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Silent embolization of an Amplatzer atrial septal closure device into the main pulmonary artery: Pivotal role of routine postprocedural surveillance echocardiography
Letters to the Editor
235
Silent embolization of an Amplatzer atrial septal closure device into the main pulmonary artery: Pivotal role of routine postprocedural surveillance echocardiography Hamza Duygu ⁎, Zehra Ilke Akyildiz, Ugur Kocabas, Cem Nazli, Oktay Ergene Fellow of Cardiology, Ataturk Training and Research Hospital, Izmir, Turkey
a r t i c l e
i n f o
Article history: Received 28 August 2009 Accepted 10 September 2009 Available online 6 November 2009 Keywords: Atrial septal defect Amplatzer occluder Device embolization Main pulmonary artery
The transcatheter closure of secundum atrial septal defects (ASDs) has become a safe and established alternative to surgery, with high closure rates and rare complications [1]. Percutaneous closure of secundum ASD may be complicated by immediate or late device embolizations. We report an asymptomatic embolization of an Amplatzer atrial septal closure device into the main pulmonary artery detected by routine postinterventional transthoracic echocardiography 24 h after deployment. An 18-year-old male who was diagnosed with ASD was referred to our clinic for percutaneous device closure because of progressive exertional dyspnea. Transthoracic echocardiography revealed a secundum type ASD with left-to-right flow documented by color Doppler evaluation. There was a moderate increase in right ventricular dimension and the pulmonary artery systolic pressure was moderately elevated (45 mm Hg). Transesophageal echocardiography (TEE) demonstrated a 29 mm secundum ASD with adequate margins of the defect and sufficient distance to the atrioventricular valves for deployment of a percutaneous closure device (Fig. 1A). Upon this, the anatomy was deemed suitable for implantation of an ASD occluder device, and he was scheduled for cardiac catheterization and device closure. Cardiac catheterization confirmed the shunt at the atrial level and revealed a pulmonary-to-systemic flow ratio of 1.8. The balloon stretched diameter was 30 mm. A 32-mm Amplatzer septal occluder device (AGA Medical Corporation, Golden Valley, Minnesota) was deployed under general anesthesia with TEE guidance. The position was confirmed by back-and-forth manipulation of the device as well as by TEE and angiographic imaging. Once positioning was confirmed, the delivery cable was disconnected from the device and removed. The device was released and TEE demonstrated a good position of the device without residual shunting or impingement on intracardiac structures (Fig. 1B). The patient was extubated and returned to the care unit. Although the patient was asymptomatic, on the first day after the procedure, routine postinterventional transthoracic echocardiography showed that the device was not seen, and echocardiography and chest x-ray confirmed device embolization into main the pulmonary artery (Fig. 2). The device did not obstruct the main pulmonary artery because it was oriented in the longitudinal plane, parallel to the direction of blood flow. The patient remained hemo-
⁎ Corresponding author. Tel.: +90 232 2444444; fax: +90 232 2431530. E-mail address: [email protected] (H. Duygu).
dynamically stable. After intravenous heparin administration, it was decided to attempt a percutaneous retrieval of the device. However, transcatheter device retrieval with snares of different sizes and bioptomes failed due to the longitudinal orientation of the device in the pulmonary artery. Therefore, the patient was referred for surgical removal. After institution of cardiopulmonary bypass, a pulmonary arteriotomy was made and device was retrieved without difficulty (Fig. 3) and the ASD closed by primary sutures. The postoperative course was uncomplicated and the patient was discharged from the hospital on the 7th postoperative day. Device embolization is a potential complication of every attempted ASD device closure. Emergency surgical intervention may be required for complications, during or after implantation of the device. Although some authors have reported cases of late device embolization after the procedure [2–4], device embolizations generally appear to occur within the first hours after implantation [5]. In a recently published study by Majunke et al. [6], a total of 650 adult patients underwent transcatheter closure of an ASD using the Amplatzer septal occluder. In this study, six device embolizations occurred. In 2 patients (0.2%), the device embolized a few minutes after release and both patients underwent surgery. Four device embolizations occured (0.6%) within 30 days after the procedures. In 2 patients, the occluder embolized into the left ventricle; in 1 patient, into the pulmonary artery; and in 1 patient, an embolized occluder was found in the descending aorta. Two embolized devices were retrieved using a catheter technique, and 2 patients underwent surgery. Peuster et al. [7] reported a clinically asymptomatic secondary embolization of a 25 mm Helex occluder into the pulmonary artery 30 h after implantation into a centrally located secundum ASD with a stretched diameter of 13 mm in a 2-year-old patient. Transcatheter device retrieval with snares of different sizes, bioptomes, and retrieval forceps failed due to the mismatch of the diameter of the device and the small diameter of the pulmonary artery. Therefore, the device was retrieved surgically. In addition to this case, Kapoor et al. [8] described a case of device embolization into the main pulmonary artery ten minutes after release in their experience of 35 Amplatzer ASD device closures. The device was surgically removed because it was not possible to retrieve the embolized device by catheterization procedures as in our case. The selection of patients with favourable ASD morphology and the choice of appropriate device sizes are crucial to prevent embolization. There may be several factors that may help predict an increased risk for device embolization. The main causes of displacement are large defects, the inadequate defect rim to hold the device, undersized device diameters, and tears in the interatrial septum during balloon sizing or the first attempt to implant [9]. We cannot explain the exact reason for the embolization of the device. However, the ASD diameter was large and the device may have been undersized. Our patient did not develop symptoms after embolization because the position of device in the pulmonary artery was in the longitudinal axis and parallel to the direction of blood flow. The device crossed the tricuspid and pulmonic valves without any damage. This case reinforces the importance of routine postprocedural echocardiographic surveillance as a screen for device embolization even if the patients are asymptomatic. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [10].
236
Letters to the Editor
Fig. 1. Transesophageal images showing atrial septal defect before (A) and after (B) device implantation.
Fig. 2. Transthoracic echocardiography (A) and chest x-ray (B) show the Amplatzer occluder device in the main pulmonary artery (arrows).
Fig. 3. Intraoperative appearance of the Amplatzer device identified into the main pulmonary artery (arrow) and surgical specimen of the retrieved device.
References [1] Giardini A, Donti A, Specchia S, et al. Long-term impact of transcatheter atrial septal defect closure in adults on cardiac function and exercise capacity. Int J Cardiol 2008;124(2):179–82. [2] Mashman WE, King SB, Jacobs WC, et al. Two cases of late embolization of Amplatzer septal occluder devices to the pulmonary artery following closure of secundum atrial septal defects. Catheter Cardiovasc Interv 2005;65 (4):588–92.
[3] Lysitsas DN, Wrigley B, Banerjee P, et al. Presentation of an embolised Amplatzer septal occluder to the main pulmonary artery 2 years after implantation. Int J Cardiol 2009;131(3):e106–7. [4] Ussia GP, Abella R, Pome G, et al. Chronic embolization of an atrial septal occluder device: percutaneous or surgical retrieval? A case report. J Cardiovasc Med (Hagerstown) 2007;8(3):197–200. [5] Chessa M, Carminati M, Butera G, et al. Early and late complications associated with transcatheter occlusion of secundum atrial septal defects. J Am Coll Cardiol 2002;39:1061–5.
Letters to the Editor [6] Majunke N, Bialkowski J, Wilson N, et al. Closure of atrial septal defect with the Amplatzer septal occluder in adults. Am J Cardiol 2009;103(4):550–4. [7] Peuster M, Reckers J, Fink C. Secondary embolization of a Helex occluder implanted into a secundum atrial septal defect. Catheter Cardiovasc Interv 2003;59(1):77–82.
