Beschreibung:
<jats:title>Abstract</jats:title>
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<jats:title>Aims</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 frequent compensatory mechanism in response to hypotension and low cardiac output or a side effect related to inotropic drugs. Ivabradine selectively acts on the 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 without mechanical circulatory support, was safe and well tolerated.</jats:p>
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<jats:title>Methods and results</jats:title>
<jats:p>We present the use of ivabradine in six patients with CS undertaking veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and a matched cohort of selected patients with similar features who did not receive ivabradine. Data regarding haemodynamic and echocardiographic monitoring, oxygenation, renal function, mechanical circulatory support, inotropes, and vasopressors doses were collected before (t0), at 12 (t1), 24 (t2), and 48 (t3) h after ivabradine administration. Ivabradine administration led to a significant heart rate reduction of 20.83 [95% confidence interval (CI) −27.2 to −14.4] b.p.m. (&lt;0.01). Echo-derived left ventricular native stroke volume (SV) significantly increased by +7.83 (95% CI 4.74–10.93) mL (P &lt; 0.001) with a parallel reduction of VA-ECMO support [−170 (95% CI −225.05 to −114.95)]. Noradrenaline was down-titrated over the observation period in all patients (P = 0.016).</jats:p>
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<jats:title>Conclusion</jats:title>
<jats:p>A significant reduction in heart rate was observed after ivabradine administration. This was associated with a native ventricular SV improvement allowing the reduction of extracorporeal flow support and vasopressors administration.</jats:p>
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