背景:主动脉瓣狭窄(AS)后负荷增加会诱导左心室(LV)重塑以保持正常的射血分数。这种代偿反应可能变得适应不良,并表现为运动异常。在早期亚临床阶段识别收缩和松弛功能障碍以防止不可逆转的恶化是临床挑战。
目的:评估随着AS重塑的进展,3D时域中区域壁动力学的变化。
方法:回顾性。
方法:共有31例射血分数降低和保留的AS患者(14例AS_rEF:7例男性,66.5[7.8]岁;17AS_pEF:12名男性,67.0[6.0]岁)和15岁健康(6名男性,61.0[7.0]岁)。
■1.5T磁共振成像/稳态自由进动和晚钆增强序列。
结果:在3D+时域和包括壁增厚(TI)在内的运动指标中重建了各个LV模型,不同步指数(DI),收缩率(CR),和松弛率(RR)自动提取,并与瘢痕形成和重塑的存在相关联。
方法:Shapiro-Wilk:数据正常性;Kruskal-Wallis:显著性差异(P<0.05);ICC和CV:变异性;Mann-Whitney:效应大小。
结果:与AS_pEF和健康组相比,AS_rEF组显示出明显的心脏运动恶化(TIAS_rEF:0.92[0.85]mm,TIAS_pEF:5.13[1.99]mm,正常:3.61[1.09]毫米,ES:0.48-0.83;DIAS_rEF:17.11[7.89]%,DIAS_pEF:6.39[4.04]%,不健康:5.71[1.87]%,ES:0.32-0.85;CRAS_rEF:8.69[6.11]毫米/秒,CRAS_pEF:16.48[6.70]mm/秒,正常:10.82[4.57]毫米/秒,ES:0.29-0.60;RRAS_rEF:8.45[4.84]毫米/秒;RRAS_pEF:13.49[8.56]毫米/秒,RR健康:9.31[2.48]毫米/秒,ES:0.14-0.43)。健康组和AS_pEF组之间的运动指标差异不明显(P值=0.16-0.72)。AS_rEF组以偏心性肥大为主(47.1%),并伴有瘢痕。相反,AS_pEF组以同心重塑和肥大为主(71.4%),与健康者相比,这可能表明运动亢进伴轻微的壁不同步。LV力学功能障碍对应于心肌瘢痕的存在(AS为54.9%),它恢复了由LV重塑启动和执行的补偿机制。
结论:提出的3D+时间建模技术可以区分AS_pEF之间的区域运动异常,AS_rEF,和健康的队列,辅助临床诊断和AS进展监测。尽管EF正常,但在AS早期,亚临床心肌功能障碍很明显。
方法:4技术效果:第一阶段。
Increased afterload in aortic stenosis (AS) induces left ventricle (LV) remodeling to preserve a normal ejection fraction. This compensatory response can become maladaptive and manifest with motion abnormality. It is a clinical challenge to identify contractile and relaxation dysfunction during early subclinical stage to prevent irreversible deterioration.
To evaluate the changes of regional wall dynamics in 3D + time domain as remodeling progresses in AS.
Retrospective.
A total of 31 AS patients with reduced and preserved ejection fraction (14 AS_rEF: 7 male, 66.5 [7.8] years old; 17 AS_pEF: 12 male, 67.0 [6.0] years old) and 15 healthy (6 male, 61.0 [7.0] years old).
1.5 T Magnetic resonance imaging/steady state free precession and late-gadolinium enhancement sequences.
Individual LV models were reconstructed in 3D + time domain and motion metrics including wall thickening (TI), dyssynchrony index (DI), contraction rate (CR), and relaxation rate (RR) were automatically extracted and associated with the presence of scarring and remodeling.
Shapiro-Wilk: data normality; Kruskal-Wallis: significant difference (P < 0.05); ICC and CV: variability; Mann-Whitney: effect size.
AS_rEF group shows distinct deterioration of cardiac motions compared to AS_pEF and healthy groups (TIAS_rEF : 0.92 [0.85] mm, TIAS_pEF : 5.13 [1.99] mm, TIhealthy : 3.61 [1.09] mm, ES: 0.48-0.83; DIAS_rEF : 17.11 [7.89]%, DIAS_pEF : 6.39 [4.04]%, DIhealthy : 5.71 [1.87]%, ES: 0.32-0.85; CRAS_rEF : 8.69 [6.11] mm/second, CRAS_pEF : 16.48 [6.70] mm/second, CRhealthy : 10.82 [4.57] mm/second, ES: 0.29-0.60; RRAS_rEF : 8.45 [4.84] mm/second; RRAS_pEF : 13.49 [8.56] mm/second, RRhealthy : 9.31 [2.48] mm/second, ES: 0.14-0.43). The difference in the motion metrics between healthy and AS_pEF groups were insignificant (P-value = 0.16-0.72). AS_rEF group was dominated by eccentric hypertrophy (47.1%) with concomitant scarring. Conversely, AS_pEF group was dominated by concentric remodeling and hypertrophy (71.4%), which could demonstrate hyperkinesia with slight wall dyssynchrony than healthy. Dysfunction of LV mechanics corresponded to the presence of myocardial scarring (54.9% in AS), which reverted the compensatory mechanisms initiated and performed by LV remodeling.
The proposed 3D + time modeling technique may distinguish regional motion abnormalities between AS_pEF, AS_rEF, and healthy cohorts, aiding clinical diagnosis and monitoring of AS progression. Subclinical myocardial dysfunction is evident in early AS despite of normal EF.
4 TECHNICAL EFFICACY: Stage 1.