Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Cardiology Unit, Clinical and Molecular Medicine Department, Faculty of Medicine and Psychology, "Sapienza" University of Rome, Rome, Italy.
Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Cardiology, University Hospital Ramón y Cajal, Madrid, Spain.
Int J Cardiol. 2020 May 1;306:102-108. doi: 10.1016/j.ijcard.2020.03.002. Epub 2020 Mar 3.
Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions.
In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133).
Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p < 0.001 vs. all groups). Native T1 and T2 were interrelated in patient groups and the strength of association was condition-specific (CKD r = 0.558, HTN r = 0.324, both p < 0.001; HCM r = 0.157, p = 0.05). Native T1 and T2 were similarly correlated in all CKD stages (S3 r = 0.501, S4 0.586, S5 r = 0.424, p < 0.001 for all). Native T1 was the strongest myocardial discriminator between patients and controls (area under the curve, AUC HCM: 0.97; CKD: 0.97, HTN 0.98), native T2 between CKD vs HCM (AUC 0.90) and native T1 and T2 between CKD vs HTN (AUC: 0.83 and 0.80 respectively), p < 0.001 for all.
Our findings reveal different CMR signatures of common hypertrophic cardiac phenotypes. Native T1 was raised in all conditions, indicating the presence of pathologic hypertrophic remodelling. Markedly raised native T2 was CKD-specific, suggesting a prominent role of intramyocardial fluid.
左心室（LV）肥厚伴舒张功能障碍和心力衰竭是慢性肾脏病（CKD）心脏重构的主要表现。先前的研究表明，CKD 中 T1 映射值的增加与弥漫性纤维化有关。心肌固有 T1 是一种非特异性的读出值，也可能与心肌内液体增加有关。我们检查了同时存在的 T1 和 T2 映射特征，并与其他肥厚性疾病进行了比较。
在这项前瞻性多中心研究中，比较了连续接受常规临床心脏磁共振（CMR）成像的 CKD 患者（n=154）与高血压（HTN，n=163）和肥厚型心肌病（HCM，n=158）患者，以及血压正常的对照组（n=133）。
所有患者组的心肌固有 T1 均显著升高，而 CKD 组仅固有 T2 升高（p<0.001 与所有组相比）。在患者组中，心肌固有 T1 和 T2 相互关联，且关联强度与疾病特异性相关（CKD r=0.558，HTN r=0.324，均 p<0.001；HCM r=0.157，p=0.05）。在所有 CKD 阶段，心肌固有 T1 和 T2 也有类似的相关性（S3 r=0.501，S4 0.586，S5 r=0.424，均 p<0.001）。心肌固有 T1 是区分患者和对照组的最强心肌鉴别指标（AUC HCM：0.97；CKD：0.97，HTN 0.98），心肌固有 T2 是 CKD 与 HCM 之间的鉴别指标（AUC 0.90），心肌固有 T1 和 T2 是 CKD 与 HTN 之间的鉴别指标（AUC：0.83 和 0.80，均 p<0.001）。
我们的研究结果揭示了常见肥厚性心脏表型的不同 CMR 特征。所有情况下的心肌固有 T1 均升高，表明存在病理性肥厚重构。明显升高的心肌固有 T2 是 CKD 特异性的，提示心肌内液体的作用突出。
