Does fluorescein-induced anaphylactic shock trigger late drug-eluting stent thrombosis and cause lethal ST-elevation myocardial infarction?

Transcription

1 Bu-Yuan Hsiao et al. Does fluorescein-induced anaphylactic shock trigger late drug-eluting stent thrombosis and cause lethal ST-elevation myocardial infarction? Bu-Yuan Hsiao 1, Tien-Ping Tsao 1, Wei-Hsian Yin 1 Abstract Anaphylaxis is an acute, potentially lethal, multisystem syndrome resulting from the sudden release of mast cell- and basophil-derived mediators into the circulation. It has been associated clinically with myocardial ischemia or acute coronary events. Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with anaphylaxis. Mast cells accumulate at sites of coronary atherosclerotic plaques, and mast cell degranulation plays an important role in pathogenesis. We describe a 60-year-old man who developed acute ST-elevation myocardial infarction post-fluorescein-induced anaphylactic shock. Coronary angiography showed intra-stent thrombosis in the proximal left anterior descending artery. Type III Kounis syndrome was impressed and led to lethal cardiogenic shock. Key Words: Kounis syndrome, anaphylaxis, myocardial infarction, stent thrombosis INTRODUCTION Anaphylaxis is an acute, potentially lethal, multisystem syndrome resulting from the sudden release of mast cell- and basophilderived mediators into the circulation. It has been associated clinically with myocardial ischemia or acute coronary events. 1 Mast cells accumulate at sites of coronary atherosclerotic plaques, and immunoglobulins bound to mast cells can trigger mast cell degranulation which may promote plaque rupture. 2 Stimulation of the H1 histamine receptor may also produce coronary artery vasospasm. 3 Platelet-activating factor induction of platelet aggregation and activation of coagulation pathways might additionally predispose to coronary artery thrombosis. We describe a 60-year-old man who developed acute STelevation myocardial infarction due to late drugeluting stent thrombosis after fluorescein-induced anaphylactic shock. CASE PRESENTATION A 60-year-old man presented to the emergency room with acute anaphylactic shock. His medical history included coronary artery disease (CAD), hypertension, dyslipidemia, and type 2 diabetes mellitus without history of allergies, eczema, or asthma. Two months prior, he underwent uneventful percutaneous coronary intervention (PCI) with implantation of sirolimus-eluting stent Correspondence: Dr.Wei-Hsian Yin Division of Cardiology, Heart Center, Cheng Hsin General Hospital; No. 45, Zhenxing St., Beitou Dist., Taipei City 112, Taiwan 1 Phone: ; Fax: ; chghyinwh@gmail.com 22

2 Fluorescein-induced lethal Kounis syndrome in the proximal left anterior descending artery (LAD). About one half-hour before admission, he received intravenous injection of sodium fluorescein for fluorescent angiography by his ophthalmologist. Generalized itchiness, flushing, conjunctival swelling, dizziness, blurred vision, and eventual collapse followed. After initial resuscitation, he went to the emergency room complaining of generalized itchiness without shortness of breath or wheezing. Physical examination revealed diffuse erythema without angioedema. His blood pressure was 82/46 mmhg and pulse rate was 97 beats per minute and regular. Electrocardiography revealed unchanged sinus rhythm with complete left bundle branch block (Fig. 1). Intravenous diphenhydramine (60 mg) and methylprednisolone (80 mg) were administered with intravenous fluid administration and supplemental oxygen. Due to persistent hypertension, 0.3 mg of 1:10000 epinephrine was subcutaneously injected. His clinical condition stabilized about 30 minutes post-treatment. However, he subsequently suffered from squeezing substernal chest pain, and became hemodynamically unstable about two hours after admission. Electrocardiography revealed sinus rhythm with complete right bundle branch block, and ST-segment elevations in precordial leads (Fig. 2). Peak serum troponin I and CK- MB levels were >800 ng/ml (normal: ng/ml) and 299 ng/ml (normal: ng/ml), respectively. Transthoracic echocardiography disclosed distal septum, anterior wall and apex akinesis, and left ventricle lateral and inferior wall hypokinesis. Cardiogenic shock complicated the diagnosed acute anterior wall ST-elevation myocardial infarction. He received immediate dual antiplatelet therapy (aspirin and ticagrelor), unfractionated heparin, and atorvastatin. We also arranged primary PCI in the meanwhile. Coronary angiography showed intra-stent thrombosis in the proximal LAD (Fig. 3). Thrombus aspiration was performed three times followed by uneventful balloon angioplasty. Subsequently, the LAD showed complete reperfusion (Fig. 4). Unfortunately, twenty minutes post-procedure, the patient had a seizure and lost consciousness. The electrocardiographic monitor showed ventricular Fig. 1. Initial electrocardiography revealed unchanged sinus rhythm with complete left bundle branch block. 23

3 Bu-Yuan Hsiao et al. tachycardia then ventricular fibrillation. Cardiopulmonary cerebral resuscitation was performed, followed by intra-aortic balloon pump insertion. Bedside echocardiography revealed cardiac arrest without pericardial effusion. He did not regain spontaneous circulation even with prolonged cardiopulmonary cerebral resuscitation. Acute recurrent intra-stent LAD thrombus formation was the suspected cause of death. Fig. 2. Two hours later, electrocardiography changed to sinus rhythm with complete right bundle branch block and ST-segment elevations in precordial leads. Acute anterior wall ST-elevation myocardial infarction was diagnosed. Fig. 3. Coronary angiography showed intra-stent thrombosis (arrow) in the proximal left anterior descending artery. Fig. 4. Left anterior descending artery showed complete reperfusion post-thrombus aspiration followed by balloon angioplasty. 24

