conclusion(s)\u0000 Patients receiving higher accumulative anthracycline doses and those with abnormal FS during the treatment period are at higher risk of having reduced cardiac function 12 months after treatment. High sensitivity troponin and NT-Pro BNP levels during the treatment period fail to discriminate patients at risk of developing early reduced systolic function. The re","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"15 16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75785977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.276
C. Sutter, K. Fischer, K. Yamaji, Y. Ueki, B. Jung, L. Raeber, H. Tengg-Kobligk, B. Eberle, Dominik P. Guensch
Type of funding sources: Public hospital(s). Main funding source(s): Local research funds of the Department of Anaesthesiology and Pain medicine, Bern University Hospital, Inselspital During anaesthesia, emergency and critical care treatment, patients with coronary artery disease (CAD) are often exposed to supraphysiologic arterial oxygen tensions. The balance between benefits and risks of hyperoxia (HO) in patients with stable CAD is controversial, with reports about reduced left ventricular contractility or increased morbidity and mortality. Effects of HO on right ventricular (RV) function in CAD are less well described. Advanced cardiovascular magnetic resonance (CMR) feature tracking software allows assessment of myocardial deformation, which may serve as early marker of ventricular dysfunction. In a CMR study we quantified the effect of HO on RV function and deformation in awake healthy participants and CAD patients. Ten healthy participants and 26 patients with stable one- or two-vessel obstructive CAD were included. In a CMR study, a short-axis function stack of both ventricles was obtained first at room air (RA), then during HO induced by breathing oxygen at 10L/min for 5 minutes via a non-rebreathing facemask. RV strain was analysed by a blinded reader who manually traced epicardial and endocardial contours of the RV for determining peak global circumferential strain (RVGCS), time to peak strain, systolic and diastolic strain rate parameters. RV ejection fraction did not change with O2 breathing in the healthy control group (RA, 56 ± 12% vs. HO, 55 ± 10%, p = 0.999) nor in the CAD group (RA, 60 ± 8% vs. HO, 60 ± 9%, p = 0.609). RV cardiac index decreased significantly in CAD patients from RA (2.62 ± 0.88 L/min/m2) to HO (2.42 ± 0.77L/min/m2, p = 0.002). The decrease in the control group was not significant (RVCI: RA 3.28 ± 1.29 vs HO 3.04 ± 1.27L/min/m2 p = 0.068). In the healthy control group, RVGCS, time to peak strain, and systolic strain rate did not change significantly with HO (RVGCS: RA, -14.6 ± 3.9% vs. HO, -13.1 ± 4.5%, p = 0.353; time to peak strain: 282 ± 45ms vs. 286 ± 29ms, p = 0.540; and systolic strain rate: -0.85 ± 0.27/s vs. -0.67 ± 0.28, p = 0.055). In CAD patients RVGCS worsened from -14.8 ± 3.3% on RA to -13.9 ± 3.6% at HO (p = 0.040). Time to peak strain became significantly prolonged from 319 ± 40ms on RA to 329 ± 49ms at HO (p = 0.046). This was accompanied by a reduction of systolic strain rate from -0.79 ± 0.27/s to -0.75 ± 0.22/s (p = 0.037). Diastolic strain parameters did not differ significantly between RA and HO in either group. In our cohort of CAD patients HO significantly reduced RV cardiac index and impaired systolic deformation as determined by CMR feature tracking. Studies are required in a larger patient cohort with regional analysis and assessment of longitudinal and radial deformation to assess the role of hyperoxia in CAD. Abstract Figure. Change in RV Peak Circ
资金来源类型:公立医院。主要资金来源:当地研究基金，伯尔尼大学医院，Inselspital麻醉科和疼痛医学系，在麻醉、急诊和重症监护治疗期间，冠状动脉疾病(CAD)患者经常暴露于生理上的动脉氧紧张。稳定性冠心病患者高氧(HO)的益处和风险之间的平衡是有争议的，有报道称左心室收缩力降低或发病率和死亡率增加。在冠心病患者中，HO对右心室(RV)功能的影响尚不清楚。先进的心血管磁共振(CMR)特征跟踪软件可以评估心肌变形，这可能是心室功能障碍的早期标志。在一项CMR研究中，我们量化了HO对清醒健康参与者和CAD患者右心室功能和变形的影响。10名健康参与者和26名稳定的单支或双支阻塞性CAD患者被纳入研究。在CMR研究中，首先在室内空气(RA)下获得两个心室的短轴功能堆栈，然后在通过非再呼吸面罩以10L/min呼吸5分钟引起的HO期间获得两个心室的短轴功能堆栈。右心室应变分析由盲眼阅读者手动跟踪心外膜和心内膜的右心室轮廓，以确定全球周应变峰值(RVGCS)，峰值应变时间，收缩和舒张应变率参数。健康对照组右心室射血分数随氧气呼吸无变化(RA, 56±12% vs. HO, 55±10%，p = 0.999)，冠心病组(RA, 60±8% vs. HO, 60±9%，p = 0.609)。冠心病患者RV心脏指数由RA(2.62±0.88 L/min/m2)降至HO(2.42±0.77L/min/m2, p = 0.002)。对照组RVCI: RA为3.28±1.29,HO为3.04±1.27L/min/m2, p = 0.068，差异无统计学意义。健康对照组RVGCS、应变峰值时间、收缩应变率与HO无显著差异(RVGCS: RA， -14.6±3.9% vs HO， -13.1±4.5%，p = 0.353;应变峰值时间:282±45ms vs. 286±29ms, p = 0.540;和收缩期应变率:-0.85±0.27 /秒和-0.67±0.28,p = 0.055)。CAD患者RVGCS从RA时的-14.8±3.3%恶化至HO时的-13.9±3.6% (p = 0.040)。峰值应变时间从RA组的319±40ms显著延长至HO组的329±49ms (p = 0.046)。收缩应变率从-0.79±0.27/s降至-0.75±0.22/s (p = 0.037)。两组患者舒张应变参数无明显差异。在我们的冠心病患者队列中，通过CMR特征跟踪，HO显著降低了右心室心脏指数和收缩变形受损。研究需要在更大的患者队列中进行纵向和径向变形的区域分析和评估，以评估高氧在CAD中的作用。抽象的图。RV峰值周向应变的变化
{"title":"Changes in right ventricular deformation during hyperoxia versus normoxaemia in patients with stable coronary artery disease and healthy controls","authors":"C. Sutter, K. Fischer, K. Yamaji, Y. Ueki, B. Jung, L. Raeber, H. Tengg-Kobligk, B. Eberle, Dominik P. Guensch","doi":"10.1093/EHJCI/JEAA356.276","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.276","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: Public hospital(s). Main funding source(s): Local research funds of the Department of Anaesthesiology and Pain medicine, Bern University Hospital, Inselspital\u0000 \u0000 \u0000 \u0000 During anaesthesia, emergency and critical care treatment, patients with coronary artery disease (CAD) are often exposed to supraphysiologic arterial oxygen tensions. The balance between benefits and risks of hyperoxia (HO) in patients with stable CAD is controversial, with reports about reduced left ventricular contractility or increased morbidity and mortality. Effects of HO on right ventricular (RV) function in CAD are less well described. Advanced cardiovascular magnetic resonance (CMR) feature tracking software allows assessment of myocardial deformation, which may serve as early marker of ventricular dysfunction. In a CMR study we quantified the effect of HO on RV function and deformation in awake healthy participants and CAD patients.\u0000 \u0000 \u0000 \u0000 Ten healthy participants and 26 patients with stable one- or two-vessel obstructive CAD were included. In a CMR study, a short-axis function stack of both ventricles was obtained first at room air (RA), then during HO induced by breathing oxygen at 10L/min for 5 minutes via a non-rebreathing facemask. RV strain was analysed by a blinded reader who manually traced epicardial and endocardial contours of the RV for determining peak global circumferential strain (RVGCS), time to peak strain, systolic and diastolic strain rate parameters.\u0000 \u0000 \u0000 \u0000 RV ejection fraction did not change with O2 breathing in the healthy control group (RA, 56 ± 12% vs. HO, 55 ± 10%, p = 0.999) nor in the CAD group (RA, 60 ± 8% vs. HO, 60 ± 9%, p = 0.609). RV cardiac index decreased significantly in CAD patients from RA (2.62 ± 0.88 L/min/m2) to HO (2.42 ± 0.77L/min/m2, p = 0.002). The decrease in the control group was not significant (RVCI: RA 3.28 ± 1.29 vs HO 3.04 ± 1.27L/min/m2 p = 0.068).\u0000 In the healthy control group, RVGCS, time to peak strain, and systolic strain rate did not change significantly with HO (RVGCS: RA, -14.6 ± 3.9% vs. HO, -13.1 ± 4.5%, p = 0.353; time to peak strain: 282 ± 45ms vs. 286 ± 29ms, p = 0.540; and systolic strain rate: -0.85 ± 0.27/s vs. -0.67 ± 0.28, p = 0.055).\u0000 In CAD patients RVGCS worsened from -14.8 ± 3.3% on RA to -13.9 ± 3.6% at HO (p = 0.040). Time to peak strain became significantly prolonged from 319 ± 40ms on RA to 329 ± 49ms at HO (p = 0.046). This was accompanied by a reduction of systolic strain rate from -0.79 ± 0.27/s to -0.75 ± 0.22/s (p = 0.037). Diastolic strain parameters did not differ significantly between RA and HO in either group.\u0000 \u0000 \u0000 \u0000 In our cohort of CAD patients HO significantly reduced RV cardiac index and impaired systolic deformation as determined by CMR feature tracking. Studies are required in a larger patient cohort with regional analysis and assessment of longitudinal and radial deformation to assess the role of hyperoxia in CAD.\u0000 Abstract Figure. Change in RV Peak Circ","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73686988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.305