237
[8] Kapoor MC, Singh S, Sharma S, et al. Case 6—2003: embolization of an atrial septal occluder device. J Cardiothorac Vasc Anesth 2003;17(6):755–63. [9] Levi DS, Moore JW. Embolization and retrieval of the Amplatzer septal occluder. Catheter Cardiovasc Interv 2004;61(4):543–7. [10] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
0167-5273/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.09.532
The conundrum of hypersensitivity cardiac disease: Hypersensitivity myocarditis, acute hypersensitivity coronary syndrome (Kounis Syndrome) or both? G.C. Almpanis, A. Mazarakis, D.A. Dimopoulos, N.A. Tragotsalou, G.N. Kounis, N.G. Kounis ⁎, D. Alexopoulos Department of Cardiology, University of Patras Medical School, Patras, Greece
a r t i c l e
i n f o
Article history: Received 18 September 2009 Accepted 27 September 2009 Available online 4 November 2009 Keywords: Cardiac magnetic resonance Hypersensitivity myocarditis Kounis syndrome
Hypersensitivity is synonymous to allergy and denotes an excessive reaction associated with gross tissue changes after antigen–antibody (IgE or IgM) reaction. The cardiac tissue can be easily affected by hypersensitivity processes, while the myocardium and the coronary arteries are especially vulnerable as well. There are two clinical entities of hypersensitivity etiology, 1) Hypersensitivity coronary syndrome or Kounis syndrome [1], a concurrence of acute coronary syndrome with conditions associated with mast cell degranulation involving interrelated and interacting inflammatory cells and including hypersensitivity or allergic and anaphylactic or anaphylactoid insults and 2) Hypersensitivity myocarditis [2], an inflammatory disease affecting the myocardium and the cardiac conduction system manifesting as an allergic complication of drug therapy. The following unique report is of a patient who presented with clinical and laboratory findings suggesting of acute coronary hypersensitivity syndrome (Kounis syndrome) but who was proved, with cardiac magnetic resonance (CMR) imaging , at a later stage, to have myocardial changes compatible with hypersensitivity myocarditis. The clinical course, the laboratory and differentiating findings of these two relative entities are discussed. A 28 year-old male had an episode of acute bronchitis with temperature of 38 °C and his family physician prescribed amoxicillin 1gr b.i d. Six hours later the patient felt generalized itching accompanied by erythematous rash covering the whole body surface. He was given 500 mg of hydrocortisone sodium succinate intramuscularly followed by oral cetirizine 10 mg b.i.d. The following 24 h, rash and itching started to subside. However, he was feeling unwell and he was admitted to our hospital for further evaluation.
⁎ Corresponding author. E-mail address: [email protected] (N.G. Kounis).
On examination, he had not any significant past medical history and was not smoker. He did not give any history of atopy and did not have any previous hospitalizations. His family history was free of any cardiac or chest disease. One hour after admission he developed severe retrosternal pain radiating to the neck and elbows. He started sweating with difficulty in breathing. His blood pressure was 120/ 80 mm Hg, the pulse 69 beats/min regular and on auscultation there was neither pericardial rub nor murmurs. The electrocardiogram showed ST elevation of 3 mm in leads II, III, AVF, V7–V9 compatible with acute inferior myocardial infarction (Fig. 1). He was, immediately, given 5 mg of nitroglycerin sublingually and 325 mg of aspirin and was transferred to the coronary care unit. The above symptoms were persisting and infusion of nitroglycerin was started at a rate of 2 mcg/min. However, electrocardiographic changes and symptoms did not subside and he was thrombolysed with 40 mg of tenectaplase. Half an hour later the patient developed sinus bradycardia of 40 beats/min with dizziness and diaphoresis. With 0.5 mg of atropine iv bradycardia and symptoms subsided and the electrocardiographic changes reverted to normal (Fig. 2). Transthoracic echocardiography revealed hypokinesia and segmental akinesia involving the inferior wall with an estimated ejection fraction of 55%. Next day cardiac catheterization revealed normal coronary arteries. The blood results showed peak CPK 855 IU/L (normal range 21–232), CPK-MB 90 IU/L (normal range 0–6), troponin 21.35 (nomal range N0.05), eosinophils 7% (normal range 3–5). Cardiac magnetic resonance imaging, two weeks later, showed hypokinesis of the inferolateral wall and late gadolinium enhancement in the subepicardial corresponding area (Fig. 3, arrows) compatible with myocardial inflammation due to focal myocarditis. A second CMR study 6 months