Interact CardioVasc Thorac Surg 2005;4:316-318. doi:10.1510/icvts.2004.103788
© 2005 European Association of Cardio-Thoracic Surgery
Case report - Cardiac general |
Temporary left ventricular assist and levosimendan for coronary artery spasm
Ulrich R. Döpfmera,*,
Jan P. Brauna,
Joachim Grossea and
Wolfgang Konertzb
a Department of Anesthesiology and Surgical Intensive Care, Charité University Hospital, Campus Mitte, Schumannstrasse 20–21, 10117 Berlin, Germany
b Department of Cardiac Surgery, Charité University Hospital, Campus Mitte, Schumannstrasse 20–21, 10117 Berlin, Germany
Received 3 December 2004;
received in revised form 22 February 2005;
accepted 1 March 2005
*Corresponding author: Dr Ulrich Döpfmer FRCA, Lindenstr. 30, 12589 Berlin, Germany. Tel.: +49 30 64399559; fax: +49 30 64398200.
E-mail address: doepfmer{at}snafu.de (U.R. Döpfmer).
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Abstract
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Coronary vasospasm is a life threatening complication in the early postoperative period after coronary artery bypass grafting. We report a 45-year-old patient with normal preoperative ventricular function who could not be stabilized using established treatments such as: systemic application of glyceryl trinitrate, diltiazem and milrinone, intraaortic balloon pumping and intracoronary injection of glyceryl trinitrate. Severe stunning of the myocardium required support with a centrifugal left ventricular assist device. Subsequent application of levosimendan, a calcium sensitizer, may have contributed to prevent recurrence of repeated episodes of coronary spasm, enabling early explantation of the assist device and a full recovery.
Key Words: Coronary artery bypass grafting; Coronary artery spasm; Left ventricular assist device; Calcium sensitizers; Levosimendan
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1. Introduction
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Severe early postoperative coronary artery spasm carries a high mortality [1,2]. Patients not responsive to conventional treatment require support with an intraaortic balloon pump and application of vasodilators directly into the coronary circulation [1,2]. We are not aware of any reported case where all the aforementioned measures failed and temporary implantation of a left ventricular assist device led to a good outcome.
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2. Patient, diagnosis and treatment
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A 45-year-old female patient was scheduled for CABG to her circumflex artery (RCx) and to a side branch of the RCx. This particular marginal branch had been subjected to repeated percutaneous interventions without maintained success. The left ventricular ejection fraction was 50%. She suffered from angina occurring on heavy physical exertion and from severe anginal attacks waking her up in the early morning hours. No tests for variant (=Prinzmetal) angina had been performed. Her medical therapy consisted of metoprolol, isosorbide dinitrate, molsidomin and losartan.
The left internal thoracic artery was anastomosed to the RCx and a saphenous vein graft to the side branch using normothermic extracorporeal circulation and intermittent antegrade blood cardioplegia. Weaning off extracorporeal circulation was possible without the use of inotropes. Two hours after transferral to the Intensive Care Unit she started to regain consciousness, started to breathe spontaneously with slightly elevated arterial carbon dioxide levels, and simultaneously developed ST-segment elevation over all lateral and inferior leads (Fig. 1). Five minutes later ventricular fibrillation developed. Repeated defibrillation, external chest compression and 0.5 mg of epinephrine were required to restore spontaneous circulation. An intraaortic balloon pump was inserted, transesophageal echocardiography (TEE) showed new akinesia in the anteroseptal region. A presumptive diagnosis of plaque rupture in the left anterior descending artery or embolisation into this vessel was made and she was transferred to the cardiac catheter suite immediately. The coronary angiogram revealed no fixed lesions, there was good patency of all anastomosis, but all branches of the left coronary artery and the internal thoracic artery were in severe spasm (see Video 1). Left ventricular ejection fraction was about 20%. No views of the small right coronary artery were obtained as it was free of lesions on previous coronary angiograms and TEE showed normal right ventricular function. The coronaries and the internal thoracic artery relaxed with repeated direct injections of glyceril trinitrate (GTN), but not sufficiently so, to stabilise the cardiac rhythm and left ventricular function. Repeated defibrillation, external chest compression and three boli of epinephrine were required during the investigation. Systemic administration of GTN 2 µg/kg/min