Resynchronization improves heart-arterial coupling reducing arterial load determinants

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Abstract

Background

Cardiac resynchronization therapy (CRT) has benefits on left ventricle (LV) performance, but its mid-term effects on LV load and LV-arterial coupling are unknown.

Aims

To evaluate CRT mid-term effects on LV-arterial coupling, arterial load and its determinants, and the association between CRT-dependent aortic haemodynamic changes and the arterial biomechanics.

Methods and results

Cardiac and aortic echographies were done in 25 patients (age: 61 ± 12 years; 14 men; New York Heart Association functional classes III–IV; LV ejection fraction = 28 ± 7%, QRS = 139 ± 20 ms) before and after (23 ± 12 days) CRT. Standard structural and functional parameters and dyssynchrony indices were evaluated. Ascending aorta flow and diameter waveforms were measured. Central pressure was derived using a transfer function and the diameter calibration method. Calculus: arterial elastance (EA); aortic impedance (Zc) and distensibility (AD); systemic resistances (SVR), total compliance (CT); global reflection coefficient; LV end-systolic elastance (EES); and LV-arterial coupling (EA/EES). After CRT EA diminished (−30%;P = 0.001), EES increased (29%; P = 0.001) and EA/EES improved (pre-CRT: 2.9 ± 0.9, post-CRT: 1.6 ± 0.7; P = 0.001). Arterial elastance changes were associated with changes in arterial properties. Cardiac resynchronization therapy was associated with pressure-independent increase in mean aortic diameter (pre-CRT: 30.0 ± 4.0 mm, post-CRT: 33.0 ± 5.1 mm; P = 0.005) and distensibility (pre-CRT: 3.8 ± 2.6 × 10−3mmHg−1, post-CRT: 6.4 ± 2.5 × 10–3 mmHg−1; P = 0.002), and Zc reduction (pre-CRT: 3.5 ± 1.8 × 10−2mmHg.s/mL, post-CRT:1.9 ± 0.8 × 10−2 mmHg.s/mL; P = 0.001) and SVR (pre-CRT:1.7 ± 0.4 mmHg.s/mL, post-CRT:1.0 ± 0.3 mmHg.s/mL; P = 0.001). Changes in EA determinants were associated with changes in aortic flow.

Conclusion

Early after CRT central and peripheral arterial biomechanics improved, determining a pressure-independent increase in aortic diameter and a reduction in arterial load. Left ventricular systolic performance and LV-arterial coupling were enhanced. Arterial biomechanical changes were associated with aortic flow changes.

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