later showed complete resolution of the inflammation (Fig. 4). The described patient developed severe retrosternal pain following an allergic reaction to amoxicillin administration for acute bronchitis. Electrocardiography and blood tests, including cardiac enzymes and troponin, confirmed the diagnosis of an acute myocardial infarction of type I variant of Kounis syndrome [3–9]. This variant includes patients with normal coronary arteries without predisposing factors for coronary artery disease in whose the acute release of inflammatory mediators during the allergic reaction can induce either coronary artery spasm without increase of cardiac enzymes and troponins or coronary artery spasm progressing to acute myocardial infarction with raised cardiac enzymes and troponins. Initially, the patient was suspected to have suffered episodes of coronary artery spasm and was treated with sublingual nitroglycerin followed by nitroglycerin infusion. However, this does
235
Silent embolization of an Amplatzer atrial septal closure device into the main pulmonary artery: Pivotal role of routine postprocedural surveillance echocardiography Hamza Duygu ⁎, Zehra Ilke Akyildiz, Ugur Kocabas, Cem Nazli, Oktay Ergene Fellow of Cardiology, Ataturk Training and Research Hospital, Izmir, Turkey
a r t i c l e
i n f o
Article history: Received 28 August 2009 Accepted 10 September 2009 Available online 6 November 2009 Keywords: Atrial septal defect Amplatzer occluder Device embolization Main pulmonary artery
The transcatheter closure of secundum atrial septal defects (ASDs) has become a safe and established alternative to surgery, with high closure rates and rare complications [1]. Percutaneous closure of secundum ASD may be complicated by immediate or late device embolizations. We report an asymptomatic embolization of an Amplatzer atrial septal closure device into the main pulmonary artery detected by routine postinterventional transthoracic echocardiography 24 h after deployment. An 18-year-old male who was diagnosed with ASD was referred to our clinic for percutaneous device closure because of progressive exertional dyspnea. Transthoracic echocardiography revealed a secundum type ASD with left-to-right flow documented by color Doppler evaluation. There was a moderate increase in right ventricular dimension and the pulmonary artery systolic pressure was moderately elevated (45 mm Hg). Transesophageal echocardiography (TEE) demonstrated a 29 mm secundum ASD with adequate margins of the defect and sufficient distance to the atrioventricular valves for deployment of a percutaneous closure device (Fig. 1A). Upon this, the anatomy was deemed suitable for implantation of an ASD occluder device, and he was scheduled for cardiac catheterization and device closure. Cardiac catheterization confirmed the shunt at the atrial level and revealed a pulmonary-to-systemic flow ratio of 1.8. The balloon stretched diameter was 30 mm. A 32-mm Amplatzer septal occluder device (AGA Medical Corporation, Golden Valley, Minnesota) was deployed under general anesthesia with TEE guidance. The position was confirmed by back-and-forth manipulation of the device as well as by TEE and angiographic imaging. Once positioning was confirmed, the delivery cable was disconnected from the device and removed. The device was released and TEE demonstrated a good position of the device without residual shunting or impingement on intracardiac structures (Fig. 1B). The patient was extubated and returned to the care unit. Although the patient was asymptomatic, on the first day after the procedure, routine postinterventional transthoracic echocardiography showed that the device was not seen, and echocardiography and chest x-ray confirmed device embolization into main the pulmonary artery (Fig. 2). The device did not obstruct the main pulmonary artery because it was oriented in the longitudinal plane, parallel to the direction of blood flow. The patient remained hemo-
⁎ Corresponding author. Tel.: +90 232 2444444; fax: +90 232 2431530. E-mail address: [email protected] (H. Duygu).
