Key result
Inhaled nitric oxide linked to ~2.5 mmHg lower mPAP in Impella-supported patients.
Why the study?
In cardiogenic shock treated with Impella-based mechanical circulatory support, pulmonary vascular load and right ventricular dysfunction may impair left ventricular preload and device flow, yet prospective data on the acute hemodynamic effects of inhaled nitric oxide in this setting were limited.
Does inhaled nitric oxide reduce mean pulmonary artery pressure in adult patients with cardiogenic shock receiving Impella or ECPELLA mechanical circulatory support?
Cohort (n=11)
No
Does inhaled nitric oxide reduce mean pulmonary artery pressure in adult patients with cardiogenic shock receiving Impella or ECPELLA mechanical circulatory support?
In patients with cardiogenic shock on Impella or ECPELLA support, inhaled nitric oxide was associated with an acute 30-minute reduction in mean pulmonary artery pressure without a sustained 24-hour difference or clear improvement in systemic hemodynamics.
Answers are grounded in this paper and cite their sources.
Acute mPAP reduction with inhaled nitric oxide in Impella patients should not yet change practice; leaves open need for RCTs on sustained hemodynamics and outcomes.
Among patients with cardiogenic shock receiving Impella-based mechanical circulatory support, pulmonary vascular load and right ventricular dysfunction may affect left ventricular preload and device flow. Prospective data on the acute hemodynamic effects of inhaled nitric oxide (iNO) in this setting are limited. We evaluated short-term hemodynamic changes after iNO initiation in patients receiving Impella or Impella combined with veno-arterial extracorporeal membrane oxygenation (ECPELLA) support. We conducted a prospective single-center pilot study of adult patients receiving Impella or ECPELLA support who were treated with iNO. iNO was initiated at 20 ppm after initial circulatory resuscitation once pulmonary artery pulse pressure could be reliably assessed. Hemodynamic variables were recorded immediately before iNO initiation (T0) and 30 min (T1) and 24 h (T2) after initiation. The primary endpoint was the change in mean pulmonary artery pressure (mPAP) from T0 to T1. We enrolled 11 patients, and 10 were analyzed. mPAP decreased from 19.0 (14.8-20.3) mmHg at T0 to 16.5 (12.8-19.3) mmHg at T1 (P = 0.004). The T0-T2 difference was not significant. Lactate levels decreased, but this temporal change could not be attributed directly to iNO without a control group. Methemoglobin levels increased slightly at T2 without clinical methemoglobinemia. iNO was temporally associated with an early reduction in mPAP in patients receiving Impella-based support, without clear improvement in systemic hemodynamic indices. These hypothesis-generating findings require confirmation in larger controlled studies.
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Hiruma et al. (2026) conducted a cohort in Cardiogenic shock receiving Impella-based mechanical circulatory support (n=11). Inhaled nitric oxide (iNO) vs. Baseline (pre-initiation at T0; no control group) was evaluated on Change in mean pulmonary artery pressure (mPAP) from immediately before iNO initiation (T0) to 30 min after initiation (T1) (p=0.004). Inhaled nitric oxide at 20 ppm decreased mean pulmonary artery pressure from 19.0 mmHg at baseline to 16.5 mmHg at 30 minutes (P=0.004) in Impella-supported patients.
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