The aim of this investigation was to examine the role of perforin (P)‐mediated cytotoxicity in the dynamics of tissue damage in patients with non‐ST‐segment elevation myocardial infarction (NSTEMI) treated with anti‐ischaemic drugs. We enrolled 48 patients with NSTEMI in this study [age, 71.5 years; 61.5/76 (median, 25th/75th percentiles)]. The percentage of total peripheral blood P+ lymphocytes was elevated owing to the increased frequency of P+ cells within natural killer (NK) subsets, T and NKT cells in patients on day 1 after NSTEMI when compared with healthy controls. Positive correlations were found between cardiac troponin I plasma concentrations and the frequency of P+ cells, P+ T cells, P+ NK cells and their CD56+dim and CD56+bright subsets during the first week after the NSTEMI. The expression of P in NK cells was accompanied by P‐mediated cytotoxicity against K‐562 targets at all days examined, except day 21, when an anti‐perforin monoclonal antibody did not completely abolish the killing. The percentage of P+ T cells, P+ NKT cells and P+ NK subsets was the highest on the day 1 after NSTEMI and decreased in the post‐infarction period. CD56+ lymphocytes were found in damaged myocardium, suggesting their tissue recruitment. In conclusion, patients with NSTEMI have a strong and prolonged P‐mediated systemic inflammatory reaction, which may sustain autoaggressive reactions towards myocardial tissue during the development of myocardial infarction.

We aimed to analyse granulysin (GNLY)‐mediated cytotoxicity in the peripheral blood of patients with non‐ST‐segment elevation myocardial infarction (NSTEMI) treated with anti‐ischaemic drug therapy. Thirty‐nine NSTEMI patients with a median age of 70 years and 28 age‐matched healthy subjects were enrolled in this study. On day 7 after MI, the number of GNLY+ lymphocytes in the peripheral blood increased approximately six‐fold of that in the healthy subjects, measured by flow cytometry. On day 14, the number of GNLY+ cells significantly decreased in T, NKT, and both CD56+dim and CD56+bright NK subsets. GNLY+ CD3+ and GNLY+ CD56+ cells infiltrated central zone of myocardial infarction (MI). In persons who died in the first week after MI, GNLY+ cells were found within accumulation of apoptotic leucocytes and reached the apoptotic cardiomyocytes in border MI zones probably due to the influence of interleukin‐15 in peri‐necrotic cardiomyocytes, as it is was shown by immunohistology. By day 28, the percentage of GNLY+ lymphocytes in peripheral blood returned to the levels similar to that of the healthy subjects. Anti‐GNLY mAb decreased apoptosis of K562 targets using peripheral blood NK cells from days 7 and 28 after MI, while in assays using cells from days 1 and 21, both anti‐GNLY and anti‐perforin mAbs were required to significantly decrease apoptosis. Using NK cells from day 14, K562 apoptosis was nearly absent. In conclusion, it seems that GNLY+ lymphocytes, probably attracted by IL‐15, not only participate partially in myocardial cell apoptosis, but also hasten resolution of cardiac leucocyte infiltration in patients with NSTEMI.

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LITERATURE 1.Murphy RT, Thaman R, Blanes JG, Ward D, Sevdalis E, Papra E, et al. Natural history and familial characteristics of isolated left ventricular noncompaction. Eur Heart J. Hypertrophic cardiomyopathy (HCM) and left ventricular noncompaction (LVNC) are both genetically determined and familial diseases. Hypertrophic cardiomyopathy (HCM) is defined as hypertrophy of the myocardium more than 1.5cm, without another identifiable cause, such as long-standing hypertension, amyloidosis, aortic stenosis, glycogen storage disease. Many of the mutations associated with HCM involve the cardiac sarcomeric proteins and include actin, myosin, or troponin component of the sarcomere and it is most frequently transmitted as an autosomal dominant trait. Left ventricular noncompaction is a rare congenital cardiomyopathy which is characterized by the presence of a thin, compacted epicardial layer and a non-compacted thicker endocardial layer of myocardium, with prominent trabeculation and deep recesses communicating with the cavity of the left ventricle. The cause of the disorder has been identified as mutations in genes associated with the mitochondrial function, like G4.5 which encodes the protein tafazzin, genes related with the cytoskeleton, like those of alpha-dystrobrevin or dystrophin, genes that code proteins of the Z line of the sarcomere, like LDB3, which codes the protein Cypher/ZASP, genes of the internal nuclear membrane proteins (LMNA, which encodes lamin A/C) and even genes that code sarcomeric proteins like cardiac alpha-actin and the beta-myosin heavy chain and cardiac troponin T. The clinical picture of both diseases, HCM and LVNC, varies from mild forms until severe forms with heart failure and complex ventricular arrhythmias. LVNC and HCM may appear as overlapping entities. Cases of patients sharing both the LVNC and HCM phenotypes have been already published, and it is speculated that mutations in sarcomere protein genes known to cause hypertrophic cardiomyopathy and dilated cardiomyopathy may be associated with left ventricular noncompaction. 1-5 In our case report, we are presenting patient with clear overlapping pheenotyp for LVNC and HCM, using the imaging method cardiac MRI.

Atrial fibrillation is an important factor associated with left atrium (LA) enlargement and thrombus formation in the LA appendage. Transesophageal echocardiography is the procedure of choice for assessment of dimension of the LA, as well as thrombus detection in the LA cavity or LA appendage. It can detect thrombi with a high degree of sensitivity and specificity varying from 93% to 100%. Cardiac CT represents a gold standard for the assessment of anatomy of the LA complex. The mean CT sensitivity for identifying thrombus in the LA was 81% and the mean specificity 90%. Because of the high spatial resolution and the excellent myocardial border detection magnetic resonance imaging (MRI) is considered the most accurate technique for the non-invasive assessment of atrial volumes. Cardiac magnetic resonance imaging helps in tissue characterization of various intra-atrial masses and thus differentiation between cardiac tumors and thrombi. Both CMR and cardiac CT currently represent very important imaging modalities used for the comprehensive evaluation of the LA. [1][2][3] In our work we show a small series of patients with suspected mass in the LA appendage on the transesophageal ultrasound in which a cardiac MSCT and/or cardiac MRI is performed.