G. Casas, J. Limeres, G. Oristrell, L. Gutiérrez, R. Barriales, P. García-Pavía, E. Zorio, J. Gimeno, E. Villacorta, J. Jiménez-Jáimez, T. Ripoll, À. Bayés, I. Ferreira, J. Rodríguez-Palomares
Type of funding sources: None. Left ventricular noncompaction (LVNC) is a heterogeneous entity with a wide phenotypic expression. Risk factors have not been well established and prognostic stratification remains challenging. Describe long term outcomes of LVNC patients and determine predictors of cardiovascular events. Prospective multicentric study of consecutive patients fulfilling imaging diangostic criteria for LVNC (Jenni echo criteria and Petersen CMR criteria). Demographic, ECG, imaging and genetic variables were collected. End points were heart failure (HF), ventricular arrhythmias (VA), systemic embolisms (SE) and all-cause death. Major adverse cardiovascular events (MACE) was the combination of the four previous end points. 585 patients from 12 referral centres were included from 2000 to 2018. Age at diagnosis was 45 ± 20 years, 334 (57%) were male, baseline LVEF was 48 ± 17% and 18% presented late gadolinium enhancement (LGE). During a median follow-up of 5.1 years (IQR 2.3-8.1), 110 (19%) patients presented HF, 87 (15%) VA, 18 (3%) SE and 34 (6%) died. MACE occurred in 223 (38%) patients. LVEF was independently associated with HF, VA, SE and MACE: HR were 1.08, 1.02, 1.04 and 1.02 respectively (all p < 0.05). LGE was more frequent in patients with reduced LVEF (39 Vs 53%, p < 0.001) and was associated with higher HF and VA risk in patients with LVEF > 35% (HR 2.69 and 2.48 respectively, p < 0.05) (Figure 1). Patients with a normal ECG, LVEF≥50%, no LGE and no family aggregation presented no MACE (0%) at long term follow-up. Among patients who underwent genetic testing (354, 61%), TTN variants and complex genotype (more than one variant) presented lower LVEF and higher HF risk. ACTC1 variants were associated with VA. LVNC carries a high long term risk of heart faliure and ventricular arrhythmias. LVEF is the most important predictor and myocardial fibrosis is associated with increased risk in patients without severe systolic dysfunction. Genotype is a modifier of outcomes. These factors might be used to risk stratify LVNC patients. Abstract Figure. Kaplan Meier survival curves
资金来源类型:无。左心室不压实(LVNC)是一种异质性实体，具有广泛的表型表达。危险因素尚未很好地确定，预后分层仍然具有挑战性。描述LVNC患者的长期预后并确定心血管事件的预测因素。满足LVNC影像学诊断标准(Jenni回声标准和Petersen CMR标准)的连续患者的前瞻性多中心研究。收集人口统计学、心电图、影像学和遗传变量。终点为心力衰竭(HF)、室性心律失常(VA)、全身性栓塞(SE)和全因死亡。主要心血管不良事件(MACE)是前四个终点的总和。2000年至2018年纳入了12个转诊中心的585名患者。诊断年龄45±20岁，男性334例(57%)，基线LVEF为48±17%，18%表现为晚期钆增强(LGE)。在中位随访5.1年(IQR 2.3-8.1)期间，110例(19%)患者出现HF, 87例(15%)出现VA, 18例(3%)出现SE, 34例(6%)死亡。223例(38%)患者发生MACE。LVEF与HF、VA、SE、MACE独立相关，HR分别为1.08、1.02、1.04、1.02(均p < 0.05)。LGE在LVEF降低的患者中更常见(39 Vs 53%， p < 0.001)， LVEF > 35%的患者HF和VA风险更高(HR分别为2.69和2.48,p < 0.05)(图1)。长期随访时，心电图正常、LVEF≥50%、无LGE、无家族聚集的患者未出现MACE(0%)。在接受基因检测的患者中(354.61%)，TTN变异和复杂基因型(多于一种变异)表现出较低的LVEF和较高的HF风险。ACTC1变异与VA相关。LVNC具有心力衰竭和室性心律失常的高长期风险。LVEF是最重要的预测因子，心肌纤维化与无严重收缩功能障碍患者的风险增加相关。基因型是结果的修饰因子。这些因素可用于LVNC患者的风险分层。抽象的图。Kaplan Meier生存曲线
{"title":"Long term outcomes in left ventricular noncompaction","authors":"G. Casas, J. Limeres, G. Oristrell, L. Gutiérrez, R. Barriales, P. García-Pavía, E. Zorio, J. Gimeno, E. Villacorta, J. Jiménez-Jáimez, T. Ripoll, À. Bayés, I. Ferreira, J. Rodríguez-Palomares","doi":"10.1093/EHJCI/JEAA356.305","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.305","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: None.\u0000 \u0000 \u0000 \u0000 Left ventricular noncompaction (LVNC) is a heterogeneous entity with a wide phenotypic expression. Risk factors have not been well established and prognostic stratification remains challenging.\u0000 \u0000 \u0000 \u0000 Describe long term outcomes of LVNC patients and determine predictors of cardiovascular events. \u0000 \u0000 \u0000 \u0000 \u0000 Prospective multicentric study of consecutive patients fulfilling imaging diangostic criteria for LVNC (Jenni echo criteria and Petersen CMR criteria). Demographic, ECG, imaging and genetic variables were collected. End points were heart failure (HF), ventricular arrhythmias (VA), systemic embolisms (SE) and all-cause death. Major adverse cardiovascular events (MACE) was the combination of the four previous end points.\u0000 \u0000 \u0000 \u0000 585 patients from 12 referral centres were included from 2000 to 2018. Age at diagnosis was 45 ± 20 years, 334 (57%) were male, baseline LVEF was 48 ± 17% and 18% presented late gadolinium enhancement (LGE). During a median follow-up of 5.1 years (IQR 2.3-8.1), 110 (19%) patients presented HF, 87 (15%) VA, 18 (3%) SE and 34 (6%) died. MACE occurred in 223 (38%) patients.\u0000 LVEF was independently associated with HF, VA, SE and MACE: HR were 1.08, 1.02, 1.04 and 1.02 respectively (all p < 0.05). LGE was more frequent in patients with reduced LVEF (39 Vs 53%, p < 0.001) and was associated with higher HF and VA risk in patients with LVEF > 35% (HR 2.69 and 2.48 respectively, p < 0.05) (Figure 1). Patients with a normal ECG, LVEF≥50%, no LGE and no family aggregation presented no MACE (0%) at long term follow-up.\u0000 Among patients who underwent genetic testing (354, 61%), TTN variants and complex genotype (more than one variant) presented lower LVEF and higher HF risk. ACTC1 variants were associated with VA.\u0000 \u0000 \u0000 \u0000 LVNC carries a high long term risk of heart faliure and ventricular arrhythmias. LVEF is the most important predictor and myocardial fibrosis is associated with increased risk in patients without severe systolic dysfunction. Genotype is a modifier of outcomes. These factors might be used to risk stratify LVNC patients.\u0000 Abstract Figure. Kaplan Meier survival curves\u0000","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74577199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.293
T. Pezel, P. Garot, T. Hovasse, S. Toupin, T. Unterseeh, M. Morice, S. Champagne, Y. Louvard, F. Sanguineti, J. Garot
