|Year : 2016 | Volume
| Issue : 3 | Page : 114-117
Type I kounis syndrome: A rare st elevation myocardial infarction with normal coronary arteries after honeybee sting
Sanjay Arun Mundhe, Sidheshwar V Birajdar, Sanjay S Chavan, Ashish K Jain
Department of General Medicine, S. R. T. R. Government Medical College, Ambajogai, Maharashtra, India
|Date of Web Publication||16-Sep-2016|
Sanjay Arun Mundhe
Department of General Medicine, S. R. T. R. Government Medical College, Ambajogai - 431 517, Maharashtra
Source of Support: None, Conflict of Interest: None
The Kounis syndrome is described as an acute coronary syndrome after hymenoptera stings or exposure to environmental toxins or drugs. Bee sting may cause hypersensitivity reaction ranging from simple allergic reaction to life-threatening anaphylactic reaction, sometimes leading to death. Although rare, cardiac involvement is a possible complication, varying from vasospasm to acute ST-elevation myocardial infarction (MI). We report a case of honeybee (Apis cerana indica) sting causing Kounis syndrome. A 36-year-old female, beekeeper in a farm with known allergy to bee venom without any significant cardiovascular risk factors and history had stung by a honeybee on the neck. She presented with features of anaphylaxis and acute inferior wall MI, which was transient and responded to therapy of anaphylaxis. Angiography revealed normal coronaries and patient responded to the standard treatment of anaphylaxis.
Keywords: Allergic myocardial infarction, Anaphylaxis, Honeybee sting, Hymenoptera, Ischemic heart disease, Kounis syndrome
|How to cite this article:|
Mundhe SA, Birajdar SV, Chavan SS, Jain AK. Type I kounis syndrome: A rare st elevation myocardial infarction with normal coronary arteries after honeybee sting. Heart India 2016;4:114-7
|How to cite this URL:|
Mundhe SA, Birajdar SV, Chavan SS, Jain AK. Type I kounis syndrome: A rare st elevation myocardial infarction with normal coronary arteries after honeybee sting. Heart India [serial online] 2016 [cited 2021 Dec 2];4:114-7. Available from: https://www.heartindia.net/text.asp?2016/4/3/114/190755
| Introduction|| |
Kounis syndrome is characterized by symptoms that range from vasospastic angina to ST elevation myocardial infarction (MI) that occurs as hypersensitivity reaction after allergen exposure.  Several drugs (nonsteroidal anti-inflammatory drugs, antibiotics, and antineoplastic agents); bee and wasp stings (hymenoptera venom) have been implicated as causes for Kounis syndrome.  The hymenoptera including honeybees and stinging hornets are widely distributed in India, especially in the rural area and their stinging is a common environmental hazard.  The acute MI (AMI) due to honeybee sting is relatively rare and only a few authors have discussed the relationship between the sting, anaphylactic shock, and MI. ,,
| Case report|| |
A 36-year-old female working as beekeeper in a farm with known allergy to bee venom and without any cardiovascular risk factors presented to our hospital with a history of bee sting over neck while handling honey. After few minutes of sting, she started having itching, feeling of being unwell, lightheadedness and strange feeling followed by sweating, dyspnea, and epigastric discomfort. On admission after 20 min, she had profuse sweating, urticaria, angioedema, local swelling with sting, bradycardia (pulse 48/min), and hypotension (blood pressure [BP] 70/40 mmHg) with lethargy. She was tachypneic and had bilateral polyphonic rhonchi. Twelve-lead electrocardiogram (ECG) showed ST segments elevations in inferior leads with sinus bradycardia [Figure 1]. Her peripheral oxygen saturation was 90% and random blood sugar was 114 mg/dl. Anaphylactic shock was the diagnosis and 0.5 ml (1:1000) adrenalin deep IM in the thigh, atropine 0.6 mg intravenous (IV), hydrocortisone 200 mg IV, and chlorpheniramine 10 mg IV with oxygen, IV fluids, and nebulization of albuterol (2.5 ml of 0.5%) were given immediately. Sting was removed with the help of card. The patient received loading doses of antiplatelets drugs with statin considering an acute coronary syndrome. Over next 10 min, she felt better and BP improved to 110/70 mmHg with a clear chest with auscultation and repeat serial ECG was normal [Figure 2]. Thrombolytic therapy was planned initially considering AMI but was withheld after normal repeat ECG with absent cardiac symptoms. The patient underwent coronary angiography which showed no significant abnormality in coronaries [Figure 3] and echocardiography revealed no wall motion abnormality or any structural defect with preserved ejection fraction done after 8-10 h [Figure 4]. Her investigations showed a normal troponin T at baseline that rose after 8 h. The patient was asymptomatic thereafter and received oral prednisolone in tapering doses and oral cetirizine 10 mg/day for next 7 days and antiplatelets and statins were stopped after normal coronary angiography report and normal serum lipid levels. She was discharged after 3 days with advice to change the job and planned for venom immunotherapy. The patient followed up in outpatient department after a week and was asymptomatic.
