<unk>  is often missed or underdiagnosed so understanding the disease process and clinical presentation while having a high suspicion for the problem is compulsory. It is important to focus on the duration of time between the trigger exposure and the onset of symptoms. Majority of the cases had a duration of under one hour while some had a duration of 6 hours. EKG, chest x-ray, echocardiography, and angiography are needed if suspicion for myocardial ischemia or infarction is present. Patients with systemic allergic reactions associated with clinical, electrocardiographic, angiographic, echocardiographic and laboratory findings of acute myocardial ischemia should be diagnosed as having<unk> . EKG changes can be consistent with infarction most commonly in the inferior leads, ischemia, sinus bradycardia or tachycardia, heart block, atrial fibrillation, ventricular fibrillation, ventricular ectopic beats, QRS and QT prolongation, and findings similar to digoxin toxicity. Echocardiography assists with finding atherosclerotic stenosis and thrombosis. Serum tryptase, histamine, immunoglobulins (IgE), cardiac enzymes, cardiac troponins are helpful to confirm the diagnosis. In<unk> , the newer techniques such as thallium-201 single-photon emission computer tomography (SPECT) and 125I-15-(p-iodophenyl)-3-(R,S) methylpentadecanoic acid (BMIPP) SPECT have revealed severe myocardial ischemia while coronary angiography showed normal coronary arteries. Furthermore, with cardiac magnetic resonance imaging (MRI), the delayed contrast-enhanced images show normal washout in the subendocardial lesion area in patients with<unk>  type I variant. Other similar presentations to rule out include Takotsubo and hypersensitivity myocarditis. Classification Three variants of<unk>  are recognised: * Type I is also known as allergic vasospastic angina due to endothelial dysfunction. It occurs in people without underlying coronary artery disease or predisposing factors who have allergic ACS secondary to coronary artery spasm. Inflammatory mediators during an allergic reaction can cause arterial spasms with normal troponins. However, this may lead to myocardial infarction which will elevate troponins. MINOCA, which stands for myocardial infarction with non-obstructive coronary arteries is new clinical presentation that includes endothelial dysfunction and can be caused by this type I variant. * Type II occurs in people with underlying asymptomatic coronary artery disease where an allergic reaction leads to either coronary artery spasm or plaque erosion. A myocardial infarction can also be seen here, in which case troponins would be elevated. * Type III occurs in the setting of coronary thrombosis (including stent thrombosis) where aspirated thrombus stained with hematoxylin-eosin and Giemsa demonstrate the presence of eosinophils and mast cells respectively. It also includes those with people who have died suddenly after previous coronary stent insertion, where evidence of an allergic reaction to the stent is found on post-mortem examination. Type III is subdivided now to stent thrombosis (subtype a) and stent restenosis (subtype b).
Kounis syndrome
Kufor–Rakeb syndrome
Zunich–Kaye syndrome
STAR syndrome
Simpson–Golabi–Behmel syndrome
RAPADILINO syndrome
Qazi–Markouizos syndrome
Malouf syndrome