Type of funding sources: None. Cardiovascular magnetic resonance imaging (CMR) has emerged as an accurate technique that can assess ventricular function, stress myocardial perfusion, and viability, without radiation. Recent studies have shown that stress CMR would be the best test to predict obstructive coronary artery disease (CAD) with a good safety. The aim of our study was to assess the feasibility and incidence of immediate complications of stress CMR in a tertiary Cardiovascular Center with CMR Laboratory dedicated. Prospective registry of vasodilator stress CMR in a French center with CMR expertise included all consecutive patients referred for vasodilator stress perfusion CMR to detect an obstructive CAD between 2008 and 2020. Stress CMR was performed at 1.5 T using dipyridamole. The clinical and demographic data, quality of test, CMR findings, haemodynamic data, and complications were prospectively recorded. Stress CMR was performed in 35,157 patients (98.2% of requested). The study could not be performed due to claustrophobia in 0.3%. Quality was optimal in 93.1%, suboptimal in 6.4%, and poor in 0.5% of studies. Images were diagnostic in 97.9% of patients. No patient died or had acute myocardial infarction during the test. Moreover, 56 patients (0.16%) had severe immediate complications, and one anaphylactic shock post-gadolinium. The only factor significantly associated with higher incidence of serious complications was the detection of inducible ischaemia (p < 0.001). Incidence of non-severe complications was low (1.5%), severe controlled chest pain being the most frequent. Minor symptoms occurred frequently (35.5%). Performance of stress CMR is safe with very high image rate of satisfactory quality to perform the diagnosis in a referral population. Inducible ischaemia was the only factor identified which was associated with serious complications. Abstract Table. Final results after stress CMR
{"title":"Vasodilatation stress cardiovascular magnetic resonance: feasibility and safety in a monocentric prospective study","authors":"T. Pezel, P. Garot, T. Hovasse, S. Toupin, T. Unterseeh, M. Morice, S. Champagne, Y. Louvard, F. Sanguineti, J. Garot","doi":"10.1093/EHJCI/JEAA356.293","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.293","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: None.\u0000 \u0000 \u0000 \u0000 Cardiovascular magnetic resonance imaging (CMR) has emerged as an accurate technique that can assess ventricular function, stress myocardial perfusion, and viability, without radiation. Recent studies have shown that stress CMR would be the best test to predict obstructive coronary artery disease (CAD) with a good safety.\u0000 \u0000 \u0000 \u0000 The aim of our study was to assess the feasibility and incidence of immediate complications of stress CMR in a tertiary Cardiovascular Center with CMR Laboratory dedicated.\u0000 \u0000 \u0000 \u0000 Prospective registry of vasodilator stress CMR in a French center with CMR expertise included all consecutive patients referred for vasodilator stress perfusion CMR to detect an obstructive CAD between 2008 and 2020. Stress CMR was performed at 1.5 T using dipyridamole. The clinical and demographic data, quality of test, CMR findings, haemodynamic data, and complications were prospectively recorded.\u0000 \u0000 \u0000 \u0000 Stress CMR was performed in 35,157 patients (98.2% of requested). The study could not be performed due to claustrophobia in 0.3%. Quality was optimal in 93.1%, suboptimal in 6.4%, and poor in 0.5% of studies. Images were diagnostic in 97.9% of patients. No patient died or had acute myocardial infarction during the test. Moreover, 56 patients (0.16%) had severe immediate complications, and one anaphylactic shock post-gadolinium. The only factor significantly associated with higher incidence of serious complications was the detection of inducible ischaemia (p < 0.001). Incidence of non-severe complications was low (1.5%), severe controlled chest pain being the most frequent. Minor symptoms occurred frequently (35.5%).\u0000 \u0000 \u0000 \u0000 Performance of stress CMR is safe with very high image rate of satisfactory quality to perform the diagnosis in a referral population. Inducible ischaemia was the only factor identified which was associated with serious complications.\u0000 Abstract Table. Final results after stress CMR\u0000","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75140218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.224
L. Dux-Santoy, G. Teixidó-Tura, A. Ruiz-Muñoz, L. Mura, F. Valente, Á. López-Sainz, L. Galián, L. Gutiérrez, T. González‐Alujas, A. Sao-Avilés, I. F. González, A. Evangelista, J. Rodríguez-Palomares, A. Guala
Type of funding sources: Public Institution(s). Main funding source(s): Spanish Ministry of Science, Innovation and Universities Instituto de Salud Carlos III Background. Dilation of the aortic root is a key feature of Marfan syndrome and it is related to the occurrence of aortic events and death. On top of maximum diameter, rapid annual growth rate is suggested by guidelines for indication of aortic root replacement. Current gold-standard for aortic root diameter assessment is manual quantification on multiplanar reformatted 3D computed tomography (CT) or magnetic resonance angiogram. However, inter- and intra-observer reproducibility are limited and different measurement methods, i.e. cusp-to-cusp and cusp-to-commissure, may be used in different clinical centres, leading to difficulties in the clinical assessment of progressive dilation. Purpose. We aimed to test whether aortic root growth rate during follow-up can be reliably quantified by semi-automatic co-registration of two CT angiograms. Methods. Seven Marfan syndrome patients, free from previous aortic surgery, with a total of 11 pairs of CT were identified. Manual assessment of six aortic root diameters (right-non coronary -RN- , right-left -RL- and left-non coronary -LN- cusp-to-cusp and R, L and N cusp-to-commissure) was obtained from all CTs by an experienced researcher blind to semi-automatic results. The thoracic aorta and the outflow tract were semi-automatically segmented in the baseline CT and commissure and cusps were manually located. A 10 mm-thick region of interest containing the aortic wall was automatically generated from segmentation boundary. Co-registration was obtained with three, fully-automatic steps. Firstly, baseline and follow-up CT scans were aligned by means of a rigid registration. Then, scans were co-registered with multi-resolution affine followed by b-spline non-rigid registrations based on mutual information metric. The transformation pertaining to the location of baseline commissure and cusps points was used to locate the same points in the follow-up scan (Fig. 1 top). Results. Follow-up duration was 35 ± 22 (range 12-70.3) months. Automatic quantification of diameter growth during the follow-up was obtained in 62 out of 66 (94%) diameter comparisons. High Pearson correlation coefficients (R) and ICC were found between manual and semi-automatic assessment of growth rate, both for cusp-to-cusp and cusp-to-commissure diameters: R = 0.727 and ICC = 0.678 for RN; R = 0.822 and ICC = 0.602 for RL; R = 0.648 and ICC = 0.668 for LN; R = 0.726 and ICC = 0.711 for R; R = 0.911 and ICC = 0.895 for L and R = 0.553 and ICC = 0.482 for N. Scatter and Bland-Altman plots for all growth rates (Fig. 1) confirmed very good correlation (R = 0.810) but a slight tendency (R=-0.270) for underestimation at high growth rate. No correlation was found between follow-up duration and difference between techniques (R = 0.06). Conclusions. Semi-automatic quantification of ao
