In a very important paper published in this journal [1], twopatients suffering from severe anaphylaxis developedelectrocardiographic ST segment elevation associated withprominent cardiovascular symptoms. The first patient’surticaria was accompanied by chest pain, tachycardia andhypotension, and skin prick tests were positive for beef,pork and milk. The second patient’s urticaria was devel-oped intra-operatively, and was accompanied by hypoten-sion culminating in ventricular tachycardia and ventricularfibrillation necessitating cardiac defibrillation. This patienthad received propofol, sevoflurane, fentanyl, atracariumand epinephrine and had positive skin prick tests to atra-carium and latex.All the above symptoms are characteristic for type Ivariant of Kounis syndrome for the first patient, and type IIvariant of Kounis syndrome for the second patient. Kounissyndrome is defined [2] as the concurrence of acute coro-nary syndromes with conditions associated with mast celldegranulation and other interacting and interrelatedinflammatory cells such as T lymphocytes and macro-phages. It is caused by inflammatory mediators such ashistamine, neutral proteases, arachidonic acid products,platelet-activating factor, and a variety of cytokines andchemokines released during the activation process. It seemspossible that the first patient suffered a type I variant ofKounis syndrome, which is seen in patients with normal ornearly normal coronary arteries without predisposing fac-tors for coronary artery disease, in whom the acute releaseof inflammatory mediators can induce either coronaryartery spasm with normal cardiac enzymes and troponins,or coronary artery spasm progressing to acute myocardialinfarction with raised cardiac enzymes and troponins.On the other hand, type II variant of Kounis syndromeincludes patients with culprit but quiescent preexisting ath-eromatous disease, in whom acute release of inflammatorymediators can induce either coronary artery spasm alone, orplaque erosion or rupture manifesting as acute myocardialinfarction with its consequences. A type III variant of Kounissyndrome has been described recently in patients with coro-nary artery stent thrombosis in whom aspirated thrombusspecimens stained with hematoxylin–eosin and Giemsa arefound infiltrated by eosinophils and mast cells, respectively.The second patient had positive skin prick tests in latexand atracarium but the other drugs he received duringanesthesia such as propofol, fentanyl and sevoflurane couldalso contribute to the allergic cascade. Therefore, thispatient was under the risk of five agents which were able toact directly or via IgE mechanism to degranulate mastcells. It is known that mast cell surface bears 500,000 to 1million IgE molecules and degranulation occurs when2,000 of these molecules, which is a critical number, make1,000 bridges with antigens. These bridges can be madewith antigens of different specificities as it happens inpatients during anesthesia [2]. It looks likely that the moreantigens an anesthetized patient is exposed to, the easierand quicker the degranulation occurs.It is generally believed, that myocardial involvementduring severe anaphylactic reactions is the result of sys-temic vasodilatation, reduced venous return, leakage ofplasma and volume loss due to increased vascular perme-ability that ensue leading to depression of the cardiacoutput, and contribute to coronary hypoperfusion withsubsequent myocardial damage.However, experimental and clinical studies have shownthat human heart is the primary site and the target of
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Oct 1, 2024
Takayuki Ishihara + 12
Open Access