We almost overlooked the cause of the infarction

Description
A 59 year old patient presented with a severe anaphylactic reaction. CPR was mandated because of ventricular tachycardia. Coronary angiography revealed a subtotal thrombotic occlusion of the LAD.  Diagnostic work up for cardiac thromboembolism was performed but no clear competing cause could be diagnosed, therefore allergic myocardial infarction (Kounis Syndrome) was diagnosed.

Patient presentation
A 59 year old patient presented with a generalized exanthema after intake of metamizole due to a headache. He complained of no respiratory symptoms, no nausea, no vomiting, but became increasingly unstable, hypotensive and tachycardic with a heart rate of 112 beats per minute, blood pressure of 95/60 mmHg,  respiratory rate of 18 breaths per minute. Oxygen saturation was 90% on ambient air. Cardiac auscultation revealed rhythmic and normal heart sounds. Medication at the time of admission was ramipril 2,5 mg.

Initial work up
Initial laboratory data revealed elevated levels of high-sensitivity cardiac troponin-T (687 pg/ml; normal: <14 pg/mL). An electrocardiogram revealed a sinus tachycardia, normal QRS axis (Img. 1,2). There was no ST-segment deviation and no QT-prolongation.
Monitoring showed a hemodynamically relevant polymorphic ventricular tachycardia (Img. 3,4). With the onset of unconsciousness, CPR was immediately initiated and successful defibrillation performed. Urgent CAG revealed a coronary 1-vessel disease with subtotal thrombotic occlusion of the proximal LAD with a high thrombus burden (Img.5). Successful direct stenting of the LAD was performed. As was already shown in a CAG two years before,  there was hardly any sclerosis of the coronary arteries.

Diagnosis and Management
Cardiac-MRI described ischemic changes consistent with anterior wall infarction. There were no indications of myocarditis or cardiomyopathies. To exclude an intracardiac source of coronary embolism, we performed transesophageal echocardiography, which showed no abnormalities.
We supplemented dual platelet inhibition and a statin. Metoprolol was added for prophylaxis of arrhythmia. Echocardiography showed a good left ventricular systolic function with no evidence of wall motion abnormalities.
No inflammation or neoplasia was found that could have caused a hypercoagulable state.

Follow-up
The patient was stable during the remainder of his hospitalization and no further complaints or arrhythmias occurred. He was discharged on day 8.
We strongly discouraged the use of metamizole. We recommended presentation in a coagulation outpatient clinic and modulation of cardiovascular risk factors, including cessation of nicotine consumption.

Conclusion
Kounis syndrome is defined as acute coronary syndrome in the setting of an anaphylactic reaction. Although mostly described as vasospastic Angina in patients with normal coronary arteries (Kounis Syndrome Type I), coronary vasospasm may lead to plaque rupture causing myocardial infarction (Kounis syndrome Type 2). Acute stent thrombosis in the presence of eosinophils and mast cells is described as Kounis syndrome type 3.
Kounis Syndrome might be more common than previously anticipated, although it is likely underdiagnosed. The role of inflammation in ACS is only partly elucidated, especially in context of the mechanism of plaque rupture in non stenotic plaques.