Allergic angina following wasp sting: Kounis syndrome

Abstract

Kounis syndrome is defined as an acute coronary syndrome triggered by the release of inflammatory mediators following an allergic insult characterized by acute onset of breathlessness, palpitations, diaphoresis and chest tightness (Gázquez V, Dalmau G, Gaig P, Gómez C, Navarro S, Mercé J. Kounis syndrome: report of 5 cases. J Investig Allergol Clin Immunol 2010;20:162–5). We report a 20-year-male patient who presented with acute myocardial infarction following a wasp sting at our institute. ECG showed non-ST-elevation myocardial infarction. Symptoms settled with hydrocortisone and adrenaline. Coronary angiogram revealed normal epicardial coronaries.

INTRODUCTION

Myocardial infarction secondary to anaphylaxis is known as Kounis syndrome. Varied etiology has been described in the literature. Physicians should be aware of this entity since thrombolysis and percutaneous coronary intervention can be avoided in such situations. Serious allergic reactions may be the cause of acute coronary syndrome in patients with healthy or altered coronary arteries and no cardiovascular risk factors.

CASE REPORT

A 20-year-old man with no cardiovascular risk factors sustained a wasp sting over his left forearm. Fifteen minutes later, he experienced sudden shortness of breath, feeling of instability, palpitations, chest tightness and excessive sweating. On admission at our institute, patient was hypotensive (80/60 mmHg) with an arterial oxygen saturation of 85%. He was given 1 mg of subcutaneous adrenaline (1 : 1000) and 100 mg of intravenous hydrocortisone. The electrocardiogram revealed T-inversion in leads I, aVL, II, aVF and V1–V6 (Fig. 1). Echocardiogram showed anterior wall hypokinesia with an LVEF of 40%. Troponin T at admission was elevated (1.1 ng/ml; ref. range <0.01 ng/ml). Following administration of adrenaline and corticosteroids, the patient became hemodynamically stable. Coronary angiogram (Fig. 2) after 8 h revealed normal epicardial coronaries. After 18 hours of admission abnormalities reverted to normal (Fig. 3) and the ejection fraction improved to 55% with no regional wall motion abnormality of anterior wall.

Figure 1:

ECG at admission showing deep T-inversion in anterior leads.

Figure 2:

Coronary angiogram showing normal epicardial coronaries.

Figure 3:

ECG after 18 hours showing almost normalization of T-inversions.

DISCUSSION

Kounis syndrome or allergic was first described in 1991 by Kounis and Zafras [1] as ‘the coincidental occurrence of chest pain and allergic reactions accompanied by clinical and laboratory findings of classic angina pectoris caused by inflammatory mediators released during the allergic insult’. They called the progression from chest pain to acute myocardial infarction ‘allergic myocardial infarction’ [2, 3]. This occurs during episodes of anaphylaxis [4], and frequently in patients with prior coronary disease, although it has also been observed in patients with healthy coronary vessels. The main mechanism implicated is vasospasm of the coronary arteries [5].

Three variants of syndrome have been described:

1. Type I variant—This applies to patients with normal or nearly normal coronary arteries without predisposing factors for coronary artery disease, and the acute mediator release can induce either coronary artery spasm [6] or coronary artery spasm progressing to acute myocardial infarction.

2. Type II variant—This applies to patients with culprit, quiescent pre-existing atheromatous disease, and the mediator release can induce either coronary artery spasm or coronary artery spasm together with plaque erosion or rupture manifesting as acute myocardial infarction.

3. Type III variant is seen in patients with stent thrombosis in whom thrombus harvested and stained with hematoxylin–eosin and Giemsa that show eosinophils and mast cells, respectively. Type III variant is diagnosed in patients with stent implantation who died suddenly and histological examination of coronary intima, media or adventitia adjacent to the stent is infiltrated by eosinophils and/or mast cells.

Following an allergic insult, arachidonic acid cascade is activated; histamine is released leading onto a series of functional and metabolic changes in the heart, termed as cardiac anaphylaxis [7, 8]. Authors have also described the role of renin released during anaphylaxis in causing cardiac dysfunction [9]. Mueller [10] has reported the role of adrenaline in causing Kounis syndrome. Elevated serum tryptase will aid in differentiating Kounis syndrome from routine forms of acute coronary syndrome, provided that the blood sample is drawn between the first and second hour after onset of symptoms.

CONCLUSIONS

Kounis syndrome is not a rare disease but an infrequently diagnosed condition.

It should be borne in mind when diagnosing patients with no cardiovascular risk factors who experience acute coronary syndrome accompanied by symptoms of anaphylaxis.

CONFLICT OF INTEREST STATEMENT

None declared.