{"title":"Semi-automatic quantification of aortic root progressive dilation by automatic co-registration of computed tomography angiograms: a preliminary comparison with manual assessment in Marfan patients","authors":"L. Dux-Santoy, G. Teixidó-Tura, A. Ruiz-Muñoz, L. Mura, F. Valente, Á. López-Sainz, L. Galián, L. Gutiérrez, T. González‐Alujas, A. Sao-Avilés, I. F. González, A. Evangelista, J. Rodríguez-Palomares, A. Guala","doi":"10.1093/EHJCI/JEAA356.224","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.224","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: Public Institution(s). Main funding source(s): Spanish Ministry of Science, Innovation and Universities Instituto de Salud Carlos III\u0000 Background. Dilation of the aortic root is a key feature of Marfan syndrome and it is related to the occurrence of aortic events and death. On top of maximum diameter, rapid annual growth rate is suggested by guidelines for indication of aortic root replacement. Current gold-standard for aortic root diameter assessment is manual quantification on multiplanar reformatted 3D computed tomography (CT) or magnetic resonance angiogram. However, inter- and intra-observer reproducibility are limited and different measurement methods, i.e. cusp-to-cusp and cusp-to-commissure, may be used in different clinical centres, leading to difficulties in the clinical assessment of progressive dilation.\u0000 Purpose. We aimed to test whether aortic root growth rate during follow-up can be reliably quantified by semi-automatic co-registration of two CT angiograms.\u0000 Methods. Seven Marfan syndrome patients, free from previous aortic surgery, with a total of 11 pairs of CT were identified. Manual assessment of six aortic root diameters (right-non coronary -RN- , right-left -RL- and left-non coronary -LN- cusp-to-cusp and R, L and N cusp-to-commissure) was obtained from all CTs by an experienced researcher blind to semi-automatic results. The thoracic aorta and the outflow tract were semi-automatically segmented in the baseline CT and commissure and cusps were manually located. A 10 mm-thick region of interest containing the aortic wall was automatically generated from segmentation boundary. Co-registration was obtained with three, fully-automatic steps. Firstly, baseline and follow-up CT scans were aligned by means of a rigid registration. Then, scans were co-registered with multi-resolution affine followed by b-spline non-rigid registrations based on mutual information metric. The transformation pertaining to the location of baseline commissure and cusps points was used to locate the same points in the follow-up scan (Fig. 1 top).\u0000 Results. Follow-up duration was 35 ± 22 (range 12-70.3) months. Automatic quantification of diameter growth during the follow-up was obtained in 62 out of 66 (94%) diameter comparisons. High Pearson correlation coefficients (R) and ICC were found between manual and semi-automatic assessment of growth rate, both for cusp-to-cusp and cusp-to-commissure diameters: R = 0.727 and ICC = 0.678 for RN; R = 0.822 and ICC = 0.602 for RL; R = 0.648 and ICC = 0.668 for LN; R = 0.726 and ICC = 0.711 for R; R = 0.911 and ICC = 0.895 for L and R = 0.553 and ICC = 0.482 for N. Scatter and Bland-Altman plots for all growth rates (Fig. 1) confirmed very good correlation (R = 0.810) but a slight tendency (R=-0.270) for underestimation at high growth rate. No correlation was found between follow-up duration and difference between techniques (R = 0.06).\u0000 Conclusions. Semi-automatic quantification of ao","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"CE-29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84568868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.047
A. Caenen, L. Keijzer, S. Bézy, J. Duchenne, M. Orłowska, A. V. D. Steen, N. Jong, P. Segers, J. Bosch, J. Voigt, J. Dhooge, H. Vos
Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Research Foundation Flanders (FWO): grant 1211620N TTW – Dutch Heart Foundation partnership program "Earlier recognition of cardiovascular diseases": project number 14740 Background Echocardiographic shear wave elastography (SWE) encompasses all ultrasound techniques tracking shear wave (SW) motion in the cardiac wall, of which the propagation speed is linked to the intrinsic mechanical properties. SWs can be induced naturally, for example by valve closure, or externally by using an acoustic radiation force (ARF). Although the latter is technically more demanding, it enables instantaneous stiffness assessment throughout the entire cardiac cycle (fig. a). However, it is unknown how factors such as cardiac loading and contractility, next to intrinsic mechanical properties, affect ARF-based SW speeds. Purpose We performed transthoracic SWE measurements in pigs to study the effects of hemodynamic alterations, inotropic state and myocardial infarction (MI) on diastolic and systolic SW speeds. Methods Different cardiac conditions were considered in three pigs: (i) baseline (BL), (ii) preload decrease (PD), (iii) afterload increase (AI), (iv) preload increase (PI), (v) administration of dobutamine (DOB), (vi) BL2, (vii) MI through 60-100 min. occlusion of the LAD and (viii) 40 min. reperfusion (REP). For each condition, transthoracic high frame rate ARF-based SWE acquisitions were taken in a parasternal long-axis view with a research ultrasound system. SWs were induced in the septum at 34 Hz during 1.5 s to track SW speeds throughout the cardiac cycle (fig. a&b). Systolic and diastolic SW speeds were determined from the 10% highest and lowest median values per condition, respectively. Left ventricular pressure-volume (PV) loops were recorded to estimate end-diastolic pressure (EDP), end-systolic pressure (ESP) and passive chamber stiffness (dPdV). dPdV was determined as the slope of the tangent to the fitted end-diastolic PV relationship at mean ED volume. Linear regressions and Pearson’s correlation coefficients were computed. Results Diastolic SW speed was correlated to EDP for conditions with changes in loading, and to dPdV for conditions with changes in chamber stiffness (fig. c). Both relationships were significant, with a moderate positive correlation for EDP (R = 0.48, p = 0.02) and a strong positive correlation for dPdV (R = 0.76, p l 0.01). Furthermore, the observed change in diastolic SW speed was smaller when altering EDP compared to dPdV (0.4 m/s vs. 1.0 m/s). For systolic SW speed, very strong positive correlations were found with ESP (R = 0.91, p l 0.01), and with dPdV (R = 0.81, p l 0.01) in fig. d. Conclusion This study shows that both diastolic and systolic SW speed are related to passive chamber stiffness. Moreover, loading also influenced systolic SW speed and, to a lesser extent, diastolic SW speed, presumably beca
资金来源类型:私人资助和/或赞助。主要资助来源:法兰德斯研究基金会(FWO): 1211620N TTW -荷兰心脏基金会合作项目“早期识别心血管疾病”:项目编号14740背景超声心动图剪切波弹性成像(SWE)包括所有跟踪心脏壁剪切波运动的超声技术，其传播速度与内在力学特性有关。声波可以自然产生，例如通过阀门关闭，或者通过外部使用声辐射力(ARF)。尽管后者在技术上要求更高，但它可以在整个心脏周期内进行瞬时刚度评估(图a)。然而，除了内在力学性能外，心脏负荷和收缩力等因素如何影响基于arf的SW速度尚不清楚。目的:我们对猪进行经胸SWE测量，研究血流动力学改变、肌力状态和心肌梗死(MI)对舒张和收缩期SW速度的影响。方法对3只猪进行不同的心脏状况研究:(i)基线(BL)， (ii)负荷前减少(PD)， (iii)负荷后增加(AI)， (iv)负荷前增加(PI)， (v)多巴酚丁胺(DOB)， (vi) BL2， (vii) 60-100分钟LAD闭塞期间心肌梗死(MI)和(viii) 40分钟再灌注(REP)。对于每种情况，使用研究超声系统在胸骨旁长轴视图下进行经胸高帧率ARF-based SWE采集。在间隔区以34 Hz频率在1.5 s内诱导SW，以跟踪整个心脏周期的SW速度(图a和b)。收缩期和舒张期SW速度分别由每种情况下10%的最高和最低中位数确定。记录左心室压力-容积(PV)循环以估计舒张末期压(EDP)、收缩末期压(ESP)和被动腔刚度(dPdV)。dPdV为平均ED容积下舒张末期PV关系的切线斜率。计算线性回归和Pearson相关系数。结果在负荷变化的情况下，舒张SW速度与EDP相关，在腔室刚度变化的情况下，与dPdV相关(图c)。两者的关系都很显著，EDP中度正相关(R = 0.48, p = 0.02)， dPdV强正相关(R = 0.76, p = 0.01)。此外，与dPdV相比，改变EDP时观察到的舒张期SW速度变化更小(0.4 m/s vs 1.0 m/s)。收缩期超声速度与ESP (R = 0.91, p < 0.01)和dPdV (R = 0.81, p < 0.01)呈正相关。结论舒张期和收缩期超声速度均与被动腔室刚度相关。此外，载荷也会影响收缩期的SW速度，并在较小程度上影响舒张期的SW速度，可能是因为材料非线性。收缩速度也与收缩力有关。因此，虽然瓣膜关闭后的SWs发生在心脏周期的某个时刻，但可以选择基于arf的SWs的时间，以评估心脏(结构和功能)状态的特定方面。抽象的图。
