e-Herz: Case study Herz 2013 DOI 10.1007/s00059-013-3919-7 Received: 5 July 2013 Accepted: 6 July 2013 © Urban & Vogel 2013
C. Akgullu1 · U. Eryilmaz1 · H. Gungor1 · C. Zencir1 · M. Selvi1 · M. Avcil2 · B. Dagli2 1 Faculty of Medicine, Department of Cardiology, Adnan Menderes University , Aydin 2 Department of Emergency Medicine , Adnan Menderes University , Aydin
Myocardial infarction secondary to morphine-induced Kounis syndrome Kounis syndrome (KS), originally known as “allergic angina syndrome,” was first described in 1991 [1]. Since then, it has been shown that this syndrome can progress to acute coronary syndromes and may cause sudden cardiac death [2]. The main cause of this syndrome is thought to be concomitant coronary artery spasm and atheromatous plaque rupture during allergic episodes and hypersensitivity reactions [3]. Some drugs, latex, foods, as well as various conditions and environmental exposures may trigger this rare-life threatening syndrome. Among these, KS due to morphine use is extremely rare. In this report, we present the case of a 36-year-old female patient who survived after acute allergic reaction and concomitant acute lateral myocardial infarction as the result of morphine administration.
phine, she complained of chest discomfort, nausea, and sweating. Her blood pressure suddenly fell to 70/35 mmHg. Following administration of intravenous fluid, parenteral corticosteroids, and antihistamines her blood pressure rose to 90/60 mmHg but her chest discomfort continued. The patient’s electrocardiogram (ECG) showed 1-mm ST-segment elevation in leads I and AVL and marked ST-segment depression in leads III and V3–V5 (. Fig. 1). Intravenous 5,000 IU
heparin and 600 mg clopidogrel were administered in the emergency department and she was transferred to the coronary care unit. Forty-five minutes after the onset of morphine-triggered symptoms, her chest discomfort totally resolved and a check-up ECG was completely normal (. Fig. 2). The following day, left heart catheterization revealed normal right and left coronary arteries (. Fig. 3). Troponin I levels were high (9.3 ng/ml) and transthoracic echocar-
Case report A 36-year-old woman with a history of atopy and allergic reactions against nonsteroidal anti-inflammatory drugs presented to our emergency department with severe colicky lower back ache lasting for 30 min. She did not have any cardiovascular risk factors or systemic illness. Physical examination revealed a blood pressure of 120/80 mmHg with a regular pulse of 70 beats/min. Renal colic was suspected and 5 mg morphine sulfate was administered intravenously. Directly after the administration of mor-
Fig. 1 8 Electrocardiogram just after the administration of morphine, demonstrating ST-segment elevation in leads I and AVL, and ST-segment depressions in V2–V6 Herz 2013
| 1
e-Herz: Case study
Fig. 2 8 Completely normal electrocardiogram, 45 min after the onset of morphine-triggered symptoms
normal coronary arteries without any cardiovascular risk factors [6]; the type-II variant includes patients with preexisting atheromatous disease; and type-III is associated with drug-eluting stent thrombosis [7, 8, 9]. In the present case, coronary angiography displayed normal coronary arteries with an elevated level of troponin and transient ST changes in the ECG following exposure to allergenic insult, morphine. Based on these date from the literature, our case corresponds to the type-I variant of KS. Activation of mast cells and the systemic release of histamine are common side effects of morphine, but KS is extremely rare. In the literature there is only one report of KS induced by the administration of two different beta-lactam antibiotics and concomitant parenteral morphine [10].
Conclusion In conclusion, anaphylaxis by morphine is most likely responsible for the severe acute coronary syndrome, leading to acute lateral myocardial infarction in the present case. We call attention to this rare clinical entity because allergic myocardial infarction, if not recognized and managed in time, may cause life-threatening conditions.
Corresponding address Fig. 3 8 a Selective right coronary angiogram demonstrating normal right coronary artery. b Selective left coronary angiogram demonstrating normal left coronary system
diography showed normal left ventricular systolic functions with an ejection fraction of 68%. Following catheterization, her medical therapy was continued with antihistamines and 75 mg/ day clopidogrel for 1 month. She was also diagnosed as having a small stone passing through the ureter to the bladder. She did not complain of recurrent back ache. Our final diagnosis was Kounis syndrome secondary to morphine sulfate. The patient did not experience recurrent angina during hospitalization, and she was discharged on the fourth day without any complications.
2 |
Herz 2013
Discussion Angina pectoris in the course of allergic reactions was first described in 1991 and is known as Kounis syndrome [1]. Several pathophysiological mechanisms have been proposed to explain this clinical entity [4, 5]. The one most accepted is mast cell activation causing vasospastic and inflammatory response on the coronary endothelium, which may further contribute to coronary plaque rupture and thrombus formation [4]. Three types of KS have been described. The type-I variant describes patients with
H. Gungor Faculty of Medicine, Department of Cardiology, Adnan Menderes University 09100 Aydin Turkey
[email protected]
Conflict of interest. On behalf of all authors, the corresponding author states that there are no conflicts of interest.
References 1. Kounis NG, Zavras GM (1991) Histamine-induced coronary artery spasm: the concept of allergic angina. Br J Clin Pract 45:121–128 2. Aykan AC, Zehir R, Karabay CY, Özkan M (2012) A case of Kounis syndrome presented with sudden cardiac death. Anadolu Kardiyol Derg12:599–600
3. Yurtdaş M, Aydin MK (2012) A case of coronary spasm with resultant acute myocardial infarction: likely the result of an allergic reaction. Intern Med 51:2161–2164 4. Kounis NG, Hahalis G, Kourelis T et al (2008) Kounis syndrome (allergic angina and allergic myocardial infarction). In: Gallo AP, Jones ML (Hrsg) Angina pectoris: etiology, pathogenesis and treatment. Nova Science Publishers, Hauppauge, S 77–150 5. Fassio F, Almerigogna F (2012) Kounis syndrome (allergic acute coronary syndrome): different views in allergologic and cardiologic literature. Intern Emerg Med 7:489–495 6. Wada T, Abe M, Yagi N et al (2010) Coronary vasospasm secondary to allergic reaction following food ingestion: a case of type I variant Kounis syndrome. Heart Vessels 25:263–266 7. Venturini E, Magni L, Kounis NG (2011) Drug eluting stent-induced Kounis syndrome. Int J Cardiol 146:e16–e19 8. Akyel A, Murat SN, Çay S et al (2012) Late drug eluting stent thrombosisdue to acemetacine: Type III Kounis syndrome Kounis syndrome due to Acemetacine. Int J Cardiol 155:461–462 9. Karasu E, Minareci K (2011) Myocardial infarction following a bee sting: an example of Type II Kounis syndrome. Int J Cardiol 148:382–384 10. Uluçay A, Aksoy MF (2012) A case of Kounis syndrome aggravated by administration of morphine. Anadolu Kardiyol Derg 12:190–191
Herz 2013
| 3