4 Fluorescein-induced lethal Kounis syndrome DISCUSSION Anaphylaxis most often results from immunologic reactions to foods, medications, and insect stings, although it can also be induced through nonimmunologic mechanisms by any agent capable of producing a sudden, systemic degranulation of mast cells or basophils. It has been associated clinically with myocardial ischemia, atrial and ventricular arrhythmias, conduction defects, and T-wave abnormalities. 1 Kounis syndrome, firstly described in 1991, is the concurrence of acute coronary syndromes with conditions associated with anaphylaxis. 4 Mast cells accumulate at sites of coronary atherosclerotic plaques, and mast cell degranulation may promote plaque rupture. 2 Histamine, acting at H 1 receptors, mediates coronary artery vasoconstriction and possibly vasospasm. 3 Plateletactivating factor decreases coronary blood flow, delays atrioventricular conduction, and has negative inotropic effects on the heart. Plateletactivating factor induction of platelet aggregation and activation of coagulation pathways might additionally predispose to coronary artery thrombosis, and thus trigger myocardial infarction. Finally, the administration of epinephrine, which is a life-saving drug to treat anaphylaxis, might aggravate pre-existing coronary spasms induced by mast cell-derived mediators. 5 There are three variants of Kounis syndrome that have been described. 6 Type I (coronary spasm), possibly representing endothelial dysfunction or microvascular angina, includes patients with normal coronary arteries without predisposing factors for CAD. Acute release of inflammatory mediators can induce coronary artery spasms with/without cardiac enzyme increases. Type II (coronary thrombosis), includes patients with pre-existing but quiescent atheromatous disease. Acute release of inflammatory mediators can induce either coronary artery spasms (with normal cardiac enzymes), or plaque erosion/rupture (manifesting as acute myocardial infarction). Type III (drug-eluting stent thrombosis), 7,8 includes patients with stent thrombosis in whom thrombus harvesting and pathological staining shows the presence of eosinophils and mast cells. Several drugs could induce Kounis syndrome. Fluorescein, a synthetic organic compound, is indicated in diagnostic fluorescein angiography or angioscopy of the retina and iris vasculature. It may cause adverse reactions, including nausea, vomiting, hives and anaphylaxis, but rarely leads to anaphylactic shock and subsequent cardiac arrest. To our knowledge, this is the first reported case of type III Kounis syndrome due to fluorescein-induced anaphylactic shock complicated by late drug-eluting stent thrombosis. Acute ST-elevation myocardial infarction complicating anaphylaxis is rare but can be lethal. The heart becomes the target of severe anaphylaxis and mast cell degranulation plays an important role in pathogenesis of cardiac complications. Physicians should be aware of this condition to provide proper diagnosis and treatment. REFERENCES 1. Marone G, Bova M, Detoraki A, Onorati AM, Rossi FW, Spadaro G. The human heart as a shock organ in anaphylaxis. Novartis Found Symp 2004;257: Kovanen PT, Kaartinen M, Paavonen T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation 1995;92: Steffel J, Akhmedov A, Greutert H, Lüscher TF, Tanner FC. Histamine induces tissue factor expression: implications for acute coronary syndromes. Circulation 2005;112: Kounis NG, Zavras GM. Histamine-induced coronary artery spasm: the concept of allergic angina. Br J Clin Pract 1991;45: Shaver KJ, Adams C, Weiss SJ. Acute myocardial infarction after administration of low-dose intravenous epinephrine for anaphylaxis. CJEM 2006;8: Biteker M. A new classification of Kounis syndrome. Int J Cardiol 2010;145: Venturini E, Magni L, Kounis NG.. Drug eluting stentinduced Kounis syndrome. Int J Cardiol 2011;146:e Kounis NG, Tsigkas G, Almpanis G, Kounis GN, Mazarakis A, Hahalis G. Coronary stent implantation, eosinophils and the Kounis hypersensitivity associated acute coronary syndrome. Atherosclerosis 2011; 217:

5 蕭卜源等 螢光素引起之過敏性休克, 是否觸發晚期塗藥支架之栓塞並造成致命性之 ST 段上升心肌梗塞? 蕭卜源 1, 曹殿萍 1 1, 殷偉賢 摘要 過敏反應乃是由於肥大細胞和嗜鹼性細胞被活化並釋放出致敏物質, 所導致的一種急性 甚至可能致命, 影響眾多系統的症候群 臨床上過敏可能跟心肌缺氧或急性冠心症有關 當急性冠心症的發生與過敏相關時, 稱之為 Kounis 症候群 過敏發生時, 肥大細胞會聚集在冠狀動脈的粥樣硬化斑塊, 此時肥大細胞的去顆粒作用就扮演非常重要的致病機轉 在此我們描述一位 60 歲的男性, 注射螢光素造成過敏性休克之後, 發生急性 ST 段上升之心肌梗塞 冠狀動脈造影顯示在左前降支的近端, 支架內有血栓形成 此病患被診斷為第三類型的 Kounis 症候群, 後來並發生心因性休克而死亡 關鍵詞 :Kounis 症候群, 過敏性反應, 心肌梗塞, 支架栓塞 通訊作者 : 殷偉賢醫師 112 台北市北投區振興街 45 號 ; 振興醫療財團法人振興醫院心臟醫學中心心臟血管內科 1 電話 : ; 傳真 : ; chghyinwh@gmail.com 26