The association of secondary hyperparathyroidism and myocardial damages in hemodialysis end-stage renal disease patients: assessed by cardiovascular magnetic resonance native T1 mapping.
The association of secondary hyperparathyroidism and myocardial damages in hemodialysis end-stage renal disease patients: assessed by cardiovascular magnetic resonance native T1 mapping.
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DOI：
10.1186/s12968-021-00713-8
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发表时间：
2021-03-11
期刊：
影响因子：
--
通讯作者：
Guo Y
中科院分区：
文献类型：
--
作者：
Xu H;Peng W;Yang Z;Zhang Y;Xia C;Li Z;Xu R;Guo Y
继发性甲状旁腺功能亢进是终末期肾病（ESRD）的常见并发症，可能与心血管疾病有关。因此，本研究的目的是探讨心肌损害使用非造影剂心血管磁共振（CMR）在接受血液透析的ESRD患者，并进一步探讨其与甲状旁腺激素（PTH）毒性的关系。72例接受常规血液透析的成人ESRD患者和30例健康受试者接受CMR检查。在短轴平面上从二尖瓣水平到左心室（LV）心尖的连续CMR电影切片，垂直双腔长轴平面和水平四腔平面的电影系列。天然T1映射使用修改后的Look-Sep反转恢复（MOLLI）序列获得。分析天然T1值和心肌应变。 从所有入组患者中获得免疫反应性甲状旁腺激素（iPTH）。发现40例（55.6%）血液透析ESRD患者iPTH水平升高。与健康对照组相比，iPTH靶向治疗组和iPTH升高组的左室射血分数（LVEF）均降低（55.9 ± 12. 0% vs. 65.0 ± 4.5%; 51.7 ± 12.8vs. 65.0 ± 4.5%，均P < 0.05）。iPTH升高的ESRD患者的平均峰值径向应变（PRS）、峰值周向应变（PCS）和峰值纵向应变（PLS）最低;然而，在这三组中未观察到显著差异。从基底部到心尖部，iPTH水平升高的ESRD患者的天然T1倾向于高于iPTH靶向治疗组和健康受试者（均P < 0.05）。在靶向iPTH治疗的ESRD患者中，基底段和中段的天然T1均显著高于正常人（基底段，1304 ± 41 ms vs. 1238 ± 36 ms，P = 0.001;中段，1300 ± 43 ms vs. 1242 ± 50 ms，P < 0.001）。比较三组的总体天然T1值，目标和iPTH水平升高的ESRD患者显示天然T1升高（分别为1305 ± 41 ms vs. 1251 ± 49 ms，P = 0.001; 1334 ± 40 ms vs. 1251 ± 49 ms，P < 0.001）。基底段和整体天然T1值与iPTH中度相关（r = 0.4，P < 0.001; r = 0.5，P < 0.001）。多元线性回归分析显示，总体天然T1值（β = 1.0，P = 0.01）与iPTH独立相关。iPTH水平升高与接受维持性血液透析的ESRD患者的心肌损伤相关，并且是其独立危险因素。试验注册：中国临床试验注册中心（http：//www.chictr.org.cn/index.aspx）ChiCTR-DND-17012976，13/12/2017，回顾性注册。
Secondary hyperparathyroidism is a common complication of end-stage renal disease (ESRD), which may be associated with cardiovascular diseases. Thus, this study aimed to explore myocardial damage using non-contrast cardiovascular magnetic resonance (CMR) in ESRD patients undergoing hemodialysis and further investigate its relationship with parathyroid hormone (PTH) toxicity. Seventy-two adult ESRD patients receiving regular hemodialysis and 30 healthy subjects underwent CMR examination. Continuous CMR cine sections from the mitral valve level to the left ventricular (LV) apex in the short-axis plane, cine series of vertical two-chamber long-axis plane, and horizontal four-chamber plane were acquired. Native T1 mapping was obtained using modified Look-Locker inversion recovery (MOLLI) sequences. Native T1 values and myocardial strain were analyzed. Immunoreactive parathyroid hormone (iPTH) was obtained from all enrolled patients. Forty (55.6%) hemodialysis ESRD patients were found to have increased iPTH levels. LV ejection fraction (LVEF) of both ESRD patients with targeted and increased iPTH levels was decreased compared with healthy subjects (55.9 ± 12.0% vs. 65.0 ± 4.5%; 51.7 ± 12.8 vs. 65.0 ± 4.5%, both P < 0.05). The mean peak radial strain (PRS), peak circumferential strain (PCS), and peak longitudinal strain (PLS) were lowest in ESRD patients with increased iPTH; however, no significant difference was observed among these three groups. Segmentally, from base to apex, the native T1 of ESRD patients with increased iPTH levels tended to be higher than those with targeted iPTH and healthy subjects (all P < 0.05). In ESRD patients with targeted iPTH, both native T1 of basal and middle segments were significantly higher than normal subjects (basal, 1304 ± 41 ms vs. 1238 ± 36 ms, P = 0.001; middle, 1300 ± 43 ms vs. 1242 ± 50 ms, P < 0.001). Comparing global native T1 values in the three groups, ESRD patients with targeted and increased iPTH level showed increased native T1 (1305 ± 41 ms vs. 1251 ± 49 ms, P = 0.001; 1334 ± 40 ms vs. 1251 ± 49 ms, P < 0.001, respectively). Native T1 values of the basal segment and global native T1 were moderately associated with iPTH (r = 0.4, P < 0.001; r = 0.5, P < 0.001). Multiple linear regression analysis showed that global native T1 values (beta = 1.0, P = 0.01) were independently associated with iPTH. Elevated iPTH level was associated with and was an independent risk factor for myocardial damage in ESRD patients undergoing maintenance hemodialysis. Trial registration: Chinese Clinical Trial Registry (http://www.chictr.org.cn/index.aspx) ChiCTR-DND-17012976, 13/12/2017, retrospectively registered.
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影响因子：
168.9
作者：
Matsushita, Kunihiro;van der Velde, Marije;Astor, Brad C.;Woodward, Mark;Levey, Andrew S.;de Jong, Paul E.;Coresh, Josef;Gansevoort, Ron T.
通讯作者：
Gansevoort, Ron T.
DOI：
10.1038/ki.2009.188
发表时间：
2009-08-01
期刊：
Kidney international. Supplement
影响因子：
--
作者：
通讯作者：
--
影响因子：
13.6
作者：
Kottgen, Anna;Russell, Stuart D.;Coresh, Josef
通讯作者：
Coresh, Josef
影响因子：
2.4
作者：
Aggarwal, Himanshu;AlJaroudi, Wael A.;Hage, Fadi G.
通讯作者：
Hage, Fadi G.
影响因子：
2.3
作者：
Asche, C. V.;Marx, S. E.;Andress, D.
通讯作者：
Andress, D.