The Role of Levosimendan in Patients with Decreased Left Ventricular Function Undergoing Cardiac Surgery

Abstract

The postoperative low cardiac output is one of the most important complications following cardiac surgery and is associated with increased morbidity and mortality. The condition requires inotropic support to achieve adequate hemodynamic status and tissue perfusion. While catecholamines are utilised as a standard therapy in cardiac surgery, their use is limited due to increased oxygen consumption. Levosimendan is calcium sensitising inodilatator expressing positive inotropic effect by binding with cardiac troponin C without increasing oxygen demand. Furthermore, the drug opens potassium ATP (KATP) channels in cardiac mitochondria and in the vascular muscle cells, showing cardioprotective and vasodilator properties, respectively. In the past decade, levosimendan demonstrated promising results in treating patients with reduced left ventricular function when administered in peri- or post- operative settings. In addition, pre-operative use of levosimendan in patients with severely reduced left ventricular ejection fraction may reduce the requirements for postoperative inotropic support, mechanical support, duration of intensive care unit stay as well as hospital stay and a decrease in post-operative mortality. However, larger studies are needed to clarify clinical advantages of levosimendan versus conventional inotropes.

Influence of Subarachnoid Anesthesia in the Prone Position on the Energy of Circulation

“…Today, it does not require additional evidence that for the vital activity and preservation of the integrity of a living organism, it needs a constant flow of energy from the outside at a sufficient speed. It had long been established that at rest, an organism weighing about 70 kg requires about 1800 kcal of energy per day, which is about 90 W [1,2]. This power must be developed, for example, when lifting a weight of 9 kg to a height of 1 m in 1 second.…”

Robot-Assisted Robotic Prostatectomy in a Patient with Dilated Cardiomyopathy and LVEF of 35%

“…Cited in a pre-anesthetic consultation, we objected to difficulty in the airway, Mallampatti IV, and a severe myocardial dysfunction with which we consulted with cardiology decided to increase the dose of carvedilol to 25 mg/12 hours and to enter the patient 48 hours before surgery in the ICU to administer Levosimendan at a loading dose of 7 micrograms/kg. Levosimendan increases calcium sensitivity by cardiac troponin myofilaments by increasing myocardial contractility and decreasing both pulmonary and systemic peripheral resistance in addition to having an antiarrhythmic effect [5].…”

Levosimendan for ECLS Weaning: A Strategy in Need of Validation

“…Overall, these changes lead to an increase in myocardial contractility; however, increased intracellular calcium levels also increase myocardial oxygen consumption, making patients prone to developing arrhythmias and cardiotoxicity. 6,7 Therefore, the use of an inodilator without the previously mentioned side effects would be the most ideal and beneficial in ECLS weaning.…”

“…Levosimendan works through an alternate pathway by increasing calcium sensitivity of cardiac myocytes by binding to cardiac troponin-C in a calcium-dependent manner. 7 This differing pharmacological approach leads to positive inotropic effects akin to milrinone, but without the associated increase in myocardial oxygen demand, as intracellular calcium concentration remains unchanged. 1,7,8,9 Additionally, levosimendan causes smooth muscle relaxation by activating potassium adenosine triphosphate channels in coronary, pulmonary, and systemic vascular smooth muscles, thereby improving coronary perfusion while unloading both ventricles by decreasing systemic and pulmonary vascular resistance.…”

“…7 This differing pharmacological approach leads to positive inotropic effects akin to milrinone, but without the associated increase in myocardial oxygen demand, as intracellular calcium concentration remains unchanged. 1,7,8,9 Additionally, levosimendan causes smooth muscle relaxation by activating potassium adenosine triphosphate channels in coronary, pulmonary, and systemic vascular smooth muscles, thereby improving coronary perfusion while unloading both ventricles by decreasing systemic and pulmonary vascular resistance. 7,10 These pharmacodynamics of levosimendan may help with myocardial recovery and may facilitate successful separation from temporary ECLS after post-cardiotomy cardiogenic shock.…”