{"title":"Closed-chest measurement of diastolic and systolic shear wave speed to assess myocardial stiffness","authors":"A. Caenen, L. Keijzer, S. Bézy, J. Duchenne, M. Orłowska, A. V. D. Steen, N. Jong, P. Segers, J. Bosch, J. Voigt, J. Dhooge, H. Vos","doi":"10.1093/EHJCI/JEAA356.047","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.047","url":null,"abstract":"Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Research Foundation Flanders (FWO): grant 1211620N TTW – Dutch Heart Foundation partnership program \"Earlier recognition of cardiovascular diseases\": project number 14740 Background Echocardiographic shear wave elastography (SWE) encompasses all ultrasound techniques tracking shear wave (SW) motion in the cardiac wall, of which the propagation speed is linked to the intrinsic mechanical properties. SWs can be induced naturally, for example by valve closure, or externally by using an acoustic radiation force (ARF). Although the latter is technically more demanding, it enables instantaneous stiffness assessment throughout the entire cardiac cycle (fig. a). However, it is unknown how factors such as cardiac loading and contractility, next to intrinsic mechanical properties, affect ARF-based SW speeds. Purpose We performed transthoracic SWE measurements in pigs to study the effects of hemodynamic alterations, inotropic state and myocardial infarction (MI) on diastolic and systolic SW speeds. Methods Different cardiac conditions were considered in three pigs: (i) baseline (BL), (ii) preload decrease (PD), (iii) afterload increase (AI), (iv) preload increase (PI), (v) administration of dobutamine (DOB), (vi) BL2, (vii) MI through 60-100 min. occlusion of the LAD and (viii) 40 min. reperfusion (REP). For each condition, transthoracic high frame rate ARF-based SWE acquisitions were taken in a parasternal long-axis view with a research ultrasound system. SWs were induced in the septum at 34 Hz during 1.5 s to track SW speeds throughout the cardiac cycle (fig. a&b). Systolic and diastolic SW speeds were determined from the 10% highest and lowest median values per condition, respectively. Left ventricular pressure-volume (PV) loops were recorded to estimate end-diastolic pressure (EDP), end-systolic pressure (ESP) and passive chamber stiffness (dPdV). dPdV was determined as the slope of the tangent to the fitted end-diastolic PV relationship at mean ED volume. Linear regressions and Pearson’s correlation coefficients were computed. Results Diastolic SW speed was correlated to EDP for conditions with changes in loading, and to dPdV for conditions with changes in chamber stiffness (fig. c). Both relationships were significant, with a moderate positive correlation for EDP (R = 0.48, p = 0.02) and a strong positive correlation for dPdV (R = 0.76, p l 0.01). Furthermore, the observed change in diastolic SW speed was smaller when altering EDP compared to dPdV (0.4 m/s vs. 1.0 m/s). For systolic SW speed, very strong positive correlations were found with ESP (R = 0.91, p l 0.01), and with dPdV (R = 0.81, p l 0.01) in fig. d. Conclusion This study shows that both diastolic and systolic SW speed are related to passive chamber stiffness. Moreover, loading also influenced systolic SW speed and, to a lesser extent, diastolic SW speed, presumably beca","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"78 1","pages":"56-57"},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78303007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.329
I. Visoiu, R. Rimbas, L. S. Magda, S. Mihăilă-Baldea, P. Bălănescu, D. Mihalcea, A. Chitroceanu, M. Stefan, L. Gheorghiu, A. Marinescu, A. Nicula, D. Vinereanu
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): PN-III-P1-1-TE-2016-0669, within PNCDI III Left ventricular non-compaction (LVNC) is associated with an increased risk of heart failure (HF). The presence of a real LVNC with HF with preserved ejection fraction (HFpEF), is still controverted. We evaluated prospectively 42 patients with HFpEF, 21 with LVNC (61 ± 9 years) and 21 without LVNC (LVC), aged and risk factor matched, by cardiac magnetic resonance (CMR) 1.5T. LVNC diagnosis was confirmed by Petersen and Jacquier criteria (NC/C ratio and the percentage of NC myocardium). We performed myocardial T1 mapping (normal value of 950 ± 21ms). We calculated a mean value of all native T1 (T1mean), and also for apical (apicalT1) and basal segments (basalT1). We also calculated ECV mean, basal and apical. All patients had NTproBNP and biomarkers for systemic inflammation (hsCRP, IL6, cystatin C and sST2), endothelial dysfunction: VCAM, von Willebrand factor (vWf), vWF metalloproteinase-ADAMTS13, and myocardial fibrosis: vascular peroxidase (VPO), and Galectin-3. In the LVNC, mean NC/C ratio was 2.9 ± 0.5 mm and the percentage of NC myocardium was 24.41 ± 8.8%. LVNC patients had significantly higher T1apical, higher ECVmean, ECV basal and apical (Table) by comparison with LVC group, suggesting an extensive fibrosis in LVNC group with significantly higher apical fibrosis. Inflammatory markers were similar between groups, LVNC patients had lower values of ADAMTS13, suggesting endothelial dysfunction, and higher values of Galectin-3, suggesting increased myocardial fibrosis (Table). Galectin-3 correlated positively only with apicalT1 (R = 0.49, p = 0.04). NTproBNP significantly correlated with VPO, a promotor of fibrosis (r = 0.61, p = 0.009) in LVNC group, whereas in LVC group correlated with cystatin C (r = 0.62, p = 0003) and VCAM (r = 0.4, p = 0.05). Native apical T1 cut off >1021 ms provided the highest sensibility and specificity to differentiate segments with and without NC in HFpEF (p = 0.002) (Figure). HFpEF patients with LVNC have significant higher NTproBNP, higher fibrosis than patients without LVNC, more extensive in non-compacted apical segments. Galectin-3 level correlates only with apical fibrosis on CMR, expressed by apicalT1 time. Moreover, endothelial dysfunction seems to play an important role in HFpEF generation in LVNC. All findings suggests that LVNC is a stand alone condition, not an adaptive hyper-trabeculation in HFpEF. Table.Comparison between groups NTproBNP (pg/ml) Galectin3 (ng/ml) ADAMTS13 (ng/ml) T1mean (ms) basalT1 (ms) apicalT1 (ms) ECV mean (%) ECV basal (%) ECV apical (%) LVNC 294 ± 282 8.44 ± 3.45 767.35 ± 335.56 1013.8 ± 31.8 1002.8 ± 27.2 1059 ± 73 27.2 ± 2.9 26.2 ± 2.9 29.6 ± 3.9 LVC 163 ± 71 6.67 ± 2.88 962.33 ± 253.78 1003.2 ± 28.1 1004.3 ± 29.5 1007 ± 40 24.3 ± 2.5 24.2 ± 2.7 25.2 ± 2.8 P value 0.031 0.048 0.049 0.26 0.865 0.007 0.002 0.03
