Improved Interpretation of Pulmonary Artery Wedge Pressures through Left Atrial Volumetry—A Cardiac Magnetic Resonance Imaging Study

TL;DR

This study shows that pulmonary artery wedge pressure (PAWP) may not reliably reflect left heart disease in patients with reduced heart function, and left atrial ejection fraction is a better indicator.

Contribution

The study identifies left atrial ejection fraction as a novel CMR predictor of elevated PAWP in patients with reduced LVEF.

Findings

Elevated PAWP was independently predicted by NT-proBNP, left atrial ejection fraction, and LV end-systolic volume index.

A normal PAWP did not reliably exclude elevated left ventricular end-diastolic pressure (LVEDP) in patients with reduced LVEF.

Left atrial ejection fraction was the only CMR variable significantly different between patients with elevated LVEDP and PAWP levels.

Abstract

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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