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. 2021 May;37(5):1745-1755.
doi: 10.1007/s10554-020-02143-6. Epub 2021 Jan 27.

Underfilling decreases left ventricular function in pulmonary arterial hypertension

Hannah Sjögren  1 , Barbro Kjellström  1   2 , Anna Bredfelt  1 , Katarina Steding-Ehrenborg  1   3 , Göran Rådegran  4 , Roger Hesselstrand  5 , Håkan Arheden  1 , Ellen Ostenfeld  6   7
Affiliations

Underfilling decreases left ventricular function in pulmonary arterial hypertension

Hannah Sjögren et al. Int J Cardiovasc Imaging. 2021 May.

Abstract

To evaluate the association between impaired left ventricular (LV) longitudinal function and LV underfilling in patients with pulmonary arterial hypertension (PAH). Thirty-nine patients with PAH and 18 age and sex-matched healthy controls were included. LV volume and left atrial volume (LAV) were delineated in short-axis cardiac magnetic resonance (CMR) cine images. LV longitudinal function was assessed from atrio-ventricular plane displacement (AVPD) and global longitudinal strain (GLS) was assessed using feature tracking in three long-axis views. LV filling was assessed by LAV and by pulmonary artery wedge pressure (PAWP) using right heart catheterisation. Patients had a smaller LAV, LV volume and stroke volume as well as a lower LV-AVPD and LV-GLS than controls. PAWP was 6 [IQR 5--9] mmHg in patients. LV ejection fraction did not differ between groups. LV stroke volume correlated with LV-AVPD (r = 0.445, p = .001), LV-GLS (r = - 0.549, p < 0.0001) and LAVmax (r = .585, p < 0.0001). Furthermore, LV-AVPD (r = .598) and LV-GLS (r = - 0.675) correlated with LAVmax (p < 0.0001 for both). Neither LV-AVPD, LV-GLS, LAVmax nor stroke volume correlated with PAWP. Impaired LV longitudinal function was associated with low stroke volume, low PAWP and a small LAV in PAH. Small stroke volumes and LAV, together with normal LA pressure, implies that the mechanism causing reduced LV longitudinal function is underfilling rather than an intrinsic LV dysfunction in PAH.

Keywords: Cardiac magnetic resonance imaging; Feature tracking strain; Left atrial volume; Left ventricular dysfunction; Pulmonary hypertension.

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Conflict of interest statement

None of the authors have any conflict of interest related to this manuscript.

Figures

Fig. 1
Fig. 1
Example of myocardial tracing in 3-chamber view (left) and delineation of left atrium (right) in a patient with associated pulmonary arterial hypertension owing to systemic sclerosis
Fig. 2
Fig. 2
Correlation between peak systolic left ventricular global longitudinal strain (GLS) and left atrial (LA) volumes in healthy controls (blue circles) and patients with pulmonary arterial hypertension (red filled circles; light red are idiopathic and dark red are associated to systemic sclerosis). LAVmax LA maximum volume indexed to body surface area, LAVmin LA minimum volume indexed to body surface area, LAEV LA emptying volume indexed to body surface area
Fig. 3
Fig. 3
Correlation between peak systolic left ventricular atrioventricular plane displacement (AVPD) and left atrial (LA) volumes in healthy controls (blue circles) and patients with pulmonary arterial hypertension (red filled circles; light red are idiopathic and dark red are associated to systemic sclerosis). LAVmax LA maximum volume indexed to body surface area, LAVmin LA minimum volume indexed to body surface area, LAEV LA emptying volume indexed to body surface area
Fig. 4
Fig. 4
Correlation between peak systolic left ventricular global longitudinal strain (GLS), and atrioventricular plane displacement (AVPD) in healthy controls (blue circles) and patients with pulmonary arterial hypertension (red filled circles; light red are idiopathic and dark red are associated to systemic sclerosis). R2 = 0.02 in healthy controls and R2 = 0.278 in patients
See this image and copyright information in PMC

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