dynamically stable. After intravenous heparin administration, it was decided to attempt a percutaneous retrieval of the device. However, transcatheter device retrieval with snares of different sizes and bioptomes failed due to the longitudinal orientation of the device in the pulmonary artery. Therefore, the patient was referred for surgical removal. After institution of cardiopulmonary bypass, a pulmonary arteriotomy was made and device was retrieved without difficulty (Fig. 3) and the ASD closed by primary sutures. The postoperative course was uncomplicated and the patient was discharged from the hospital on the 7th postoperative day. Device embolization is a potential complication of every attempted ASD device closure. Emergency surgical intervention may be required for complications, during or after implantation of the device. Although some authors have reported cases of late device embolization after the procedure [2–4], device embolizations generally appear to occur within the first hours after implantation [5]. In a recently published study by Majunke et al. [6], a total of 650 adult patients underwent transcatheter closure of an ASD using the Amplatzer septal occluder. In this study, six device embolizations occurred. In 2 patients (0.2%), the device embolized a few minutes after release and both patients underwent surgery. Four device embolizations occured (0.6%) within 30 days after the procedures. In 2 patients, the occluder embolized into the left ventricle; in 1 patient, into the pulmonary artery; and in 1 patient, an embolized occluder was found in the descending aorta. Two embolized devices were retrieved using a catheter technique, and 2 patients underwent surgery. Peuster et al. [7] reported a clinically asymptomatic secondary embolization of a 25 mm Helex occluder into the pulmonary artery 30 h after implantation into a centrally located secundum ASD with a stretched diameter of 13 mm in a 2-year-old patient. Transcatheter device retrieval with snares of different sizes, bioptomes, and retrieval forceps failed due to the mismatch of the diameter of the device and the small diameter of the pulmonary artery. Therefore, the device was retrieved surgically. In addition to this case, Kapoor et al. [8] described a case of device embolization into the main pulmonary artery ten minutes after release in their experience of 35 Amplatzer ASD device closures. The device was surgically removed because it was not possible to retrieve the embolized device by catheterization procedures as in our case. The selection of patients with favourable ASD morphology and the choice of appropriate device sizes are crucial to prevent embolization. There may be several factors that may help predict an increased risk for device embolization. The main causes of displacement are large defects, the inadequate defect rim to hold the device, undersized device diameters, and tears in the interatrial septum during balloon sizing or the first attempt to implant [9]. We cannot explain the exact reason for the embolization of the device. However, the ASD diameter was large and the device may have been undersized. Our patient did not develop symptoms after embolization because the position of device in the pulmonary artery was in the longitudinal axis and parallel to the direction of blood flow. The device crossed the tricuspid and pulmonic valves without any damage. This case reinforces the importance of routine postprocedural echocardiographic surveillance as a screen for device embolization even if the patients are asymptomatic. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [10].
236
Letters to the Editor
Fig. 1. Transesophageal images showing atrial septal defect before (A) and after (B) device implantation.
Fig. 2. Transthoracic echocardiography (A) and chest x-ray (B) show the Amplatzer occluder device in the main pulmonary artery (arrows).
Fig. 3. Intraoperative appearance of the Amplatzer device identified into the main pulmonary artery (arrow) and surgical specimen of the retrieved device.
References [1] Giardini A, Donti A, Specchia S, et al. Long-term impact of transcatheter atrial septal defect closure in adults on cardiac function and exercise capacity. Int J Cardiol 2008;124(2):179–82. [2] Mashman WE, King SB, Jacobs WC, et al. Two cases of late embolization of Amplatzer septal occluder devices to the pulmonary artery following closure of secundum atrial septal defects. Catheter Cardiovasc Interv 2005;65 (4):588–92.
[3] Lysitsas DN, Wrigley B, Banerjee P, et al. Presentation of an embolised Amplatzer septal occluder to the main pulmonary artery 2 years after implantation. Int J Cardiol 2009;131(3):e106–7. [4] Ussia GP, Abella R, Pome G, et al. Chronic embolization of an atrial septal occluder device: percutaneous or surgical retrieval? A case report. J Cardiovasc Med (Hagerstown) 2007;8(3):197–200. [5] Chessa M, Carminati M, Butera G, et al. Early and late complications associated with transcatheter occlusion of secundum atrial septal defects. J Am Coll Cardiol 2002;39:1061–5.
Letters to the Editor [6] Majunke N, Bialkowski J, Wilson N, et al. Closure of atrial septal defect with the Amplatzer septal occluder in adults. Am J Cardiol 2009;103(4):550–4. [7] Peuster M, Reckers J, Fink C. Secondary embolization of a Helex occluder implanted into a secundum atrial septal defect. Catheter Cardiovasc Interv 2003;59(1):77–82.
