Author`s Reply.

To the Editor,

We would like to thank the authors for their comments regarding our article in their letter entitled “Kounis syndrome not induced but prevented by the implantation of a drug-eluting stent,” published in Anatol J Cardiol 2017; 17: 412-3 (1).

Cardiovascular disease is an increased risk factor for anaphylactic severity. Various pathophysiologic mechanisms have been reported to explain cardiac anaphylaxis. In healthy individuals, a large number of mast cells exist in cardiac tissues, particularly among myocardial fibers, around the blood vessels, and in the intima of the coronary arteries. Because of the allergic reaction, the activation of mast cells in the skin and lungs, as well as in the heart, results in the release of various mediators such as histamine, leukotriene C4, prostaglandin D2, tryptase, kinase, and renin. The release of these mediators leads to cardiac symptoms such as coronary artery spasm, hypotension, dysfunction of cardiac contractility, and arrhythmia.

In patients with coronary artery disease, there is an increase in the number and concentration of mast cells in the coronary arteries and atherosclerotic plaques. In allergic reactions in patients with an atherosclerotic heart disease, activation of mast cells and release of mediators can lead to acute coronary syndrome by causing coronary artery spasm, plaque erosion, and rupture (2).

Our case was diagnosed with type 2 variant of Kounis syndrome because the patient already had an underlying coronary artery disease, and the first drug induced an allergic reaction that resulted in myocardial infarction. Our patient had a single 90% lesion in the midportion of the left circumflex artery, and the implanted stent completely restored the coronary circulation.

Following the intake of the same drug for the second time, in which a similar or more severe hypersensitivity reaction is expected, the patient developed anaphylaxis without cardiac involvement. It is likely that the coronary artery disease was treated and active and the vulnerable plaques were stabilized, and therefore, Kounis syndrome did not occur during the second drug reaction.

Although drug-releasing stents themselves cause hypersensitivity in rare cases when applied to the patient with correct indications, microvascular function recovery and increased microcirculatory resistance index are reduced (3).

Thus, it is possible to prevent an anaphylaxis from becoming more severe.