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Effect of levosimendan on ventriculo-arterial coupling in patients with ischemic cardiomyopathy
F Guarracino1, C Cariello, A Danella
1Cardiothoracic Anaesthesia and Intensive Care Unit, Cardiothoracic Department, University Hospital of Pisa, Italy. fabiodoc64@hotmail.com
Insights
Levosimendan improves ventriculo-arterial coupling in patients with left ventricular dysfunction. This drug enhances myocardial contractility and reduces arterial elastance, boosting cardiovascular performance.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Levosimendan is a calcium sensitizer that enhances myocardial contractility and dilates peripheral arteries.
- Ventriculo-arterial coupling (Ea/Ees) assesses cardiovascular efficiency by relating ventricular and arterial elastance.
- Ischemic cardiomyopathy presents challenges in maintaining adequate cardiac output.
Purpose of the Study:
- To evaluate the effects of levosimendan on ventriculo-arterial coupling in patients with ischemic cardiomyopathy.
- To assess changes in myocardial contractility and arterial system interaction.
- To determine the drug's impact on overall cardiovascular performance.
Main Methods:
- Prospective clinical investigation involving 15 patients with stable angina and left ventricular dysfunction.
- Invasive monitoring and transesophageal echocardiography were used to assess cardiovascular variables.
- Levosimendan was administered as a 12 mug/kg bolus before coronary surgery.
Main Results:
- Levosimendan significantly increased cardiac index and ejection fraction.
- Mean arterial pressure and systemic vascular resistances were significantly decreased.
- Arterial elastance (Ea) decreased, while ventricular elastance (Ees) increased, significantly improving the Ea/Ees ratio.
Conclusions:
- Levosimendan effectively improves ventriculo-arterial coupling in coronary patients with left ventricular dysfunction.
- The drug enhances myocardial contractility and reduces arterial elastance, leading to better cardiovascular performance.
- Levosimendan represents a potential therapeutic option for managing cardiac dysfunction in this patient population.
Background:
Levosimendan, a novel calcium sensitizer, enhances myocardial contractility without affecting intracellular calcium concentration. It also dilates peripheral arterial vessels by acting on ATP-dependent K(+) channels. Ventriculo-arterial coupling, the relationship between myocardial contractility and the arterial system, describes the efficiency of the cardiovascular system by analysing the relationship between myocardial contractility expressed by ventricular elastance (E(es)) and arterial elastance (E(a)). The aim of this prospective clinical investigation was to evaluate the effects of levosimendan on ventriculo-arterial coupling in patients with ischemic cardiomyopathy.
Methods:
Fifteen patients with stable angina and left ventricular dysfunction underwent elective coronary surgery. Before surgery started, ventriculo-arterial coupling and several variables of cardiovascular performance were assessed by invasive monitoring and transoesophageal echocardiography before and after administration of levosimendan (12 mug/kg bolus) in coronary patients under general anesthesia.
Results:
The cardiac index and ejection fraction increased significantly [from 1.92 +/- 0.4 to 2.1 +/- 0.4 l/min/m(2) (P = 0.0004) and from 31% +/- 6 to 40% +/- 9 (P = 0.001), respectively], while mean arterial pressure and systemic vascular resistances decreased significantly [from 83 +/- 10 to 72 +/- 5 mmHg (P = 0.0016) and from 997 +/- 341 to 855 +/- 324 dyne s/cm(5) (P = 0.0002), respectively]. After administration of levosimendan, E(a) decreased significantly (from 4.3 +/- 1.8 to 3.2 +/- 1.3 mmHg/ml/m(2), P= 0.005), while E(es) significantly increased (from 2.8 +/- 1.6 to 4.4 +/- 2.3 mmHg/ml/m(2), P= 0.05); as a result, E(a)/E(es) decreased significantly (from 1.76 +/- 1 to 0.83 +/- 0.2, P= 0.002).
Conclusion:
Levosimendan improves ventriculo-arterial coupling and cardiovascular performance in coronary patients with left ventricular dysfunction by enhancing myocardial contractility and reducing arterial elastance.
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