Beschreibung:
<jats:title>Abstract</jats:title>
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<jats:title>Background</jats:title>
<jats:p>Cardiogenic shock (CS) is a life threatening condition due to primary cardiac dysfunction. First line therapy involves drug administration (including inotropes and/or vasopressors) up to mechanical circulatory support. Tachycardia is a compensatory mechanism in response to hypotension and low cardiac output or a side effect related to inotropic drugs. Ivabradine selectively acts on IKf channel in the sinoatrial node to reduce sinus heart rate without affecting inotropism. Its use in small non-randomized series of patients with CS was safe and well tolerated [1].</jats:p>
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<jats:title>Methods</jats:title>
<jats:p>We present the use of ivabradine in six patients with CS undertaking veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Data regarding haemodynamic and echocardiographic monitoring were collected before, at 12, 24 and 48 hours after ivabradine administration.</jats:p>
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<jats:title>Results</jats:title>
<jats:p>Ivabradine was administered through naso-gastric tube with a median time of 23 hours [IQR 18–28] since VA-ECMO implantation at the starting dose of 2.5 mg twice a day. Haemodynamic and echocardiographic parameters are shown in table. Ivabradine was well tolerated and led to a significant reduction of heart rate after first administration (p&lt;0.01) (Fig. 1, panel A). Echo-derived stroke volume increased significantly (p&lt;0.001) (Fig. 1, panel B); so did cardiac index (p&lt;0.001) and left ventricular cardiac power index (p 0.005) (Fig. 1, panel C). VA-ECMO rate pump and blood flow significantly decreased (respectively p 0.002, p 0.001). No significant changes were observed in arterial blood pressure (p&gt;0.05). Norepinephrine was down-titrated in all patients (p 0.01). Patients presented with cardiac arrest died due to neurological injury whereas the others were weaned off VA-ECMO and discharged alive.</jats:p>
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<jats:title>Conclusions</jats:title>
<jats:p>Ivabradine administration resulted in an effective reduction of heart rate leading to ventricular stroke volume allowing the reduction of extracorporeal flow support and vasopressors administration.</jats:p>
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<jats:title>Funding Acknowledgement</jats:title>
<jats:p>Type of funding sources: None.</jats:p>
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