and diltiazem 4 µg/kg/min did not improve the coronary spasm. As all the aforementioned measures seemed to fail we urgently transferred the patient into the operating room and a left ventricular assist device (LVAD) (Capiox, Terumo Cardiovascular Systems, Tokyo, Japan) was inserted using extracorporeal circulation. During the procedure cardiac denervation was attempted by dissection of tissue surrounding the aorta and pulmonary artery. Diltiazem and GTN were continued during and after implantation, norepinephrine had to be added for low sytemic vascular resistance. Once the left ventricle was unloaded ST-segments normalized. Three hours after the procedure she again developed elevated ST-segments and the partially unloaded ventricle showed generalized severe hypokinesia. These signs responded to intravenous administration of 2.5 mg of milrinone. After a further two hours a similar episode occurred during continuous administration of GTN, diltiazem and milrinone. Coronary spasm responded rapidly to levosimendan 20 µg/kg given over 15 min. During application of this loading dose TEE showed marked improvement of regional and overall contractility of the partially unloaded ventricle. A maintenance infusion of 0.2 µg/kg/min was continued for 36 h. No further episode of vasospasm occurred, LVAD explantation was possible after 40 h, 10 h thereafter she could be extubated and another 10 h later the balloon pump was removed. One year after the event she is back in her employment and remains free of symptoms with medical therapy consisting of diltiazem, metoprolol, losartan and simvastatin.
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Fig. 1. Shows the electrocardiograms on admission to the Intensive Care Unit (on the left) and roughly 2 h later, shortly before onset of ventricular fibrillation (on the right).
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Video 1. Shows postoperative angiographic views of the left main stem and the left internal thoracic artery, starting with a left ventriculogram.
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3. Discussion
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Postoperative CS can have disastrous consequences [1]. It seems to occur more often in patients suffering from angina at rest [2], but it has occurred in patients without a suggestive history. Successful management of this condition requires early recognition. Cardiac catheterization is the gold standard for diagnosis. Intracoronary injection of GTN and possibly calcium channel antagonists seems to be vital for successful management [2–4]. During angiography we saw relaxation of the spastic coronary arteries on direct injection of GTN, but this could not be maintained long enough to reestablish a stable rhythm and hemodynamic situation. Severe left ventricular dysfunction secondary to stunning forced us to implant a LVAD. Once this decision was made we removed the coronary catheter, as it might have become dislodged during the implant procedure.
Recurrent coronary spasm responded to intravenous milrinone, once the left ventricle was partially unloaded by the LVAD. This response only lasted two hours despite continuous infusion of three coronary vasodilators with different modes of action. Sustained control of vasospasm could be achieved by additional systemic application of levosimendan. This calcium sensitizer has positive inotropic action and dilatation of the systemic and coronary vasculature via activation of adenosine triphosphate-dependent potassium channels is well documented [5,6]. It is an approved drug in Scandinavia, Austria, Belgium and Spain. The hemodynamic effects of levosimendan last for several days, presumably due to the long half life of active metabolites [7,8]. This fact, in combination with possible spontaneous resolution of the spasm, made a trial of levosimendan withdrawal – and reinstitution, had symptoms recurred – pointless. Despite this we still believe that levosimendan application contributed to the early successful weaning off all mechanical assist systems by maintaining coronary vasodilatation and providing inotropic support for the stunned myocardium. In our opinion, it may well turn out to be the inotrope of choice in patients with documented or presumed vasospasm, as it has no negative effect on myocardial oxygen balance. Its successful use in cardiac failure post-myocardial infarction, is well documented [9].
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4. Conclusion
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Severe postoperative coronary spasm does not always respond to established treatments and a temporary mechanical assist device may be required. Levosimendan seems to be a logical choice for inotropic support of the stunned myocardium in this situation.
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References
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Abstract
1. Introduction