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特征追踪 CMR 评价抗高血压药物治疗的顽固性高血压患者左心室心肌应变对慢性压力超负荷的反应。

Left ventricular myocardial strain responding to chronic pressure overload in patients with resistant hypertension evaluated by feature-tracking CMR.

机构信息

Department of Diagnostic and Interventional Radiology and Nuclear Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Department of Cardiology, University Heart & Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246, Hamburg, Germany.

出版信息

Eur Radiol. 2023 Sep;33(9):6278-6289. doi: 10.1007/s00330-023-09595-z. Epub 2023 Apr 10.

DOI:10.1007/s00330-023-09595-z
PMID:37032365
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10415476/
Abstract

OBJECTIVES

The study aimed to investigate the alterations of myocardial deformation responding to long-standing pressure overload and the effects of focal myocardial fibrosis using feature-tracking cardiac magnetic resonance (FT-CMR) in patients with resistant hypertension (RH).

METHODS

Consecutive RH patients were prospectively recruited and underwent CMR at a single institution. FT-CMR analyses based on cine images were applied to measure left ventricular (LV) peak systolic global longitudinal (GLS), radial (GRS), and circumferential strain (GCS). Functional and morphological CMR variables, and late gadolinium enhancement (LGE) imaging were also obtained.

RESULTS

A total of 50 RH patients (63 ± 12 years, 32 men) and 18 normotensive controls (57 ± 8 years, 12 men) were studied. RH patients had a higher average systolic blood pressure than controls (166 ± 21 mmHg vs. 116 ± 8 mmHg, p < 0.001) with the intake of 5 ± 1 antihypertensive drugs. RH patients showed increased LV mass index (78 ± 15 g/m vs. 61 ± 9 g/m, p < 0.001), decreased GLS (- 16 ± 3% vs. - 19 ± 2%, p = 0.001) and GRS (41 ± 12% vs. 48 ± 8%, p = 0.037), and GCS was reduced by trend (- 17 ± 4% vs. - 19 ± 4%, p = 0.078). Twenty-one (42%) RH patients demonstrated a LV focal myocardial fibrosis (LGE +). LGE + RH patients had higher LV mass index (85 ± 14 g/m vs. 73 ± 15 g/m, p = 0.007) and attenuated GRS (37 ± 12% vs. 44 ± 12%, p = 0.048) compared to LGE - RH patients, whereas GLS (p = 0.146) and GCS (p = 0.961) were similar.

CONCLUSION

Attenuation of LV GLS and GRS, and GCS decline by tendency, might be adaptative changes responding to chronic pressure overload. There is a high incidence of focal myocardial fibrosis in RH patients, which is associated with reduced LV GRS.

CLINICAL RELEVANCE STATEMENT

Feature-tracking CMR-derived myocardial strain offers insights into the influence of long-standing pressure overload and of a myocardial fibrotic process on cardiac deformation in patients with resistant hypertension.

KEY POINTS

• Variations of left ventricular strain are attributable to the degree of myocardial impairment in resistant hypertensive patients. • Focal myocardial fibrosis of the left ventricle is associated with attenuated global radial strain. • Feature-tracking CMR provides additional information on the attenuation of myocardial deformation responding to long-standing high blood pressure.

摘要

目的

本研究旨在应用特征追踪心脏磁共振(FT-CMR)探讨长期压力超负荷状态下心肌变形的变化,并研究局灶性心肌纤维化对其的影响,研究对象为耐药性高血压(RH)患者。

方法

连续纳入 RH 患者,在一家医疗机构进行前瞻性 CMR 检查。应用电影图像的 FT-CMR 分析来测量左心室(LV)收缩期整体纵向应变(GLS)、径向应变(GRS)和圆周应变(GCS)峰值。还获得了功能和形态学 CMR 变量以及钆延迟增强(LGE)图像。

结果

共纳入 50 例 RH 患者(63±12 岁,32 名男性)和 18 名血压正常的对照者(57±8 岁,12 名男性)。RH 患者的平均收缩压高于对照组(166±21mmHg 比 116±8mmHg,p<0.001),同时服用 5±1 种降压药。RH 患者的 LV 质量指数(78±15g/m 比 61±9g/m,p<0.001)更高,GLS(-16±3%比-19±2%,p=0.001)和 GRS(41±12%比 48±8%,p=0.037)更低,GCS 也呈下降趋势(-17±4%比-19±4%,p=0.078)。21 例(42%)RH 患者存在局灶性心肌纤维化(LGE+)。与 LGE- RH 患者相比,LGE+ RH 患者的 LV 质量指数(85±14g/m 比 73±15g/m,p=0.007)更高,GRS 更低(37±12%比 44±12%,p=0.048),而 GLS(p=0.146)和 GCS(p=0.961)无显著差异。

结论

LV GLS 和 GRS 的减弱以及 GCS 的下降可能是对慢性压力超负荷的适应性变化。RH 患者存在局灶性心肌纤维化的高发生率,与 LV GRS 降低有关。

临床相关性

特征追踪 CMR 衍生的心肌应变提供了有关长期压力超负荷和心肌纤维化过程对耐药性高血压患者心脏变形影响的深入了解。

关键点

  1. 左心室应变的变化归因于耐药性高血压患者心肌损伤的程度。

  2. 左心室局灶性心肌纤维化与整体径向应变减弱有关。

  3. 特征追踪 CMR 可提供有关长期高血压状态下心肌变形减弱的附加信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/1bcbbf413c6a/330_2023_9595_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/38e644ad0563/330_2023_9595_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/278290843fda/330_2023_9595_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/1bcbbf413c6a/330_2023_9595_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/38e644ad0563/330_2023_9595_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/278290843fda/330_2023_9595_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ed/10415476/1bcbbf413c6a/330_2023_9595_Fig3_HTML.jpg

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