ABSTRACT
Acute coronary syndromes secondary to hypersensitivity reactions related with allergic factors are defined as Kounis syndrome. Doxycycline is an antibiotic commonly used in clinical practice. In this report, we described an atypical presentation of Kounis syndrome in a patient who was admitted to the emergency service complaining of chest pain, generalized rash and fever. She was taking doxycycline for 3 days because of urinary tract infection. Non specific ST-T changes were seen on electrocardiography, positive troponin levels were detected and global left ventricular wall motion abnormalities were defined by echocardiography. The patient had no conventional risk factor for acute coronary syndrome. Normal coronary angiography results, improved left ventricular functions and symptoms by antihistaminic and steroid treatments were consistent with Kounis syndrome.
Introduction
Allergic myocardial infarction, known as Kounis syndrome, is caused by inflammatory mediators and should be considered in all patients presenting with hypersensitivity reactions. Many factors, such as drugs, foods, environmental exposures (animal stings) and latex contact can trigger this clinical situation. According to our knowledge, this is the first case of Kounis syndrome with its late presentation and being a consequence of doxycycline treatment.
Case
A 24-year-old female patient was admitted to our emergency department with chest pain, generalized rash and fever that began 24 hours ago. She was taking doxycycline for 3 days because of urinary tract infection. Electrocardiography (ECG) was performed and non-specific ST-T changes were seen (Figure 1). Increased troponin levels as 0.56 ng/ml (normal value: <0.05 ng/ml) and mild leukocytosis as 15x10³/µL (normal value: <10x10³/µL) were detected. Transthoracic echocardiography showed global hypokinesis of the left ventricle and, ejection fraction was calculated as 50%. The patient was hospitalized in the intensive care unit and coronary angiography (CAG) was performed (Figure 2a and 2b). Normal coronary arteries without any culprit lesion were observed on ergotamine provocation test and intravascular ultrasonography (IVUS). The patient was diagnosed with Kounis syndrome. In addition to antihistaminic treatment, parenteral steroid was started. During the 3 days of follow-up, no chest pain developed, rashes disappeared, troponin levels returned to normal range and echocardiographic abnormalities improved completely. The patient was discharged with the suggestion to consult the allergy department for detailed examination about other possible allergens that may cause hypersensitivity reactions such as allergic myocardial infarction.
Discussion
In this case report, we presented a patient diagnosed with allergic myocardial infarction known as Kounis syndrome. Our case is interesting in terms of its late presentation and being related with doxycycline treatment. Kounis syndrome is defined as the coincidental occurrence of chest pain and allergic reactions accompanied by clinical and laboratory findings of acute coronary syndrome caused by inflammatory mediators released during the allergic insult (1). The main pathophysiology in Kounis syndrome is coronary artery vasospasm due to release of vasoactive mediators, such as histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines, and chemokines secondary to mast cell activation (2). Two different types of Kounis syndrome has been defined. Type 1 Kounis syndrome is the development of acute allergic reaction in patients without predisposing factors for coronary artery disease as a result of coronary artery spasm by allergic insults. This type can be related with endothelial dysfunction and, cardiac biomarkers are either normal or elevated. Type 2 variant includes patients with culprit but quiescent coronary disease and atherosclerotic plaque erosion or rupture manifesting as acute myocardial infarction (3). In recent years, Biteker et al. have proposed a new classification for Kounis syndrome including Type 3 in relation with drug-eluting stent thrombosis after percutaneous coronary interventions (4). Our case was consistent with Type 1 Kounis syndrome. The patient had normal coronary arteries, elevated troponin levels and a history of antibiotic use which led to an allergic insult. With its late presentation after exposure to an allergic insult and also with its occurrence due to a new type of antibiotic subgroup, such as tetracycline, were the main properties of our case different from other cases.
Multifactorial aetiology of Kounis syndrome usually challenges the diagnosis. Drugs, especially antibiotics, environmental exposures, foods, latex contact, insect stings and many other conditions can cause Kounis syndrome (5). In Type 1, vasodilatator agents, such as nitrates and calcium blockers, in addition to antihistaminic and steroid therapy, usually improve symptoms and cardiac functions whereas conventional acute coronary syndrome protocols, including antithrombotic and anticoagulant drugs are required for Type 2 Kounis syndrome (6). Clinicians must be aware of allergic myocardial infarction presenting with chest pain, elevated troponin levels, electrocardiographic and echocardiographic abnormalities concurrent with allergic findings as a result of hypersensitivity reactions.
