Gen Thorac Cardiovasc Surg (2008) 56:559–562 DOI 10.1007/s11748-008-0298-8
CASE REPORT
Tricuspid valve replacement and levosimendan Ferit Cicekcioglu, MD · Ali Ihsan Parlar, MD Levent Altinay, MD · Kerem Yay, MD Salih Fehmi Katircioglu, MD
Received: 19 December 2007 / Accepted: 27 June 2008 © The Japanese Association for Thoracic Surgery 2008
Abstract Isolated tricuspid valve replacement, which is not a common operation, is associated with poor shortand long-term results, and the postoperative morbidity and mortality rates are high. The main reason for these adverse effects is the acute manifestation of chronic right heart failure. To treat right heart failure, we used levosimendan for its inotropic and vasodilatatory effects, and it does not increase the calcium overload in myocardial cells. We report two cases of tricuspid valve replacement operations performed using levosimendan. Both patients receiving levosimendan tolerated the operations well, and their postoperative courses were uneventful. Key words Cardiac surgical procedures · Levosimendan · Tricuspid valve
Introduction Tricuspid valve replacement (TVR) is not a common operation. It is generally agreed that tricuspid valve repair techniques should be chosen for functional disease if possible. In some specific cases, TVR is usually unavoidable if there is significant valve degeneration, especially in cases of multiple reoperation procedures.1,2 F. Cicekcioglu · A.I. Parlar · L. Altinay · K. Yay · S.F. Katircioglu (*)1 Cardiovascular Surgery Clinic, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey Present address: 1 Turkiye Yuksek Ihtisas Hastanesi, Kalp ve Damar Cerrahisi Klinigi, 06100 Sihhiye, Ankara, Turkey Tel. +90-312-306-1188; Fax +90-312-229-5868 e-mail:
[email protected]
Isolated TVR is associated with poor short- and longterm results and high rates of postoperative complications. The hospital mortality rate has been reported in a range of 12%–27%.1–4 Patients with decreased functional capacity [New York Hospital Association (NYHA) class III/IV], congestive symptoms, rheumatic origin, and reoperation are more prone to develop low cardiac output syndrome. Elevated pulmonary artery pressure (PAP) and rheumatic etiology have unfavorably affected the long-term results.3,4 Levosimendan is a new drug currently introduced into clinical use. Its widely accepted indications are acute postinfarction cardiac failure, diastolic cardiac failure, and low-cardiac output syndrome following coronary artery bypass grafting.5 In the literature, levosimendan reduced the right ventricular afterload and PAP.6,7 We can clearly benefit from the vasodilatory effects of levosimendan for reduction of high PAP and right ventricular protection.
Case report Case 1 A 69-year-old woman admitted to the outpatient clinic with symptoms of dyspnea, orthopnea, and congestive symptoms (ascites 4+, pretibial edema 4+). Her complaint had started 2 years ago and had increased during the last few months. Her medical history indicated that she had undergone an aortic valve replacement operation 5 years ago for aortic stenosis. She had NYHA class IV functional capacity. The electrocardiogram showed atrial fibrillation rhythm. Transthoracic (TTE) and transesophageal echocardiography (TEE) revealed a
560 Fig. 1 Case 1. Intraoperative hemodynamics: systolic and diastolic blood pressure (BP) and heart rate. CPB, cardiopulmonary bypass; Levo, levosimendan
Gen Thorac Cardiovasc Surg (2008) 56:559–562 Systolic BP Diastolic BP Heart Rate
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normally functioning aortic mechanical prosthetic valve, 4° tricuspid insufficiency associated with annular enlargement, valvular tissue loss, perimembranous ventricular septal defect (VSD), ejection fraction 45%, and 70 mmHg systolic pulmonary artery pressure (sPAP). Coronary angiography and catheterization were performed and revealed normal coronary artery anatomy, perimembranous VSD [pulmonary-to-systemic flow ratio (Qp/Qs) 2.6], and sPAP 75 mmHg. During surgery, a degenerative native tricuspid valve was excised and replaced with a 31-mm mechanical prosthesis; the VSD was repaired with a Dacron patch. No problems occurred during the operation or the period of weaning from cardiopulmonary bypass (CPB). The cross-clamp and CPB times were 65 min and 103 min, respectively. Intraoperative hemodynamics (systolic and diastolic blood pressure, heart rate) are shown in Fig. 1. The intensive care unit (ICU) follow-up time was 48 h, and the patient was discharged from the hospital on the postoperative day (POD) 8. Before discharge, a control TTE showed a functional prosthetic valve, no residual VSD, 40% ejection fraction, and 40 mmHg sPAP. On POD 30, patient was observed with NYHA class II functional capacity, and neither ascites nor congestive symptoms were found. Case 2 A 35-year-old woman was admitted to the outpatient clinic with palpitation, dyspnea, orthopnea, and pretibial edema. She had NYHA class III functional capacity. Her medical history indicated that a mitral valve replacement (MVR) operation was carried out 17 years ago because of mitral stenosis. Her electrocardiogram
