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Ann Thorac Surg 2006;82:1529-1531
© 2006 The Society of Thoracic Surgeons
a Department of Anesthesiology and Intensive Care Medicine, Helsinki University Hospital, Helsinki, Finland
b Department of Cardiothoracic Surgery, Helsinki University Hospital, Helsinki, Finland
Accepted for publication February 9, 2006.
* Address correspondence to Dr Petäjä, Department of Anesthesiology and Intensive Care Medicine, PL 340, 00029 HUS, Finland. (Email: liisa.petaja{at}hus.fi).
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Abstract |
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Introduction |
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Levosimendan is a new positive inotropic drug belonging to the group of calcium sensitizers. It has been recently introduced into cardiac surgery. We describe a case of severe low output syndrome after cardiac transplantation that significantly improved with levosimendan.
The heart donor was a previously healthy 44-year-old man who died of a sub-arachnoid hemorrhage. His transthoracic echocardiography and electrocardiography suggested left ventricular hypertrophy. Due to his good physical condition, no angiography was considered necessary. Systolic function of the heart and cardiac biomarker levels were normal. The recipient was a 51-year-old man with end-stage heart failure due to ischemic cardiomyopathy. His pulmonary pressures were modestly elevated (40/14 mm Hg; mean, 33 mm Hg), and his glomerular filtration rate was normal (90.1 mL/min/1.73 m2).
Despite the good preoperative systolic function of the donor heart, dobutamine and norepinephrine were used perioperatively, based on the judgement of the local anesthesiologist. The heart relaxed, and asystole was attained with cold crystalloid cardioplegia. The graft was transported in an ice-cold saline solution for several hundred kilometers and was implanted by means of bi-caval anastamosis. Total graft ischemia time reached 205 minutes. Recurrent ventricular fibrillation occurring after aortic de-clamping was treated with amiodarone, lidocaine, magnesium sulphate, and direct current shocks.
The heart was reperfused for 60 minutes before weaning from cardiopulmonary bypass. Only after the starting of several inotropic agents his sinus rhythm was regained and the atrial pacing of 100 bpm was introduced. Although the weaning succeeded, a low output state remained for the next hours despite vigorous titration of the inotropic agents (Fig 1). After cardiopulmonary bypass, norepinephrine was infused until the introduction of the intraaortic balloon pump, due to the low systolic blood pressure. The intraaortic balloon pump and discontinuation of norepinephrine caused his cardiac index to rise significantly; however this proved temporary. Consequently we increased the dose of epinephrine, which only resulted in a further drop in his cardiac index. Trials of inhaled nitric oxide and altering of the pacing rate had no impact on his cardiac index (not shown in the figure). Severe global biventricular hypokinesia observed by transesophageal echocardiography persisted, and his blood lactate level was increasing.
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The recovery continued during the following days (Fig 1). Diuresis remained good, and serum creatinine (89 micromol/L) and urea concentration (12.9 mmol/L), peaked on the fourth postoperative day. Immunosuppression was carried out by induction with anti-thymocyte globuline and triple-drug therapy (ie, mycophenolate mofetil, prednisolone, and cyclosporine [the cyclosporine was started on the third postoperative day]). Two weeks after surgery, central venous line infection occurred and was easily cured by removal of the catheter and antibiotics. Thereafter, recovery has been uncomplicated. The patient was discharged from the hospital on postoperative day 26. During the 3-month follow-up, repeated endomyocardial biopsies and cardiac contractility assessed by transthoracic echocardiography have been normal.
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Comment |
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The possible causing factors for primary graft failure in this case were a suboptimal graft due to the left ventricular hypertrophy, the prolonged ischemia, or the use of norepinephrine prior to cardiectomy [3]. However, primary graft failures are occasionally unavoidable, because of the long distances in the Nordic countries and a substantial shortage of donor hearts. Because primary graft failure accounts for 41% of the early deaths after heart transplantation, it is essential to develop treatment options for this condition to improve short-term and long-term survival [1].
