Can a Bee Sting Really Trigger a Heart Attack? Decoding Kounis Syndrome

Introduction – When Allergy Meets the Coronary Arteries

Most people associate insect stings with hives or throat tightness, yet the same burst of allergy chemicals can also clamp down the coronary arteries or rupture an existing plaque. This under-recognized emergency—Kounis syndrome—mimics or precipitates a classic myocardial infarction but is driven by mast-cell mediators rather than atherosclerosis alone. Clinicians who overlook the allergic component risk missing the real culprit and delaying lifesaving therapy.

What Is Kounis Syndrome?

Kounis syndrome describes acute coronary events triggered by an allergic or hypersensitivity reaction. Researchers classify three clinical variants:

• Type I – Coronary spasm of angiographically normal vessels.
• Type II – Plaque erosion or rupture in patients with silent coronary disease.
• Type III – Thrombosis of a recently implanted coronary stent. ^[1]

Mast-cell degranulation releases histamine, tryptase, platelet-activating factor, leukotrienes, and proteases. These substances constrict coronary smooth muscle, boost heart-rate and oxygen demand, activate platelets, and erode plaque caps—all within minutes of allergen exposure. ^{[1, 2]}

Pathophysiology – From Venom to Vasospasm

• Phospholipase A2 and melittin in bee venom directly trigger mast-cell activation and complement pathways. ^[2]
• Histamine acting on H1 and H2 receptors causes intense vasoconstriction while increasing inotropy and chronotropy, further stressing the myocardium. ^[3]
• Tryptase and chymase weaken the fibrous cap of atherosclerotic plaque, encouraging rupture [4].
• Platelet-activating factor and thromboxane-A2 amplify in-situ thrombosis, explaining sudden transitions from spasm to complete vessel occlusion. ^[4]

How Common Is It—and What Sets It Off?

Kounis syndrome remains under-diagnosed, but systematic reviews estimate it accounts for 1 – 3 percent of patients hospitalised with anaphylaxis and up to 2 percent of those presenting with acute coronary syndrome accompanied by allergic features. ^{[5, 6]}

Major triggers

• Hymenoptera venom (bees, wasps, fire ants).
• Medications such as non-steroidal anti-inflammatory drugs, antibiotics, muscle relaxants, and iodinated contrast dye. ^{[3, 7]}
• Foods (peanuts, shellfish, sesame) and food additives (sulfites).
• Environmental proteins, including latex and cold stimuli.

Middle-aged men with unrecognised coronary disease dominate case series, although cases range from children to nonagenarians. ^[6]

Clinical Clues that Differentiate It from Typical Myocardial Infarction

Key diagnostic pointers

• Serum tryptase above 11.4 µg L⁻¹ in the first one-to-two hours strongly supports mast-cell activation.^[3]
• Electrocardiograms may display transient ST-segment elevation in inferior or anterior leads, resolving with nitrates or calcium-channel blockers. ^[2]
• Sudden hemodynamic collapse resistant to standard advanced cardiac life support should prompt a search for an allergic trigger and immediate intramuscular epinephrine.

Management Dilemmas – Epinephrine vs. Vasospasm

The cornerstone of anaphylaxis treatment is intramuscular epinephrine 0.5 mg. Delaying this medication to avoid vasospasm greatly increases mortality. However, epinephrine’s alpha-adrenergic effects can exacerbate coronary constriction, especially in patients taking non-selective beta-blockers. Evidence-based expert panels therefore recommend: ^{[3, 4]}

• Give epinephrine first—the survival benefit outweighs vasospastic risk.
• If hypotension or bronchospasm persists in a beta-blocked patient, administer intravenous glucagon 1 – 2 mg over five minutes; glucagon bypasses beta-adrenergic receptors and improves cardiac output. ^[4]
• Initiate dual histamine blockade (an H1 antihistamine plus an H2 antihistamine) and intravenous corticosteroid once epinephrine is given.
• For the coronary component, use nitrates or calcium-channel blockers to relieve spasm. Avoid beta-blockers during the acute episode.
• Activate the catheterisation laboratory if plaque rupture or stent thrombosis is suspected.

Post-crisis, every patient should receive an allergology work-up. Venom immunotherapy lowers the chance of another severe reaction by up to 98 percent and is recommended after any systemic sting reaction. ^[7]

Prevention Tips for At-Risk Patients

• Carry two epinephrine auto-injectors, not one. A second dose is required in up to 20 percent of severe reactions.
• Seek evaluation for venom immunotherapy if you have had systemic symptoms to insect stings.
• Review chronic medications: non-selective beta-blockers and angiotensin-converting-enzyme inhibitors may worsen anaphylaxis outcomes.
• Outdoor event organisers should stock auto-injectors and train staff in rapid recognition and use.

A Real-World Reminder

On 12 June 2025, Indian businessman Sunjay Kapur collapsed during a polo match in England after reportedly swallowing a bee. Bystanders described immediate respiratory distress followed by cardiac arrest. Media outlets later suggested that Kounis syndrome precipitated the fatal event. ^[9] His death highlights the lethal, time-sensitive junction of allergy and cardiology and underscores why prompt epinephrine and accurate diagnosis matter on sports fields, in rural clinics, and in every emergency department worldwide.

Key Take-Aways

• A single bee sting can ignite an allergic storm that strangles the coronary arteries or ruptures plaque—Kounis syndrome is real and often fatal if missed.
• Look for the triad of recent allergen exposure, skin or airway symptoms, and chest pain.
• Treat the allergy first with intramuscular epinephrine, then tackle the coronary problem with nitrates or calcium-channel blockers—reserve beta-blockers until the allergic phase is over.
• Long-term prevention hinges on venom immunotherapy, medication review, and universal access to epinephrine auto-injectors.

References:

Also Read:

• Sweat Bee Sting: Signs, Symptoms and Treatment
  
• 10 Bug Bites You Should Know
• Does Scratching Mosquito Bites Make Them Worse?