showed atrial fibrillation. TTE revealed 4° of tricuspid insufficiency secondary to valve fibrosis as well as annular dilatation with the giant right atrium (13 × 13 cm), ejection fraction 55%, and 55 mmHg sPAP with a normally functioning mechanical mitral prosthesis valve. During the operation, a degenerated native tricuspid valve was excised and replaced with a 33-mm biological valve prosthesis, and the right atrial cavity was reduced with the plication suture technique. The patient was weaned from CPB without any problems. Cross-clamping was not used in this operation. CPB time was 71 min. Intraoperative hemodynamics (systolic and diastolic blood pressure and heart rate) are showed in Fig. 2. ICU follow-up time was 24 h, and the patient was discharged from the hospital on POD 5. Before discharge, a control TTE showed normally functioning mitral and tricuspid valve prostheses with minimal insufficiency, ejection fraction 50%–55%, and sPAP 25 mmHg. Surgical technique and levosimendan administration After induction of general anesthesia, levosimendan was administered to decrease preload and afterload. We administered this drug with a bolus dose of 12 μg/kg/min for 10 min and then continued the infusion at a rate of 0.1 μg/kg/min.8 The levosimendan infusion was continued for 24 h in the ICU. According to our usual clinical practice, we did not monitor the right heart via a pulmonary artery catheter during TVR. After right femoral artery cannulation, remedian sternotomy was performed. Then, a pericardial adhesion was dissected, and bicaval venous cannulation was performed. CPB was initiated with flow of 2.5 l/m2. For case
Gen Thorac Cardiovasc Surg (2008) 56:559–562 Fig. 2 Case 2. Intraoperative hemodynamics: systolic and diastolic blood pressure (BP) and heart rate. CPB, cardiopulmonary bypass; Levo, levosimendan
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1, the standard cardioplegic technique and aortic crossclamping were used during closure of the VSD, with the cross-clamp being released following VSD closure. The venae cavae were surrounded by encircling tapes and tightened. In both cases, TVR were performed with the use of standard CPB without cross-clamping the aorta using the beating-heart technique.
Discussion Patients requiring TVR are considered to be at high risk because of the reoperation, concomitant cardiac procedures, and end-stage functional classes. Heart failure was the predominant cause of early and late deaths after TVR.9 We were able to demonstrate that preservation of right ventricular contractility and reduction of PAP can be achieved with levosimendan. PAP of >50 mmHg is referred to as pulmonary hypertension. We selected two patients whose sPAP was >50 mmHg and who had congestive symptoms. Patients with tricuspid valve disease generally have elevated PAP associated with impaired right ventricular function. The main cause of this problem is an increased afterload. The main aim of this therapy is to restore right ventricular function. We believe that conventional inotropic agents associated with vasodilator agents do not restore right ventricular function because they increase myocardial contractility at the expense of an increased afterload. This type of physiology prolongs the ICU stay and myocardial recovery. Major determinants of ventricular performance are preload, afterload, and contractility. The right ventricle
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works in a volume-dependent manner and is susceptible to changes in the afterload. In contrast to the left ventricle, a small increase in afterload leads to a significant reduction in right ventricular function, which later leads to left ventricular failure. Levosimendan acts by increasing myocardial contractility without increasing oxygen demand and by relaxing the ATP-sensitive potassium channels in small vessels and calcium-activated potassium and voltage-dependent potassium channels in large vessels.8 It is probable that the vasodilatation effect of levosimendan on pulmonary arteries is related to this pathway. In light of this explanation, while at the same time that the reduced afterload increases the CO, the systolic blood pressure is slightly reduced. The therapeutic target of this problem is a reduction of PAP and an increase in right ventricular contractility without causing systemic hypotension. Levosimendan became the focus of our interest for treating this type of disorder, as it has vasodilator and positive inotropic effects with different mechanisms. It is currently being introduced into clinical use.8,10 Our patients were weaned from CPB smoothly without the need of any other inotropic agent and were discharged from the hospital shortly after their operations.
Conclusion Tricuspid valve replacement with perioperative levosimendan administration in patients who had high PAP and right ventricular failure is an acceptable subject for investigation. More clinical and randomized trials should be carried out.
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