Pimobendan and levosimendan appear more beneficial than traditional inotropic agents, which carry risks of calcium overload, arrhythmias, and myocardial injury in acute heart failure.
Traditional inotropic agents carry significant risks of arrhythmias and cell death, highlighting the potential benefit of calcium sensitizers like levosimendan.
Inotropic agents are indispensable for the improvement of cardiac contractile dysfunction in acute or decompensated heart failure. Clinically available agents, including sympathomimetic amines (dopamine, dobutamine, noradrenaline) and selective phosphodiesterase-3 inhibitors (amrinone, milrinone, olprinone and enoximone) act via cAMP/protein kinase A (PKA)-mediated facilitation of intracellular Ca2+ mobilisation. Phosphodiesterase-3 inhibitors also have a vasodilatory action, which plays a role in improving haemodynamic parameters in certain patients, and are termed inodilators. The available inotropic agents suffer from risks of Ca2+ overload leading to arrhythmias, myocardial cell injury and ultimately, cell death. In addition, they are energetically disadvantageous because of an increase in activation energy and cellular metabolism. Furthermore, they lose their effectiveness under pathophysiological conditions, such as acidosis, stunned myocardium and heart failure. Pimobendan and levosimendan (that act by a combination of an increase in Ca2+ sensitivity and phosphodiesterase-3 inhibition) appear to be more beneficial among existing agents. Novel Ca2+ sensitisers that are under basic research warrant clinical trials to replace available inotropic agents.
Endoh et al. (Tue,) conducted a review in Acute or decompensated heart failure. Inotropic agents was evaluated. Pimobendan and levosimendan appear more beneficial than traditional inotropic agents, which carry risks of calcium overload, arrhythmias, and myocardial injury in acute heart failure.
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