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Cardiac troponins have a crucial role in diagnosing acute myocardial infarction, but have been considered by some authors to have a high false positive rate. Such opinions may decrease the confidence in troponin with important clinical consequences. The aim of the paper is to analyze three different meanings of the phrase »false positive troponin«: A) analytic (technical) false positive, with no real myocardial damage; B) false positive considering AMI: cardiac injury is present, but there is no AMI; C) false positive considering CAD: there is myocardial damage, but no CAD. The most frequent and the most important source of misunderstanding is the confusion between aspects A) and B). Namely, there has been a relatively small percentage of false positive troponin elevations due to analytic reasons. On the contrary, there has been a relatively large percentage of »false positive« results in patients with myocardial necrosis due to causes other than AMI; for them - instead of »FP troponin elevation« - another phrase ought to be used, e.g., »non-AMI troponin elevation« until the etiopathogenesis in an individual patient is recognized. The phrase »false positive troponin« should be restricted to the artificial increase in troponin due to preanalytic and analytic reasons. By doing so, we may decrease the degree of confusion about troponin and increase the confidence in this highly specific marker of myocardial injury. The possibility of an analytic false positive result should always be kept in mind when one interprets elevated troponin.

The modern treatment of patients with acute coronary syndrome (ACS) is justified and effective, but carries a higher risk of bleeding. The study aimed to determine the basic risk factors for bleeding and included 177 patients with ACS who were hospitalized at the Clinic for Crdiology Niš, in the period from May to September 2013. Based on the presence of bleeding, patients were first divided into patients with bleeding and patients without bleeding. Patients with bleeding were further divided into patients with significant bleeding and patients with less significant bleeding. The study took into account: demographic and anamnestic data, a form of ACS, basic laboratory tests and applied therapy for ACS. In the group of patients with bleeding, there were statistically significantly more non-smokers (X2 = 6.527, p = 0.038), patients with chronic kidney disease (CKD) (X2 = 4.192, p = 0.041) and patients with higher CRP values (p = 0.039). In the subgroup of patients with significant bleeding, there were a statistically significantly more frequent patients with CKD (36.4% vs. 6.5%, Fisher's tests: p = 0.007) and higher CRP values (z = 2.452, p = 0.014). In the subgroup of patients with less significant bleeding, the values of hemoglobin (t = 3,496, p = 0,003) were statistically significantly lower compared to other patients. It is interesting to note that the values of hemoglobin, creatinine clearance, and leukocyte count (as a parameter of inflammation) are variables of the PRECISE-DAPT scoring system that appeared in 2017, after our study. [ABSTRACT FROM AUTHOR]

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Introduction. Kounis syndrome is a simultaneous manifestation of acute coronary syndrome and conditions associated with mast cell activation, such as allergies or anaphylactic reactions. We present early stent thrombosis in a female with an atopic constitution without previous atherosclerosis of coronary arteries. Case report. A 50-year-old woman with typical anginal pain was admitted to the Clinic for Cardiology, University Clinical Center Niš. A few hours earlier, she had passed by a linden tree in bloom. She immediately felt chest pain, paresthesia and numbness in her left arm throat tightness, heaviness of the tongue, and swelling of the lips. The symptoms disappeared for 60 min after taking 10 mg of loratadine, but then they recurred. On the electrocardiographic (ECG) findings, 30 minutes after admission, ST elevation was seen in leads D2, D3, aVF, and V6. She underwent an emergency percutaneous coronary intervention procedure. Occlusive thrombosis was seen in the ostium of the left anterior descending (LAD) coronary artery. A sirolimus-coated stent was placed and thrombolysis in myocardial infarction (TIMI) 3 flow was obtained. A few hours after the intervention, the patient reported a new onset of chest pain followed by ventricular fibrillation (VF), DC shock, and the occurrence of new ST-segment elevation in aVR and V1-V3 on the ECG. Repeated angiography showed acute in-stent thrombotic occlusion. Balloon angioplasty was performed, which restored TIMI 3 flow in LAD coronary artery. Anticoagulant and corticosteroid therapy was administered. Three days after the intervention, optical coherence tomography imaging was performed, which showed good stent expansion and apposition, without atherosclerosis and thrombosis. Conclusion. Coronary angiography proved type I Kounis syndrome after exposure to an allergen, and type III Kounis syndrome developed shortly after stent placement when acute in-stent thrombosis occurred. Newly described causes of acute and subacute stent thrombosis in type III Kounis syndrome are stent-associated hypersensitivity reactions. [ABSTRACT FROM AUTHOR]