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Legionella pneumophila infection (legionellosis) usually presents as a multisystemic disease, predominantly affecting the lungs (Legionnaires' disease - LD). Immunodeficiency, chemotherapy or chronic steroids use increase the risk of developing LD. Extrapulmonary manifestations of LD include cardiac complications: myocarditis, pericarditis or endocarditis. A CASE REPORT: The authors describe a case of a 51-year-old female with a history of cryoglobulinemic vasculitis, Sjögren syndrome and chronic lymphocytic leukemia who was admitted due to a high fever, fatigue, tachycardia, dyspnea and cough. Chest X-ray and CT showed bilateral pulmonary infiltrations and pleural effusion. LD was diagnosed on positive L. pneumophila urinary antigen test. Echocardiography revealed severe left ventricular (LV) dysfunction with substantially decreased ejection fraction and global longitudinal strain (GLS), with a pattern resembling reverse takotsubo syndrome (rTTS). The coronary arteries in non-invasive coronary angiography were normal. During therapy with levofloxacin and intravenous immunoglobulins as well as with carvedilol, ramipril and diuretics, gradual clinical improvement with complete normalization of LV function was observed within 5 weeks. Cardiac magnetic resonance (CMR) performed on day 35 revealed only small intramural foci of late gadolinium enhancement (LGE) with localization not corresponding to the most decreased regional longitudinal strain in the initial echocardiographic examination. The authors suggest that the mechanism of transient LV dysfunction in the case presented may have been of complex nature, including LD myocarditis and stress-induced cardiomyopathy (with the prevalence of the latter) which has not so far been reported in the literature.

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BACKGROUND: Before our study, there were no data concerning complex evaluation of: plasma PCSK9 concentrations, transcript LDL receptor (LDLR), as well as the total amount of monocytes' LDLR in acute coronary syndrome (ACS) patients. PCSK9 levels in a few cohort studies were found to correlate with the number of white blood cells (WBC) or platelets (PLT). The study aims to evaluate PCSK9-LDLR concentrations, as well as to find any association between PCSK9 and WBC or PLT. METHODS: The study group included 95 consecutive patients with acute myocardial infarction, in whom angiography/angioplasty of the culprit vessel was performed. The control group consisted of 10 healthy young volunteers. Thirty patients from the studied group were qualified for further percutaneous revascularization after 3 months. Laboratory tests were performed using commercially available kits. LDLR expression on monocyte surface was measured by flow cytometry, but the mRNA level for LDLR was established by real time polymerase chain reaction. The PCSK9 plasma concentration was measured by ELISA kits. RESULTS: Higher concentration of PCSK9 and amount of LDLR on monocytes surface were observed in patients with ACS compared with healthy young volunteers (number of LDLRs on monocytes [reaction units] 10.8 ± 9.6 vs. 41.8 ± 11.8, p < 0.001, PCSK9 [ng/mL] 295.4 ± 76.4 vs. 213 ± 63.2, p < 0.001). A similar relationship was observed after application of 3-month intensive lipid-lowering therapy in patients with ACS (n = 30, PCSK9 [ng/mL] 281.1 ± 59.5 vs. 358.5 ± 74.7, p < 0.001, LDLR transcript [reaction units] 0.6 ± 0.32 vs. 1.87 ± 0.24, p < 0.001, number of LDLRs on monocytes [reaction units] 5.9 ± 3.1 vs. 22.3 ± 3.8, p < 0.001). There were no significant differences in levels of PCSK9, LDLR between patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). There was no relation of the PCSK9 with WBC as well as with PLT. CONCLUSIONS: We observed significantly higher concentration of PCSK9, and significantly higher levels of mRNA LDLR transcript in patients with ACS compared with healthy young volunteers. A similar pattern was observed after 3 months of intensive statin therapy among patients with ACS. There were no differences in these parameters between patients with STEMI vs. NSTEMI. The results of the study require confirmation in a larger population of patients.

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Acute Coronary Syndromes (ACS) are a group of disorders caused by the significant reduction of circulation in coronary arteries. The most common reason of the dysfunction is a blood clot formed in place of plaque rupture. The role of scavenger receptors in development and progression of atherosclerosis has been confirmed in many animal experiments, however the knowledge about contribution of the receptors in the development of ACS symptoms in humans still remains insufficient. The aim of this work was to define the expression of two scavenger receptors: CD36 and MSR1 in monocytes of patients with ACS after the onset of symptoms and after the 6 months of treatment. The analysis of CD36 and MSR1 expression was carried out with the use of real-time PCR and flow cytometry. Analyses of lipid and glucose concentration in blood and the level of inflammatory markers in plasma were performed additionally for all ACS patients. All data obtained during the research were analyzed using statistical tests, such as Mann Whitney test, Wilcoxon test, or correlation. In all patients with symptoms of ACS the amount of CD36 and MSR1 mRNA in circulating monocytes, as well as the density of both receptors on the cells surface was significantly higher. Re-analysis of subjects after 6 months of treatment, showed a significant decrease in the CD36 and MSR1 expression in all patients who received atorvastatin. The results of presented studies demonstrate that both investigated receptors are involved in the development and/or progression of ACS.