{"title":"Multimodality approach by cardiac magnetic resonance and biological markers in left ventricular non-compaction with heart failure with preserved ejection fraction - revealing the unknown","authors":"I. Visoiu, R. Rimbas, L. S. Magda, S. Mihăilă-Baldea, P. Bălănescu, D. Mihalcea, A. Chitroceanu, M. Stefan, L. Gheorghiu, A. Marinescu, A. Nicula, D. Vinereanu","doi":"10.1093/EHJCI/JEAA356.329","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.329","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: Public grant(s) – National budget only. Main funding source(s): PN-III-P1-1-TE-2016-0669, within PNCDI III\u0000 \u0000 \u0000 \u0000 Left ventricular non-compaction (LVNC) is associated with an increased risk of heart failure (HF). The presence of a real LVNC with HF with preserved ejection fraction (HFpEF), is still controverted.\u0000 \u0000 \u0000 \u0000 We evaluated prospectively 42 patients with HFpEF, 21 with LVNC (61 ± 9 years) and 21 without LVNC (LVC), aged and risk factor matched, by cardiac magnetic resonance (CMR) 1.5T. LVNC diagnosis was confirmed by Petersen and Jacquier criteria (NC/C ratio and the percentage of NC myocardium). We performed myocardial T1 mapping (normal value of 950 ± 21ms). We calculated a mean value of all native T1 (T1mean), and also for apical (apicalT1) and basal segments (basalT1). We also calculated ECV mean, basal and apical. All patients had NTproBNP and biomarkers for systemic inflammation (hsCRP, IL6, cystatin C and sST2), endothelial dysfunction: VCAM, von Willebrand factor (vWf), vWF metalloproteinase-ADAMTS13, and myocardial fibrosis: vascular peroxidase (VPO), and Galectin-3.\u0000 \u0000 \u0000 \u0000 In the LVNC, mean NC/C ratio was 2.9 ± 0.5 mm and the percentage of NC myocardium was 24.41 ± 8.8%. LVNC patients had significantly higher T1apical, higher ECVmean, ECV basal and apical (Table) by comparison with LVC group, suggesting an extensive fibrosis in LVNC group with significantly higher apical fibrosis. Inflammatory markers were similar between groups, LVNC patients had lower values of ADAMTS13, suggesting endothelial dysfunction, and higher values of Galectin-3, suggesting increased myocardial fibrosis (Table). Galectin-3 correlated positively only with apicalT1 (R = 0.49, p = 0.04). NTproBNP significantly correlated with VPO, a promotor of fibrosis (r = 0.61, p = 0.009) in LVNC group, whereas in LVC group correlated with cystatin C (r = 0.62, p = 0003) and VCAM (r = 0.4, p = 0.05). Native apical T1 cut off >1021 ms provided the highest sensibility and specificity to differentiate segments with and without NC in HFpEF (p = 0.002) (Figure).\u0000 \u0000 \u0000 \u0000 HFpEF patients with LVNC have significant higher NTproBNP, higher fibrosis than patients without LVNC, more extensive in non-compacted apical segments. Galectin-3 level correlates only with apical fibrosis on CMR, expressed by apicalT1 time. Moreover, endothelial dysfunction seems to play an important role in HFpEF generation in LVNC. All findings suggests that LVNC is a stand alone condition, not an adaptive hyper-trabeculation in HFpEF.\u0000 Table.Comparison between groups NTproBNP (pg/ml) Galectin3 (ng/ml) ADAMTS13 (ng/ml) T1mean (ms) basalT1 (ms) apicalT1 (ms) ECV mean (%) ECV basal (%) ECV apical (%) LVNC 294 ± 282 8.44 ± 3.45 767.35 ± 335.56 1013.8 ± 31.8 1002.8 ± 27.2 1059 ± 73 27.2 ± 2.9 26.2 ± 2.9 29.6 ± 3.9 LVC 163 ± 71 6.67 ± 2.88 962.33 ± 253.78 1003.2 ± 28.1 1004.3 ± 29.5 1007 ± 40 24.3 ± 2.5 24.2 ± 2.7 25.2 ± 2.8 P value 0.031 0.048 0.049 0.26 0.865 0.007 0.002 0.03","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78836269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.410
N. Pavšič, P. Koritnik, M. Dolenc Novak, M. Štalc, B. Gužič Salobir, R. Zbačnik, P. Berden, Katja Prokselj
Type of funding sources: None. Myocardial fibrosis is a known prognostic factor in patients with systemic right ventricle (SRV). In these patients fixed myocardial perfusion defects are a common finding and are thought to represent areas of myocardial infarction and fibrosis. However, no study has yet correlated myocardial perfusion imaging findings with cardiac magnetic resonance (CMR) imaging, which is the imaging gold standard for detecting myocardial fibrosis. Our aim was to evaluate whether fixed myocardial perfusion defects in adult patients with SRV represent myocardial fibrosis. Patients with SRV followed at our outpatient clinic for congenital heart disease were prospectively included. Myocardial perfusion was evaluated with a two-day stress/rest single-photon emission computed tomography (SPECT) protocol, focal myocardial fibrosis with late gadolinium enhancement (LGE) and diffuse myocardial fibrosis with T1 mapping by CMR. The 12-segment model of the right ventricle was used to report segments with myocardial perfusion defects and fibrosis (Figure 1). Fifteen patients with SRV (12 patients with transposition of the great arteries following atrial switch procedure and 3 patients with congenitally corrected transposition of the great arteries; 4 (26.7%) females; mean age 34.6 ± 10.0 years) were included. Myocardial perfusion defects were present in 14 patients (93%), with predominate fixed perfusion defects (73%) and less common reversible perfusion defects (27%). Fixed myocardial perfusion defects were most frequent in anterior RV segments (figure 1), with multiple segments affected in 11 patients (median number of affected segments – 2 segments). CMR was possible in 11 (73%) patients, others had a permanent pacemaker. LGE indicating focal myocardial fibrosis was detected in only 1 (9%) patient, while increased T1 values indicating diffuse myocardial fibrosis were present in 7 (64%) patients. There was no matching between areas of fixed myocardial perfusion defects and focal myocardial fibrosis in individual patients. In our study, fixed myocardial perfusion defects detected on SPECT in patients with SRV did not represent areas of focal myocardial fibrosis on CMR. Other causes than scar may explain the frequently reported fixed perfusion defects, such as SRV anatomy with anterior position of the outflow tract and aorta, SRV morphology with variable degree of wall thickness and hypertrophy that influences tracer accumulation and image quality, or difficulties due to complex image acquisition and interpretation. To improve the diagnostic accuracy, the use of fused imaging modalities (SPECT-CT or PET-CT) is recommended in patients with SRV. Figure 1. Bull`s eye 12-segment plots of the right ventricle (RV) representing the number of segments with fixed myocardial perfusion defects detected by SPECT (1A) and LGE by CMR (1B) in patients with SRV. ANT – anterior, FW – free wall, INF – inferior, SEP – s
{"title":"Fixed myocardial perfusion defects on SPECT are not associated with focal myocardial fibrosis on CMR in adult patients with systemic right ventricle","authors":"N. Pavšič, P. Koritnik, M. Dolenc Novak, M. Štalc, B. Gužič Salobir, R. Zbačnik, P. Berden, Katja Prokselj","doi":"10.1093/EHJCI/JEAA356.410","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.410","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: None.\u0000 \u0000 \u0000 \u0000 Myocardial fibrosis is a known prognostic factor in patients with systemic right ventricle (SRV). In these patients fixed myocardial perfusion defects are a common finding and are thought to represent areas of myocardial infarction and fibrosis. However, no study has yet correlated myocardial perfusion imaging findings with cardiac magnetic resonance (CMR) imaging, which is the imaging gold standard for detecting myocardial fibrosis.\u0000 \u0000 \u0000 \u0000 Our aim was to evaluate whether fixed myocardial perfusion defects in adult patients with SRV represent myocardial fibrosis.