237
[8] Kapoor MC, Singh S, Sharma S, et al. Case 6—2003: embolization of an atrial septal occluder device. J Cardiothorac Vasc Anesth 2003;17(6):755–63. [9] Levi DS, Moore JW. Embolization and retrieval of the Amplatzer septal occluder. Catheter Cardiovasc Interv 2004;61(4):543–7. [10] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
0167-5273/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.09.532
The conundrum of hypersensitivity cardiac disease: Hypersensitivity myocarditis, acute hypersensitivity coronary syndrome (Kounis Syndrome) or both? G.C. Almpanis, A. Mazarakis, D.A. Dimopoulos, N.A. Tragotsalou, G.N. Kounis, N.G. Kounis ⁎, D. Alexopoulos Department of Cardiology, University of Patras Medical School, Patras, Greece
a r t i c l e
i n f o
Article history: Received 18 September 2009 Accepted 27 September 2009 Available online 4 November 2009 Keywords: Cardiac magnetic resonance Hypersensitivity myocarditis Kounis syndrome
Hypersensitivity is synonymous to allergy and denotes an excessive reaction associated with gross tissue changes after antigen–antibody (IgE or IgM) reaction. The cardiac tissue can be easily affected by hypersensitivity processes, while the myocardium and the coronary arteries are especially vulnerable as well. There are two clinical entities of hypersensitivity etiology, 1) Hypersensitivity coronary syndrome or Kounis syndrome [1], a concurrence of acute coronary syndrome with conditions associated with mast cell degranulation involving interrelated and interacting inflammatory cells and including hypersensitivity or allergic and anaphylactic or anaphylactoid insults and 2) Hypersensitivity myocarditis [2], an inflammatory disease affecting the myocardium and the cardiac conduction system manifesting as an allergic complication of drug therapy. The following unique report is of a patient who presented with clinical and laboratory findings suggesting of acute coronary hypersensitivity syndrome (Kounis syndrome) but who was proved, with cardiac magnetic resonance (CMR) imaging , at a later stage, to have myocardial changes compatible with hypersensitivity myocarditis. The clinical course, the laboratory and differentiating findings of these two relative entities are discussed. A 28 year-old male had an episode of acute bronchitis with temperature of 38 °C and his family physician prescribed amoxicillin 1gr b.i d. Six hours later the patient felt generalized itching accompanied by erythematous rash covering the whole body surface. He was given 500 mg of hydrocortisone sodium succinate intramuscularly followed by oral cetirizine 10 mg b.i.d. The following 24 h, rash and itching started to subside. However, he was feeling unwell and he was admitted to our hospital for further evaluation.
⁎ Corresponding author. E-mail address: [email protected] (N.G. Kounis).
On examination, he had not any significant past medical history and was not smoker. He did not give any history of atopy and did not have any previous hospitalizations. His family history was free of any cardiac or chest disease. One hour after admission he developed severe retrosternal pain radiating to the neck and elbows. He started sweating with difficulty in breathing. His blood pressure was 120/ 80 mm Hg, the pulse 69 beats/min regular and on auscultation there was neither pericardial rub nor murmurs. The electrocardiogram showed ST elevation of 3 mm in leads II, III, AVF, V7–V9 compatible with acute inferior myocardial infarction (Fig. 1). He was, immediately, given 5 mg of nitroglycerin sublingually and 325 mg of aspirin and was transferred to the coronary care unit. The above symptoms were persisting and infusion of nitroglycerin was started at a rate of 2 mcg/min. However, electrocardiographic changes and symptoms did not subside and he was thrombolysed with 40 mg of tenectaplase. Half an hour later the patient developed sinus bradycardia of 40 beats/min with dizziness and diaphoresis. With 0.5 mg of atropine iv bradycardia and symptoms subsided and the electrocardiographic changes reverted to normal (Fig. 2). Transthoracic echocardiography revealed hypokinesia and segmental akinesia involving the inferior wall with an estimated ejection fraction of 55%. Next day cardiac catheterization revealed normal coronary arteries. The blood results showed peak CPK 855 IU/L (normal range 21–232), CPK-MB 90 IU/L (normal range 0–6), troponin 21.35 (nomal range N0.05), eosinophils 7% (normal range 3–5). Cardiac magnetic resonance imaging, two weeks later, showed hypokinesis of the inferolateral wall and late gadolinium enhancement in the subepicardial corresponding area (Fig. 3, arrows) compatible with myocardial inflammation due to focal myocarditis. A second CMR study 6 months later showed complete resolution of the inflammation (Fig. 4). The described patient developed severe retrosternal pain following an allergic reaction to amoxicillin administration for acute bronchitis. Electrocardiography and blood tests, including cardiac enzymes and troponin, confirmed the diagnosis of an acute myocardial infarction of type I variant of Kounis syndrome [3–9]. This variant includes patients with normal coronary arteries without predisposing factors for coronary artery disease in whose the acute release of inflammatory mediators during the allergic reaction can induce either coronary artery spasm without increase of cardiac enzymes and troponins or coronary artery spasm progressing to acute myocardial infarction with raised cardiac enzymes and troponins. Initially, the patient was suspected to have suffered episodes of coronary artery spasm and was treated with sublingual nitroglycerin followed by nitroglycerin infusion. However, this does