|Figure 1: Electrocardiogram on admission showing ST segment elevation in inferior leads with sinus bradycardia constituent with acute inferior wall myocardial infarction|
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|Figure 2: Repeat electrocardiogram showing resolution of ST segment elevation without any other significant changes|
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|Figure 4: Two-dimensional echocardiography apical view showing no wall regional motion abnormality|
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| Discussion|| |
The term "venomous animals" is applied to creatures producing poisons in secretory glands and delivering it during biting or stinging act. Arthropods, such as spiders, scorpions, and hymenoptera (bees, wasps), are found worldwide and some of them are venomous animals. Acute coronary syndrome after hymenoptera stings and other environment exposures is referred as Kounis syndrome. ,,,, The pathophysiology of Kounis syndrome is considered to be due to activation of mast cells induced by allergic or hypersensitivity reactions releasing serotonin; histamine and formation of leukotrienes, some of which are potent coronary vasoconstrictors. , These substances can provoke myocardial ischemia either through profound hypotension or by increasing myocardial oxygen demand through direct ionotropic or chronotropic effect in the presence of compromised myocardial blood supply due to vasospasm. There are three variants of Kounis syndrome.  Type I variant includes patients with normal coronaries without predisposing factors for coronary artery disease, in which acute allergic insult induces either coronary artery spasm with normal cardiac enzymes or coronary artery spasm progressing to AMI with raised cardiac enzymes. This variant might represent a manifestation of endothelial dysfunction. Type II variant has quiescent preexisting atheromatous disease in whom acute allergic episode induces plaque erosion or rupture manifesting as AMI.  Type I variant has a better prognosis than Type II variant. However, in both types, prognosis depends on the magnitude of initial allergic response, patient's sensitivity, comorbidity, allergen concentration, and route of allergen entrance.  Type III variant is described as a coincidence of hypersensitivity reactions following implantation of drug-eluting stents, causing stent thrombosis.  Our patient had no cardiovascular risk factors and had nonsignificant angiographic findings suggesting Type I Kounis syndrome. The treatment of Kounis syndrome consists of acute coronary syndrome management and suppression of allergic reaction.  Our patient with known bee venom allergy presented with bee sting and features of anaphylaxis. Her ECG suggested cardiac involvement in the form of acute inferior wall MI. She was managed with the standard treatment of anaphylaxis and received only loading doses of antiplatelets and statins. Her ECG changes of AMI reverted within 5-10 min. With regards to therapeutic approach of coronary spasms following allergic reaction, medications should include vasodilators, such as nitrates, beta blockers, and calcium channel inhibitors which are the treatment of choice in every case of coronary spasm. There are case reports of Kounis syndrome occurring secondary to hymenoptera stings and having structural coronary artery lesions and were managed with percutaneous coronary intervention and other standard treatment of AMI. ,, However, our patient did not receive any of vasodilators due to hypotension and bradycardia or thrombolytic therapy for MI and recovered with treatment of anaphylaxis suggesting role of these medications in the treatment of Kounis syndrome.
| Conclusion|| |
Although allergic reactions to bee stings are common, recognition of Kounis syndrome in bee sting is important to provide appropriate treatments. Despite increasing number of cases, exact pathophysiology and treatment guidelines of Kounis syndrome remain unanswered. Kounis syndrome should be considered in differential diagnosis while diagnosing patients with no cardiovascular risk factors who experience acute coronary syndrome and report bee sting accompanied by symptoms of anaphylaxis. In future, further studies are needed to understand the mechanisms of allergy causing acute coronary syndromes as this will pave the way to effective therapeutic interventions.
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There are no conflicts of interest.
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