Kounis Nicholas G, Cervellin Gianfranco, Koniari Ioanna, Bonfanti Laura, Dousdampanis Periklis, Charokopos Nikolaos, Assimakopoulos Stelios F, Kakkos Stavros K, Ntouvas Ioannis G, Soufras George D, Tsolakis Ioannis
Department of Cardiology University of Patras Medical School, Rion, Patras, Achaia, Greece.
Emergency Department, Academic Hospital of Parma, Parma, Italy.
Ann Transl Med. 2018 Sep;6(17):332. doi: 10.21037/atm.2018.09.05.
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 so-called 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.
首次有报道的人类过敏性死亡被认为是法老美尼斯的死亡，死因是黄蜂蜇伤。目前，过敏性心血管事件是最常见的医疗紧急情况之一。快速诊断、及时且恰当的治疗可挽救生命。过敏反应背后的主要概念在于心肌损伤和心室功能障碍，进而导致心血管衰竭。全身血管舒张引起的冠状动脉灌注不足导致的心输出量降低、血浆渗漏和血管通透性增加导致的容量丢失，以及静脉回流减少，被视为心血管衰竭的主要原因。临床报告和实验表明，一般而言，人类心脏，尤其是冠状动脉，可能是释放的过敏介质的主要靶标。由组胺、糜酶、类胰蛋白酶、组织蛋白酶D、白三烯、血栓素和血小板活化因子（PAF）等释放的介质诱导的冠状动脉收缩和血栓形成可导致进一步的心肌损伤以及与过敏反应相关的急性冠状动脉综合征，即所谓的库尼斯综合征。伴有心肌肌钙蛋白和其他心脏生物标志物升高的库尼斯综合征可进展为心力衰竭和心血管衰竭。在实验性过敏反应中，心内组胺和其他过敏介质释放引起的心脏反应之后会出现继发性心血管反应，如心律失常、房室传导阻滞、急性心肌缺血、冠状动脉血流量和心输出量降低、脑血流量、左心室压力上升速率（LVdp/dtmax）降低，以及门静脉和冠状动脉血管阻力增加，表明血管痉挛。临床上，一些过敏性心肌梗死患者对适当的介入治疗和药物治疗反应良好，而使用抗组胺药、皮质类固醇和补液进行抗过敏治疗可能无效。因此，在过敏性心脏衰竭期间，区分由于全身血管舒张和血浆渗漏导致的心肌组织灌注不足引起的心输出量降低与由于冠状动脉收缩和血栓形成导致的心肌组织灌注不足可能具有挑战性。联合抗过敏、抗缺血和抗血栓治疗目前似乎有益。使用包括心脏磁共振成像（MRI）和心肌闪烁显像在内的更新诊断技术同时测量外周动脉阻力和冠状动脉血流量，可能有助于阐明过敏性心血管衰竭的病理生理学，从而使治疗更加迅速有效。