In our case, levosimendan served as a "bridge to healing" (ie, to support the compromised heart during the most critical hours of ischemia-reperfusion injury). Compared with the use of levosimendan, use of ventricular assist devices exposes these immunocompromised patients to infections and requires more resources. Ventricular assist devices as a rescue therapy in primary graft failure are related to high mortality rates [2].
Due to its inotropic efficacy in the failing heart, levosimendan serves as a bridge to transplantation for patients with end-stage heart failure. In studies of chronic heart failure, levosimendan has been safe and effective, whereas results of its survival benefits are inconsistent [4]. We can hardly extrapolate these results to cardiac surgery, in which we are often confronted by only temporarily depressed contractility of previously well-functioning myocardium. In studies concerning cardiac surgery, levosimendan has indeed enhanced cardiac contractility [5], but no large randomized controlled trials exist yet.
As a novel drug, levosimendan was started here as a rescue medicine only after epinephrine, norepinephrine, and milrinone had proven insufficient. Because vasodilatation alone or chronotropy was undesirable, we considered neither nitroprusside nor dobutamine [6]. However, the main problem was not vasoplegia and resultant hypotension, but depressed contractility with low pulse pressure, the inodilator profile of levosimendan was thus considered suitable. We chose to use a bolus for a quick effect (ie, a steady state achieved only after 4 hours with infusion) and an average infusion rate of 0.1 micrograms/kg/min (with 0.05 to 0.2 being the recommended range) to avoid deep hypotension. Because of the extended hemodynamic effect of levosimendan (7 to 9 days), due to its active metabolite, infusion was limited to the recommended 24 hours [7].
Several features of levosimendan may render its use feasible even after other inotropic agents fail. Other agents act through adrenergic receptors or second messengers to raise cytosolic calcium concentration. Levosimendan instead acts directly on the contractile apparatus of the myocardial cell, thus enhancing contractility regardless of beta blockade. Side effects related to high cytosolic calcium (eg, arrhythmias and relaxation impairment) are also likely to be absent. By activating KATP channels, levosimendan exerts a direct vasodilatory effect on the coronary and pulmonary vasculature and may induce a cardioprotective effect resembling ischemic preconditioning. Furthermore, levosimendan reduces renal medullary and cortical vascular resistance, thus potentially impeding the development of renal failure [5, 7, 8].
In conclusion, in this case of cardiogenic shock after heart transplantation, levosimendan improved hemodynamics significantly after failure of beta-adrenergic and alpha-adrenergic inotropic agents and a phosphodiesterase inhibitor. With its new type of mechanism, levosimendan is a feasible new noninvasive option to treat primary graft failure.
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This article has been cited by other articles:
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  H. I. Eriksson, J. R. Jalonen, L. O. Heikkinen, M. Kivikko, M. Laine, K. A. Leino, A. H. Kuitunen, K. T. Kuttila, T. K. Perakyla, T. Sarapohja, et al. Levosimendan Facilitates Weaning From Cardiopulmonary Bypass in Patients Undergoing Coronary Artery Bypass Grafting With Impaired Left Ventricular Function Ann. Thorac. Surg., February 1, 2009; 87(2): 448 - 454. [Abstract] [Full Text] [PDF]
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— = CI; —
— = PCWP. Bottom graph: the left Y-axis shows doses of infusions of epinephrine and norepinephrine in ng/kg/min. The right Y-axis shows doses of the infusions of milrinone and levosimendan in micrograms/kg/min. – – = epinephrine; - – = milrinone; - - - - = norepinephrine; —— = levosimendan. (CI = cardiac index; FIO2 = inspired oxygen fraction; IABP = intraaortic balloon pump; MAP = mean arterial pressure; mRVD = mild right ventricular dysfunction; PCWP = pulmonary capillary wedge pressure; SvO2 = mixed central venous hemoglobin saturation; TTE = transthoracic echocardiography.)