Resuscitation 81 (2010) 919–920
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Letter to the Editor Cardiac arrest caused by coronary vasospasm treated with isosorbide dinitrate and left ventricular assistance We report a case of a patient who presented with out-of-hospital cardiac arrest (OHCA) caused by coronary artery spasm in whom cardiac assistance was required to administer nitrates to alleviate coronary artery vasoconstriction. A 59-year-old male patient was admitted to the emergency department for chest pain. Six months before, he was hospitalized for an acute coronary syndrome (ACS) without ST segment elevation. A coronary angiogram revealed no significant lesion but spontaneous spasm of the third segment of the right coronary artery occurred which disappeared after intracoronary injection of 1 mg of isosorbide dinitrate (ISDN). The left ventricular ejection fraction (LVEF) was 55%. He was discharged with a prescription of aspirin, statin, verapamil 240 mg and amlodipine 10 mg. He had no chest pain for six months. He was then admitted for several bouts of chest pain. The electrocardiogram (ECG) showed numerous premature ventricular beats and depression of the segment ST in the apical-lateral leads. Shortly afterwards, the chest pain reappeared and was followed by ventricular fibrillation (VF) cardiac arrest, which was treated with immediate cardioversion. The patient’s trachea was intubated and mechanical ventilation started. An intravenous infusion of adrenaline was administered to treat hypotension (systolic blood pressure 90 mm Hg). An immediate coronary angiogram showed severe and diffuse vasospasm (Fig. 1A). ISDN 5 mg was administered in the left coronary artery and the coronary spasm disappeared (Fig. 1B). The LVEF was evaluated at 25% with a left ventricle end diastolic pressure (LVEDP) of 10 mm Hg. In the intensive care unit, VF occurred 3 times and was treated by cardioversion. An infusion of nitrates was attempted but rapidly
stopped because of low blood pressure. It was decided to implant an extra corporeal life support (ECLS). Adrenaline was rapidly tapered and replaced with noradrenaline. Nitrates were administered. The patient was weaned off the ECLS after 24 h and noradrenaline was stopped after 48 h. Oral calcium channel blockers were reintroduced. At day 4, transthoracic echocardiography (TTE) showed a marked improvement with an LVEF of 50%. On day 15, a coronary angiogram showed no coronary artery spasm at rest. Three months later, a coronary angiogram with spasm provocation test using methylergometrine maleate showed normal coronary arteries with no spasm. The patient is currently asymptomatic. Coronary artery disease is the most frequent cause of OHCA.1 Variant angina has been reported as a rare cause.2 In our patient, sub occlusive vasospasm was confirmed on the coronary angiogram performed at admission. Recommended treatments for coronary spasm are vasodilators. However, the use of these drugs is limited because they decrease systemic blood pressure. In the setting of post cardiac arrest shock, blood pressure is difficult to maintain at an adequate level because of myocardial stunning and vasoplegia.3,4 The challenge in treating this patient was to break the cycle between coronary spasm and hemodynamic instability. Catecholamines were necessary because of cardiogenic shock but worsened the vasospasm, which was the cause of shock. ECLS has been evaluated in resuscitated patients5 but never in a case of cardiac arrest due to variant angina. This transient cardiac assist device allowed the weaning of inotropic support and introduction of vasodilators. Coronary vasospasm is an underestimated cause of cardiac arrest. In the setting of cardiogenic shock complicating variant angina, management of vasodilators is challenging and transient cardiac assist may be considered.
Fig. 1. Coronary angiography. Panel A: front view revealing severe vasospasm of the mid left circumflex artery and diffuse spasm of the left anterior descending artery. Panel B: after administration of intracoronary isosorbide dinitrate, reversal of the vasospastic sub occlusion. 0300-9572/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2010.03.023
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Letter to the Editor / Resuscitation 81 (2010) 919–920
Conflict of interest None of the authors is involved in any commercial or noncommercial affiliations or consultancies that are, or may be perceived to be, a conflict of interest with the work. References 1. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation 2008;118:2452–83. 2. Myerburg RJ, Kessler KM, Mallon SM, et al. Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm. N Engl J Med 1992;326:1451–5. 3. Laurent I, Monchi M, Chiche JD, et al. Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol 2002;40:2110–6. 4. Adrie C, Laurent I, Monchi M, Cariou A, Dhainaou JF, Spaulding C. Postresuscitation disease after cardiac arrest: a sepsis-like syndrome? Curr Opin Crit Care 2004;10:208–12. 5. Megarbane B, Leprince P, Deye N, et al. Emergency feasibility in medical intensive care unit of extracorporeal life support for refractory cardiac arrest. Intensive Care Med 2007;33:758–64.
Stéphane Manzo-Silberman a,∗ Jérôme Fichet b Pascal Leprince c Nicolas Marque a Gwenhael Collin b Alain Cariou b Christian Spaulding a a Interventional Cardiology, Cochin Hospital Paris, Descartes University, 27 Rue du Faubourg Saint-Jacques, Paris, France b Intensive Care Unit, Cochin Hospital Paris, Descartes University, 27 Rue du Faubourg Saint-Jacques, Paris, France c Cardiac surgery, Pitié Salpetrière Hospital, Paris VI University, 47-83 Bd de l’Hôpital, Paris, France ∗ Corresponding
author. E-mail address:
[email protected] (S. Manzo-Silberman) 12 March 2010