Anaphylactic cardiovascular collapse and Kounis syndrome: systemic vasodilation or coronary vasoconstriction?

Abstract

The first reported human anaphylactic death is considered to be the Pharaoh Menes death, caused by a wasp sting. Currently, anaphylactic cardiovascular events represent one of most frequent medical emergencies. Rapid diagnosis, prompt and appropriate treatment can be life saving. The main concept beyond anaphylaxis lies to myocardial damage and ventricular dysfunction, thus resulting in cardiovascular collapse. Cardiac output depression due to coronary hypoperfusion from systemic vasodilation, leakage of plasma and volume loss due to increased vascular permeability, as well as reduced venous return, are regarded as the main causes of cardiovascular collapse. Clinical reports and experiments indicate that the human heart, in general, and the coronary arteries, in particular, could be the primary target of the released anaphylactic mediators. Coronary vasoconstriction and thrombosis induced by the released mediators namely histamine, chymase, tryptase, cathepsin D, leukotrienes, thromboxane and platelet activating factor (PAF) can result to further myocardial damage and anaphylaxis associated acute coronary syndrome, the socalled Kounis syndrome. Kounis syndrome with increase of cardiac troponin and other cardiac biomarkers, can progress to heart failure and cardiovascular collapse. In experimental anaphylaxis, cardiac reactions caused by the intracardiac histamine and release of other anaphylactic mediators are followed by secondary cardiovascular reactions, such as cardiac arrhythmias, atrioventricular block, acute myocardial ischemia, decrease in coronary blood flow and cardiac output, cerebral blood flow, left ventricular developed pressure (LVdp/dtmax) as well as increase in portal venous and coronary vascular resistance denoting vascular spasm. Clinically, some patients with anaphylactic myocardial infarction respond satisfactorily to appropriate interventional and medical therapy, while anti-allergic treatment with antihistamines, corticosteroids and fluid replacement might be ineffective. Therefore, differentiating the decrease of cardiac output due to myocardial tissue hypoperfusion from systemic vasodilation and leakage of plasma, from myocardial tissue due to coronary vasoconstriction and thrombosis might be challenging during anaphylactic cardiac collapse. Combined antiallergic, anti-ischemic and antithrombotic treatment seems currently beneficial. Simultaneous measurements of peripheral arterial resistance and coronary blood flow with newer diagnostic techniques including cardiac magnetic resonance imaging (MRI) and myocardial scintigraphy may help elucidating the pathophysiology of anaphylactic cardiovascular collapse, thus rendering treatment more rapid and effective.

Sugammadex-induced atropine-resistant bradycardia: clinical, pathophysiologic, and electrocardiographic considerations

“…The bradycardia and hypotension following sugammadex could have been attributed to reduced cardiac output from leakage of plasma and volume loss. Volume loss reduces venous return and hampers or delays the release of mediators for reaching the skin areas and thus none applying their action [10].…”

Immunological Mechanisms Explaining the Role of Vaccines, IgE, Mast Cells, Histamine, Elevating Ferritin, IL-6, D-dimer, VEGF Levels in COVID-19 and Dengue, Potential Treatments Such as Mast Cell Stabilizers, Antihistamines: Predictions and Confirmations

“…Kounis syndrome is cardiac injury due to an allergic reaction (Kounis et al 2018). Cardiac injury is reported in COVID-19 (Lala et al 2020) and secondary dengue infections (Macedo 2018).…”

“Too Many Cooks Spoil the Broth”: The More Antigens Present, the Easier, the Quicker, and the More Severe the Anaphylaxis

“…The patient reported developed severe anaphylaxis without skin manifestations that could have rendered the diagnosis of anaphylaxis difficult [9]. However, there are reports of severe anaphylaxis without skin involvement, and this has been attributed to shock due to reduced cardiac output from leakage of plasma and volume loss that reduces venous return and prevents or delays the released anaphylactic mediators from reaching and acting on the skin, thus inducing redness, rash, and/ or itching [10]. Physicians should always remember that drugs used with minimally invasive techniques, such as skin prick tests, could join forces with multiple concurrent medications and induce atypical but severe anaphylactic reactions with cardiovascular collapse.…”