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BACKGROUND: Thoracic fluid content (TFC) is one of the basic parameters measured by impedance cardiography (ICG). The B-type natriuretic peptide (BNP) is a neuroendocrine mediator produced in the ventricular myocardium and released in response to the increase of wall tension. AIM: To determine the relationship between TFC measured by ICG and BNP serum level in patients with systolic heart failure (HF). METHODS: The study population included 50 patients: a group of 30 patients with systolic HF in functional NYHA class II and III [27 males and 3 females, aged 53 +/- 6 years, with mean left ventricular ejection fraction (LVEF) 23 +/- 6%], and 20 controls without HF symptoms and preserved LVEF. The TFC and BNP serum level were measured on the same day. RESULTS: Mean BNP serum concentration was 521 +/- 882 pg/ml in HF patients and 44 +/- 36 pg/ml in healthy controls (p = 0.02). The TFC values did not differ significantly between the two groups (27.3 +/- 4.5 1/kW in the study group versus 26.3 +/- 2.8 1/kW in control subjects, NS). A significant correlation between TFC and BNP was found in patients with overt HF (r = 0.57, p = 0.001); however, after excluding one patient with exacerbation of HF symptoms, the correlation was non-significant (r = 0.24, p = 0.22). No correlation between these parameters was observed in healthy controls (r = 0.17, p = 0.51). CONCLUSIONS: There was no significant correlation between TFC measured by ICG and BNP serum level in haemodynamically stable patients with HF symptoms. The usefulness of ICG measurements in patients with exacerbated chronic HF needs further investigations.

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BACKGROUND: In recent years, increased serum immunoglobulin E (IgE) concentration in patients with cardiovascular diseases has been generating more and more interest. It is as yet unknown, however, if the increased IgE level is a marker of future coronary incidents and whether it may be regarded as an ischemic heart disease risk factor, or if it is indicative of the participation of antibodies in an inflammatory reaction to tissue damage. The aim of the study was to evaluate what significant changes in the total IgE concentration occur in patients with different forms of ischemic heart disease (IHD) and whether the concentration differs in comparison to healthy people. Additionally, we evaluated the dynamics of serum IgE concentration in patients with acute myocardial infarction. METHODS: The study included 195 patients: 80 acute myocardial infarction (AMI) patients, 58 patients with troponin-negative acute coronary syndrome (ACS) and 57 patients with stable angina pectoris, with negative personal and family history of allergy. The control group consisted of 39 healthy, age-matched individuals. Serum IgE concentration measurements were carried out with an Uni-cap Total IgE kit, using the FEIA technique. RESULTS: In patients suffering from any form of ischemic heart disease, significantly increased concentrations of serum immunoglobulin E were found, as compared to the control group of healthy individuals. Changes of IgE serum concentration on the 1(st) day, 7(th) day, 14(th) day and 40(th) day after AMI did not reveal any significant differences. Males with AMI turned out to have significantly higher immunoglobulin concentrations than females. CONCLUSION: The observed higher serum IgE concentration in patients with IHD may serve as evidence contribution to atherogenesis and myocardial ischemia.

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BACKGROUND: Clot formation is a crucial moment in the patophysiology of acute coronary syndromes. The aim of this research was to assess the relationship between immunoglobulin E (IgE), lipid parameters and chosen hemostatic markers. The role of IgE as a possible participant in the atherothrombotic process was also investigated. METHODS: A total of 80 patients with acute myocardial infarction (MI) was enrolled in the study. Concentrations of IgE, plasma lipid parameters, lipoprotein(a), markers of thrombin generation (TAT, AT III), markers of fibrinolysis (tPA:Ag, PAI-1:Ag, PAP, D-dimers) and markers of endothelial damage (von Willebrand factor) were measured in blood samples collected immediately after admission, before any treatment administration. RESULTS: In patients with acute MI and with IgE concentration above 100 kU/l, IgE values were strongly, positively correlated with LDL concentration (p < 0.05), lipoprotein(a) concentration (p < 0.02) and negatively correlated with HDL plasma levels (p < 0.02). Exclusion of patients with IgE concentration lower than 150 kU/l strengthened the correlation between IgE concentration and LDL (p < 0.002) and lipoprotein(a) (p < 0.01) levels. It also revealed a significant correlation between IgE and TAT (p < 0.001), IgE and AT III (p < 0.002), and IgE and D-dimers (p < 0.05). IgE and TAT values measured 7, 14 and 40 days after infarction also showed significant positive correlation between increments of these parameters. CONCLUSIONS: In patients with acute MI, a significant increase of thrombinogenesis and fibrinolysis markers is observed. Positive correlation between IgE concentration above 100 kU/l and markers of thrombinogenesis activation, lipid parameters and lipoprotein(a) levels, with significance increasing with IgE concentration and constant positive correlation between increments of IgE and TAT, can serve as evidence of IgE participation in the atherothrombotic process. (Cardiol J 2007; 14: 266-273).