\u0000 \u0000 \u0000 \u0000 Patients with SRV followed at our outpatient clinic for congenital heart disease were prospectively included. Myocardial perfusion was evaluated with a two-day stress/rest single-photon emission computed tomography (SPECT) protocol, focal myocardial fibrosis with late gadolinium enhancement (LGE) and diffuse myocardial fibrosis with T1 mapping by CMR. The 12-segment model of the right ventricle was used to report segments with myocardial perfusion defects and fibrosis (Figure 1).\u0000 \u0000 \u0000 \u0000 Fifteen patients with SRV (12 patients with transposition of the great arteries following atrial switch procedure and 3 patients with congenitally corrected transposition of the great arteries; 4 (26.7%) females; mean age 34.6 ± 10.0 years) were included. Myocardial perfusion defects were present in 14 patients (93%), with predominate fixed perfusion defects (73%) and less common reversible perfusion defects (27%). Fixed myocardial perfusion defects were most frequent in anterior RV segments (figure 1), with multiple segments affected in 11 patients (median number of affected segments – 2 segments). CMR was possible in 11 (73%) patients, others had a permanent pacemaker. LGE indicating focal myocardial fibrosis was detected in only 1 (9%) patient, while increased T1 values indicating diffuse myocardial fibrosis were present in 7 (64%) patients. There was no matching between areas of fixed myocardial perfusion defects and focal myocardial fibrosis in individual patients.\u0000 \u0000 \u0000 \u0000 In our study, fixed myocardial perfusion defects detected on SPECT in patients with SRV did not represent areas of focal myocardial fibrosis on CMR. Other causes than scar may explain the frequently reported fixed perfusion defects, such as SRV anatomy with anterior position of the outflow tract and aorta, SRV morphology with variable degree of wall thickness and hypertrophy that influences tracer accumulation and image quality, or difficulties due to complex image acquisition and interpretation. To improve the diagnostic accuracy, the use of fused imaging modalities (SPECT-CT or PET-CT) is recommended in patients with SRV.\u0000 Figure 1. Bull`s eye 12-segment plots of the right ventricle (RV) representing the number of segments with fixed myocardial perfusion defects detected by SPECT (1A) and LGE by CMR (1B) in patients with SRV. ANT – anterior, FW – free wall, INF – inferior, SEP – s","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"64 3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88353539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.435
N. V. Osta, Feddo P. Kirkels, A. Lyon, T. Koopsen, Tam Van Loon, M. Cramer, T. Delhaas, A. Teske, J. Lumens
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): NWO-ZonMw, VIDI grant 016.176.340 Dutch Heart Foundation (2015T082) Introduction Arrhythmogenic Cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. Geno-positive subjects with and without symptoms may suffer from sudden cardiac death. Therefore, early disease detection and risk stratification is important. Right ventricular (RV) longitudinal deformation abnormalities in early stages of disease have been shown to be of prognostic value. We propose an imaging-based patient-specific computer modelling approach for non-invasive quantification of regional ventricular tissue abnormalities. Purpose To non-invasively reveal the individual patient’s myocardial tissue substrates underlying the regional RV deformation abnormalities in AC mutation carriers. Methods In 65 individuals carrying a plakophilin-2 or desmoglein-2 mutation and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS) and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography (Figure: left). This cohort was subdivided into 3 consecutive clinical stages i.e. subclinical (concealed, n = 18) with no abnormalities, electrical stage (n = 13) with only electrocardiographic abnormalities, and structural stage (n = 34) with both electrical and structural abnormalities defined by the 2010 Task Force AC criteria. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects (Figure: middle). Using the individuals’ RVfw, IVS, and LVfw strain patterns as model input, this protocol automatically estimated regional RV and global IVS and LVfw tissue properties, such as myocardial contractility, stiffness, and activation delay. Results The computational model was able to reproduce the regional deformation patterns as measured clinically. Patient-specific parameter estimation results (Figure: right) revealed that clinical AC disease progression is characterized by a decrease in contractility and an increase in stiffness and mechanical delay of the RV myocardial tissue in the basal segment compared to the apex. The subclinical stage subjects showed tissue properties comparable to the control group, including a small apex-to-base heterogeneity in tissue properties. Our patient-specific modelling approach is able to reveal individual myocardial substrates underlying the regional RV deformation abnormalities. Early abnormalities in RV longitudinal strain are most likely caused by increased heterogeneity in local tissue properties, such as an apex-to-base decrease of contractility, increased of myocardial stiffness, and time to peak stress. Abnormalities in tissue properties may be found already in the subcl
{"title":"Arrhythmogenic cardiomyopathy is characterized by apex-to-base heterogeneity of right ventricular myocardial contractility, stiffness, and mechanical delay: a patient-specific modeling study","authors":"N. V. Osta, Feddo P. Kirkels, A. Lyon, T. Koopsen, Tam Van Loon, M. Cramer, T. Delhaas, A. Teske, J. Lumens","doi":"10.1093/EHJCI/JEAA356.435","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.435","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: Public grant(s) – National budget only. Main funding source(s): NWO-ZonMw, VIDI grant 016.176.340 Dutch Heart Foundation (2015T082)\u0000 Introduction\u0000 Arrhythmogenic Cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. Geno-positive subjects with and without symptoms may suffer from sudden cardiac death. Therefore, early disease detection and risk stratification is important. Right ventricular (RV) longitudinal deformation abnormalities in early stages of disease have been shown to be of prognostic value. We propose an imaging-based patient-specific computer modelling approach for non-invasive quantification of regional ventricular tissue abnormalities.\u0000 Purpose\u0000 To non-invasively reveal the individual patient’s myocardial tissue substrates underlying the regional RV deformation abnormalities in AC mutation carriers.\u0000 Methods\u0000 In 65 individuals carrying a plakophilin-2 or desmoglein-2 mutation and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS) and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography (Figure: left). This cohort was subdivided into 3 consecutive clinical stages i.e. subclinical (concealed, n = 18) with no abnormalities, electrical stage (n = 13) with only electrocardiographic abnormalities, and structural stage (n = 34) with both electrical and structural abnormalities defined by the 2010 Task Force AC criteria. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects (Figure: middle). Using the individuals’ RVfw, IVS, and LVfw strain patterns as model input, this protocol automatically estimated regional RV and global IVS and LVfw tissue properties, such as myocardial contractility, stiffness, and activation delay.