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Described in 1991 by Kounis and Zavras as an allergic angina syndrome that could lead to myocardial infarction secondary to an allergic reaction to penicillin.
Later, several causes were identified: other antibiotics, metamizole, Non-steroidal anti-inflammatory drugs, corticosteroids, general anesthetics, radiological contrast agents, proton pump inhibitors, thrombolytics, anticoagulants, food, hymenoptera stings, mastocytosis, stents intracoronary active drug, etc.
In short, Kounis syndrome It is an acute coronary syndrome (ACS) that includes: coronary spasm, acute myocardial infarction and/or stent thrombosis, associated with the activation of mast cells and platelets in anaphylactic or anaphylactoid episodes.
Mast cell degranulation with the release of multiple vasoactive mediators into the systemic circulation. For example, histamine and leukotrienes, potent coronary vasoconstrictors, and tryptase and chymase, which induce erosion or rupture of the atheromatous plaque, constitute the pathophysiological mechanism involved in the coronary event.
Classification
- Type I (majority 72%) without prior coronary disease: it is due to a coronary spasm that produces electrocardiographic changes secondary to ischemia, cardiac enzymes may be normal or reflect progression to an acute myocardial infarction.
- Type II with previous coronary artery disease: erosion or rupture of the atheromatous plaque, causing an acute myocardial infarction.
- Type III patients with thrombosis of the stents drug-active.
The diagnosis is primarily clinical and based on suspicion. An acute allergic reaction associated with acute coronary syndrome should raise suspicion of a Kounis syndrome (KS).
Diagnostic tests
– Electrocardiogram and determination of cardiac enzymes: ST segment elevation, although it may be normal or nonspecific; elevation of cardiac enzymes, which may also be normal,
- Determination of plasma tryptase or histamine. Elevated serum tryptase is a marker of mast cell activity and when elevated supports the diagnosis of hypersensitivity reaction. It is the most useful test for diagnostic support. Histamine only has a half-life of 60 minutes, with a maximum peak at 5-10 minutes after the start of the reaction. Tryptase reaches its maximum peak at 90 minutes after the start of the reaction and remains elevated in the blood for between 6 and 9 hours.
Treatment
The treatment of this condition is complex. Drugs used to treat allergic reactions can worsen cardiac symptoms (adrenaline, the drug of choice for anaphylaxis, can cause cardiac arrhythmias, vasoconstriction, and prolong ischemia), and medications used for acute coronary syndrome (ACS) can worsen the allergic reaction.
Therefore, it is necessary to select and use medications carefully to avoid further release of mediators or exacerbation of coronary vasospasm. Treatment of Kaposi's sarcoma requires elimination of the causative allergen, treatment of the coronary artery abnormality (depending on the type), and treatment of the allergic reaction.
As a general rule, hemodynamic stabilization, oxygen therapy, use of corticosteroids, anti-H1 and H2 antihistamines, and non-dihydropyridine calcium antagonists are recommended, which may be a good alternative to beta-blockers in anti-ischemic therapy.
Aspirin can worsen allergic reactions by increasing leukotrienes. Its use is not recommended in the SK (Syndrome Association). Nitrates may worsen hypotension and tachycardia. They are safe as long as the patient is not hypotensive.
Morphine can cause mast cell degranulation and worsen anaphylaxis. Fentanyl and its derivatives, which are less histamine-releasing, are preferable. Beta-blockers can worsen vasospasm and bronchospasm.
In Kounis syndrome, allergic and coronary alterations are combined, so once the acute event has been resolved, these patients should be referred for specialized studies in Cardiology and Allergology.
Finally, this is an entity in which the emergency physician must have a high index of suspicion for proper diagnosis and treatment.
