Abstract 4368476: Total Support by a Trans-Aortic Valve Micro-Axial Flow Pump Reduces Coronary Blood Flow in Both Normal and Post-reperfusion Coronary Arteries in a Goat Model of Ischemia-Reperfusion

K Kenta Ohba (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) M Masahiro Otake (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) N NANA HIRAKI (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) Y Yuki Yoshida H Hidetaka Morita (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) K Kei Sato T Takuya Nishikawa (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) M Masafumi Fukumitsu (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) K Kazunori Uemura (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) T Toru Kawada (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan) K Keita Saku (National Cerebral and Cardiovascular Center, Suita, Osaka, Japan)

Abstract

Introduction: In cases of cardiogenic shock, the transaortic micro-axial flow pump (Impella) improves systemic circulation and increases coronary perfusion pressure (CPP) while reducing myocardial oxygen consumption (MVO 2 ) via its left ventricular (LV) unloading effect. The Impella 5.5, in particular, enables stronger LV unloading due to its higher flow capacity. Physiologically, coronary blood flow (CBF) increases with CPP, while reduced MVO 2 may activate autoregulatory mechanisms that limit CBF. Hypothesis: We hypothesized that a marked reduction in MVO 2 by the Impella 5.5 may attenuate CBF. This study evaluates the impact of Impella 5.5 support on CBF in normal and post-reperfusion coronary arteries using a goat model of ischemia-reperfusion. Methods: Saanen goats (N=8, BW: 61.6±4.5 kg) were used under general anesthesia. The Impella 5.5 was inserted via the carotid artery into the LV. We measured blood pressure, LV pressure, pulmonary artery flow, arterial and coronary sinus oxygen saturation, and CBF in the left anterior descending artery (LAD) and left circumflex artery (LCX). We occluded the proximal LAD with a 3 mm balloon for 90 minutes, then deflated for reperfusion (Fig. A). At 30-min after reperfusion, Impella support was set at three stages: Control (P1), Partial support with residual native cardiac output (P3-7), and Total support (P6-9). Results: Increasing Impella support augmented CPP (37.8 ± 10.6 vs. 47.1 ± 8.5 vs. 75.2 ± 12.7 mmHg, P < 0.05) and reduced MVO 2 (298.3 ± 161.0 vs. 257.9 ± 122.2 vs. 161.0 ± 121.6, P < 0.05) (Fig. B). Total support with the Impella 5.5 suppressed MVO 2 by 53.0 ± 18.8% compared to the Control condition. LCX flow decreased with increasing Impella support (46.9 ± 26.6 vs. 45.0 ± 28.5 vs. 37.8 ± 31.0 mL/min, P < 0.05). Similarly, LAD flow was significantly reduced under Total support (30.9 ± 11.4 vs. 28.5 ± 11.7 vs. 23.7 ± 12.2 mL/min, P < 0.05) (Fig. C). Conclusion: In a goat model of ischemia–reperfusion, total support with the Impella 5.5 reduced CBF in both the normal LCX and the injured LAD. These results may be influenced by factors such as the severity of coronary injury, the timing of measurement, and the specific animal model used. Nevertheless, the findings suggest that autoregulatory mechanisms triggered by suppressed MVO 2 play a critical role in determining CBF, even in post-reperfusion setting, and should be carefully considered when evaluating the effects of Impella5.5 support on coronary circulation.

Article Details

Journal Circulation
Volume / Issue Vol. 152, Issue Suppl_3
Published November 04, 2025
ISSN 0009-7322
Publisher Lippincott Williams & Wilkins

Journal Info

Circulation

Lippincott Williams & Wilkins

ISSN: 0009-7322 Health Sciences

Authors (11)

K

Kenta Ohba

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

M

Masahiro Otake

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

N

NANA HIRAKI

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

Y

Yuki Yoshida

H

Hidetaka Morita

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

K

Kei Sato

T

Takuya Nishikawa

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

M

Masafumi Fukumitsu

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

K

Kazunori Uemura

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

T

Toru Kawada

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan

K

Keita Saku

National Cerebral and Cardiovascular Center, Suita, Osaka, Japan