\u0000 Results\u0000 The computational model was able to reproduce the regional deformation patterns as measured clinically. Patient-specific parameter estimation results (Figure: right) revealed that clinical AC disease progression is characterized by a decrease in contractility and an increase in stiffness and mechanical delay of the RV myocardial tissue in the basal segment compared to the apex. The subclinical stage subjects showed tissue properties comparable to the control group, including a small apex-to-base heterogeneity in tissue properties.\u0000 \u0000 \u0000 \u0000 Our patient-specific modelling approach is able to reveal individual myocardial substrates underlying the regional RV deformation abnormalities. Early abnormalities in RV longitudinal strain are most likely caused by increased heterogeneity in local tissue properties, such as an apex-to-base decrease of contractility, increased of myocardial stiffness, and time to peak stress. Abnormalities in tissue properties may be found already in the subcl","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"2903 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86516802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-02-08DOI: 10.1093/EHJCI/JEAA356.243
P. A. Diemen, M. Bom, R. Driessen, H. Everaars, R. Winter, P. M. Ven, M. Freiman, L. Goshen, E. Langzam, J. Min, J. Leipsic, P. Raijmakers, A. Rossum, I. Danad, P. Knaapen
Type of funding sources: None. Inflammation is a key component in the atherosclerotic process, initiating and sustaining plaques and serving as a trigger for plaque rupture leading to myocardial infarction. Coronary computed tomography angiography (CCTA) derived pericoronary adipose tissue attenuation (PCATa) has been proposed as surrogate marker for coronary inflammation and might improve risk assessment on top of CCTA derived cardiovascular risk-factors: atherosclerotic burden and plaque vulnerability. To assess the prognostic value of PCATa beyond atherosclerotic burden and high-risk plaques (HRPs). A total of 543 patients who underwent CCTA because of suspected CAD were included. CCTA assessment comprised coronary artery calcium score (CACS), presence of obstructive CAD (≥50% stenosis) and HRPs, total plaque volume (TPV), non-calcified plaque volume (NCPV), and PCATa. The endpoint was a composite of death and non-fatal myocardial infarction (MI). Prognostic thresholds were determined for quantitative CCTA variables. During a median follow-up of 6.6 [interquartile range: 4.7-7.8] years, the endpoint was observed in 42 (20 MI/22 death) patients. CACS >83, obstructive CAD, HRPs, TPV >269mm3, and NCPV >83mm3 were associated with shorter time to the endpoint with unadujsted hazard ratio’s (HR) of 5.37 (95% confidence interval (CI): 2.56-11.29), 5.70 (95% CI: 2.40-13.55), 3.31 (95% CI: 1.80-6.07), 7.76 (95% CI: 3.59-16.81), and 6.77 (95% CI: 3.24-14.16), respectively (p < 0.001 for all). PCATa of the RCA >-74.4 Hounsfield units was associated with worse prognosis (unadjusted HR: 1.99, 95% CI: 1.04-3.79, p = 0.037), whereas PCATa of the LAD and Cx were not associated with prognosis. PCATa of the RCA remained a significant predictor of death and non-fatal MI corrected for CCTA variables and clincal chacteristics associated with the endpoint (adjusted HR: 2.11, 95% CI: 1.11-4.04, p = 0.024). Coronary inflammation determined by PCATa of the RCA provides incremental prognostic value beyond clinical characteristics and comprehensive CCTA assessment. Abstract Figure. Take-home figure
资金来源类型:无。炎症是动脉粥样硬化过程中的一个关键组成部分，它启动和维持斑块，并作为斑块破裂导致心肌梗死的触发因素。冠状动脉ct血管造影(CCTA)衍生的冠状动脉周围脂肪组织衰减(PCATa)已被提议作为冠状动脉炎症的替代标志物，并可能在CCTA衍生的心血管危险因素(动脉粥样硬化负担和斑块易损)的基础上改善风险评估。评估PCATa在动脉粥样硬化负荷和高危斑块(HRPs)之外的预后价值。共纳入543例因疑似CAD而行CCTA的患者。CCTA评估包括冠状动脉钙评分(CACS)、阻塞性CAD(≥50%狭窄)和心率、总斑块体积(TPV)、非钙化斑块体积(NCPV)和PCATa。终点是死亡和非致死性心肌梗死(MI)的复合。确定定量CCTA变量的预后阈值。在中位随访6.6年(四分位数间距:4.7-7.8年)期间，42例(20例MI/22例死亡)患者观察到终点。CACS >83、阻塞性CAD、HRPs、TPV >269mm3和NCPV >83mm3与到达终点的时间较短相关，未调整的风险比(HR)分别为5.37(95%可信区间2.56-11.29)、5.70 (95% CI 2.40-13.55)、3.31 (95% CI 1.80-6.07)、7.76 (95% CI 3.59-16.81)和6.77 (95% CI 3.24-14.16) (p -74.4 Hounsfield单位与较差的预后相关(未调整的HR: 1.99, 95% CI:1.04-3.79, p = 0.037)，而LAD和Cx的PCATa与预后无关。RCA的PCATa仍然是死亡和非致死性心肌梗死的重要预测因子，校正了CCTA变量和与终点相关的临床特征(校正HR: 2.11, 95% CI: 1.11-4.04, p = 0.024)。通过RCA的PCATa检测冠状动脉炎症，除了临床特征和综合CCTA评估外，还提供了更多的预后价值。抽象的图。实得图
{"title":"Pericoronary adipose tissue attenuation leads to improved prognostication beyond atherosclerotic burden and high-risk plaques in patients with suspected coronary artery disease","authors":"P. A. Diemen, M. Bom, R. Driessen, H. Everaars, R. Winter, P. M. Ven, M. Freiman, L. Goshen, E. Langzam, J. Min, J. Leipsic, P. Raijmakers, A. Rossum, I. Danad, P. Knaapen","doi":"10.1093/EHJCI/JEAA356.243","DOIUrl":"https://doi.org/10.1093/EHJCI/JEAA356.243","url":null,"abstract":"\u0000 \u0000 \u0000 Type of funding sources: None.\u0000 \u0000 \u0000 \u0000 Inflammation is a key component in the atherosclerotic process, initiating and sustaining plaques and serving as a trigger for plaque rupture leading to myocardial infarction. Coronary computed tomography angiography (CCTA) derived pericoronary adipose tissue attenuation (PCATa) has been proposed as surrogate marker for coronary inflammation and might improve risk assessment on top of CCTA derived cardiovascular risk-factors: atherosclerotic burden and plaque vulnerability.\u0000 \u0000 \u0000 \u0000 To assess the prognostic value of PCATa beyond atherosclerotic burden and high-risk plaques (HRPs).\u0000 \u0000 \u0000 \u0000 A total of 543 patients who underwent CCTA because of suspected CAD were included. CCTA assessment comprised coronary artery calcium score (CACS), presence of obstructive CAD (≥50% stenosis) and HRPs, total plaque volume (TPV), non-calcified plaque volume (NCPV), and PCATa. The endpoint was a composite of death and non-fatal myocardial infarction (MI). Prognostic thresholds were determined for quantitative CCTA variables.\u0000 \u0000 \u0000 \u0000 During a median follow-up of 6.6 [interquartile range: 4.7-7.8] years, the endpoint was observed in 42 (20 MI/22 death) patients. CACS >83, obstructive CAD, HRPs, TPV >269mm3, and NCPV >83mm3 were associated with shorter time to the endpoint with unadujsted hazard ratio’s (HR) of 5.37 (95% confidence interval (CI): 2.56-11.29), 5.70 (95% CI: 2.40-13.55), 3.31 (95% CI: 1.80-6.07), 7.76 (95% CI: 3.59-16.81), and 6.77 (95% CI: 3.24-14.16), respectively (p < 0.001 for all). PCATa of the RCA >-74.4 Hounsfield units was associated with worse prognosis (unadjusted HR: 1.99, 95% CI: 1.04-3.79, p = 0.037), whereas PCATa of the LAD and Cx were not associated with prognosis. PCATa of the RCA remained a significant predictor of death and non-fatal MI corrected for CCTA variables and clincal chacteristics associated with the endpoint (adjusted HR: 2.11, 95% CI: 1.11-4.04, p = 0.024).\u0000 \u0000 \u0000 \u0000 Coronary inflammation determined by PCATa of the RCA provides incremental prognostic value beyond clinical characteristics and comprehensive CCTA assessment.\u0000 Abstract Figure. Take-home figure\u0000","PeriodicalId":11963,"journal":{"name":"European Journal of Echocardiography","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90345785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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