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Effects of left ventricular unloading by Impella recover LP2.5 on coronary hemodynamics

✍ Scribed by Maurice Remmelink; Krischan D. Sjauw; José P.S. Henriques; Robbert J. de Winter; Karel T. Koch; René J. van der Schaaf; Marije M. Vis; Jan G.P. Tijssen; Jan J. Piek; Jan Baan Jr.


Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
99 KB
Volume
70
Category
Article
ISSN
1522-1946

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✦ Synopsis


Abstract

Objectives:

We studied the effects of LV unloading by the Impella on coronary hemodynamics by simultaneously measuring intracoronary pressure and flow and the derived parameters fractional flow reserve (FFR), coronary flow velocity reserve (CFVR), and coronary microvascular resistance (MR).

Background:

Patients with compromised left ventricular (LV) function undergoing high‐risk percutaneous coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on coronary hemodynamics.

Methods:

Eleven patients (mean LV ejection fraction of 35 ± 11%) underwent PCI during LV support by the LV unloading device (Impella Recover® LP2.5). Intracoronary measurements were performed in a nonstenotic coronary artery after the PCI, before and after adenosine‐induced hyperemia at four different support levels (0–2.5 L/min).

Results:

Aortic and coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 ± 24 to 72 ± 27 cm/sec, P = 0.001 and 1.88 ± 0.52 to 2.34 ± 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 ± 1.32 to 1.89 ± 1.43 mm Hg cm^−1^ sec, P = 0.005).

Conclusions:

Unloading of the LV by the Impella increased aortic and intracoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella‐induced increase in coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume‐related intramyocardial resistance. © 2007 Wiley‐Liss, Inc.


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