通过左心房容积测量改进肺动脉楔压的解读--心脏磁共振成像研究

Gülmisal Güder, Theresa Reiter, M. Drayss, Wolfgang Bauer, B. Lengenfelder, P. Nordbeck, G. Fette, S. Frantz, C. Morbach, Stefan Störk
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摘要

背景:肺动脉楔压(PAWP)被认为是左心室舒张末压(LVEDP)的可靠指标,但在左侧心脏病(LHD)患者中这种关联性较弱。我们比较了心力衰竭(HF)和左心室射血分数(LVEF)降低、PAWP 或 LVEDP 升高或未升高的患者心脏磁共振成像(CMR)的形态学差异。方法我们回顾性地确定了 121 名 LVEF < 50% 的患者,他们都接受了右心导管检查 (RHC) 和 CMR。75例患者的LVEDP数据可用。研究结果研究样本的平均年龄为 63 ± 14 岁,平均 LVEF 为 32 ± 10%,72% 为男性。约 53% 的患者 PAWP 升高(>15 mmHg)。在多变量逻辑回归分析中,NT-proBNP、左心房射血分数(LAEF)和左心室收缩末期容积指数可独立预测 PAWP 升高。在 75 位有 LVEDP 数据的患者中,79% 的患者 LVEDP 升高,70% 的患者同时伴有 PAWP 升高。相比之下,除一名患者外,所有 PAWP 升高的患者和一半 PAWP 正常的患者都伴有 LVEDP 升高。Bland-Altman图显示,LVEDP和PAWP之间存在+5.0 mmHg的系统性偏差。值得注意的是,LAEF 是 LVEDP 升高且 PAWP ≤ 或大于 15 mmHg 的患者之间唯一存在显著差异的 CMR 变量。结论:在 LVEF < 50% 的患者中,PAWP 正常并不能可靠地排除 LHD,LVEDP 升高比 PAWP 升高更常见。LAEF是决定PAWP是否升高的最重要因素,这表明LHD患者保留LAEF可防止向肺后衰竭及随后的肺压升高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Improved Interpretation of Pulmonary Artery Wedge Pressures through Left Atrial Volumetry—A Cardiac Magnetic Resonance Imaging Study
Background: The pulmonary artery wedge pressure (PAWP) is regarded as a reliable indicator of left ventricular end-diastolic pressure (LVEDP), but this association is weaker in patients with left-sided heart disease (LHD). We compared morphological differences in cardiac magnetic resonance imaging (CMR) in patients with heart failure (HF) and a reduced left ventricular ejection fraction (LVEF), with or without elevation of PAWP or LVEDP. Methods: We retrospectively identified 121 patients with LVEF < 50% who had undergone right heart catheterization (RHC) and CMR. LVEDP data were available for 75 patients. Results: The mean age of the study sample was 63 ± 14 years, the mean LVEF was 32 ± 10%, and 72% were men. About 53% of the patients had an elevated PAWP (>15 mmHg). In multivariable logistic regression analysis, NT-proBNP, left atrial ejection fraction (LAEF), and LV end-systolic volume index independently predicted an elevated PAWP. Of the 75 patients with available LVEDP data, 79% had an elevated LVEDP, and 70% had concomitant PAWP elevation. By contrast, all but one patient with elevated PAWP and half of the patients with normal PAWP had concomitant LVEDP elevation. The Bland–Altman plot revealed a systematic bias of +5.0 mmHg between LVEDP and PAWP. Notably, LAEF was the only CMR variable that differed significantly between patients with elevated LVEDP and a PAWP ≤ or >15 mmHg. Conclusions: In patients with LVEF < 50%, a normal PAWP did not reliably exclude LHD, and an elevated LVEDP was more frequent than an elevated PAWP. LAEF was the most relevant determinant of an increased PAWP, suggesting that a preserved LAEF in LHD may protect against backward failure into the lungs and the subsequent increase in pulmonary pressure.
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