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. 2021 Oct;8(5):4334-4342.
doi: 10.1002/ehf2.13544. Epub 2021 Aug 10.

Left atrial conduit flow rate at baseline and during exercise: an index of impaired relaxation in HFpEF patients

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Left atrial conduit flow rate at baseline and during exercise: an index of impaired relaxation in HFpEF patients

Paolo N Marino et al. ESC Heart Fail. 2021 Oct.

Abstract

Aims: In healthy subjects, adrenergic stimulation augments left ventricular (LV) long-axis shortening and lengthening, and increases left atrial (LA) to LV intracavitary pressure gradients in early diastole. Lower increments are observed in patients with heart failure with preserved ejection fraction (HFpEF). We hypothesized that exercise in HFpEF would further impair passive LV filling in early-mid diastole, during conduit flow from pulmonary veins.

Methods and results: Twenty HFpEF patients (67.8 ± 9.8 years; 11 women), diagnosed using 2007 ESC recommendations, underwent ramped semi-supine bicycle exercise to submaximal target heart rate (∼100 bpm) or symptoms. Seventeen asymptomatic subjects (64.3 ± 8.9 years; 7 women) were controls. Simultaneous LA and LV volumes were measured from pyramidal 3D-echocardiographic full-volume datasets acquired from an apical window at baseline and during stress, together with brachial arterial pressure. LA conduit flow was computed from the increase in LV volume from its minimum at end-systole to the last frame before atrial contraction (onset of the P wave), minus the reduction in LA volume during the same time interval; the difference was integrated and expressed as average flow rate, according to a published formula. The slope of single-beat preload recruitable stroke work (PRSW) quantified LV inotropic state. 3D LV torsion (rotation of the apex minus rotation of the base divided by LV length) was also measurable, both at rest and during stress, in 10 HFpEF patients and 4 controls. There were divergent responses in conduit flow rate, which increased by 40% during exercise in controls (+17.8 ± 37.3 mL/s) but decreased by 18% in patients with HFpEF (-9.6 ± 42.3 mL/s) (P = 0.046), along with congruent changes (+1.77 ± 1.13°/cm vs. -1.94 ± 2.73°/cm) in apical torsion (P = 0.032). Increments of conduit flow rate and apical torsion during stress correlated with changes in PRSW slope (P = 0.003 and P = 0.006, respectively).

Conclusions: In HFpEF, conduit flow rate decreases when diastolic dysfunction develops during exercise, in parallel with changes in LV inotropic state and torsion, contributing to impaired stroke volume reserve. Conduit flow is measurable using 3D-echocardiographic full-volume atrio-ventricular datasets, and as a marker of LV relaxation can contribute to the diagnosis of HFpEF.

Keywords: 3D echocardiography; Diastolic function; Exercise; Heart failure with preserved ejection fraction.

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Conflict of interest statement

No conflict of interest disclosures reported for the authors.

Figures

Figure 1
Figure 1
pyramidal 3D‐echocardiographic full‐volume dataset acquired from the apex in a patient, using a 3 V transducer. Volume data can be displayed in real‐time: three orthogonal apical views and one cross‐sectional slice, with optional volume rendering. The vertical red line corresponds to the P wave on the electrocardiographic trace. The light blue line identifies minimum ventricular systolic volume (ES). The light blue and red lines identify timing of conduit flow.
Figure 2
Figure 2
Left ventricular and simultaneous atrial data at baseline and during stress in two patients enrolled in the study. Light blue and red vertical lines identify minimum cavity volume and timing of the P wave on the ECG, respectively. PRSW, slope of single‐beat preload recruitable stroke work.
Figure 3
Figure 3
Behaviour of the single‐beat preload recruitable stroke work (PRSW) relation at baseline and during stress in the two populations considered. LV inotropic state, as reflected by the slope of the relation, increases with stress only in controls (P < 0.001, interaction P = 0.004). Refer also to text and Table 2 for details. HFpEF, heart failure with preserved ejection fraction.
Figure 4
Figure 4
Dispersion plot and regression line of the difference (stress minus baseline) of apical LV torsion (y‐axis) vs. slope of single‐beat preload recruitable stroke work (PRSW, x‐axis) in 10 HFpEF patients and 4 controls. There is a significant relation between the two variables. HFpEF, heart failure with preserved ejection fraction.
Figure 5
Figure 5
Dispersion plot of the difference (stress minus baseline) of conduit flow rate (y‐axis) vs. slope of single‐beat preload recruitable stroke work (PRSW, x‐axis) in 20 HFpEF patients and 17 controls. The two patients depicted in Figure 2 are identified by arrows. HFpEF, heart failure with preserved ejection fraction.

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