Hypereosinophilic syndrome presenting with progressive cardiac cachexia: a case report.

Background: Hypereosinophilic syndrome (HES) is a rare haematologic disorder defined by persistent eosinophilia associated with organ damage. Cardiac involvement occurs in HES patients frequently and represents major cause of their morbidity and mortality. Case summary: A 66-year-old female patient underwent comprehensive cancer screening due to significant weight reduction. Screening showed negative results except for echocardiography, which revealed a large right ventricular mass imitating malignant cardiac tumour. Patient thus underwent biopsy of the intracardial mass. The procedure was complicated with right ventricular perforation causing cardiac tamponade, successfully resolved by immediate pericardiocentesis. Subsequent echocardiography revealed an echodense mass also in left ventricular apex, resembling a thrombus. Laboratory findings with mildly elevated eosinophil count and presence of formations in both ventricular apexes arose suspicion of non-malignant disease origin, specifically eosinophilic endomyocarditis. The presumption was supported by medical history of bronchial asthma, pansinusitis, and hypereosinophilia. Cardiac magnetic resonance (CMR) confirmed signs of eosinophilic endomyocarditis of both ventricles, together with presence of several intracardiac thrombi. However, despite intensive treatment, patient died due to progressive heart failure 3 months later. Discussion: As seen in our case, establishing diagnosis of eosinophilic endomyocarditis may represent a challenge in clinical practice, since it represents a rare disease with variable clinical manifestations. However, presence of formations in both ventricles together with peripheral eosinophilia should raise suspicion of this diagnosis. Our case also highlights the importance of CMR imaging in diagnostic process of eosinophilic endomyocarditis, since it represents a non-invasive diagnostic modality able to detect distinctive signs of eosinophilic endomyocarditis.

Inflammatory marker sTREM-1 reflects the clinical stage and respiratory tract obstruction in allergic asthma bronchiale patients and correlates with number of neutrophils.

The knowledge that asthma is an inflammatory disorder has prompted us to investigate the plasma levels of a new inflammatory marker sTREM-1 that is released from the surfaces of activated neutrophils and monocytes. The plasma levels of sTREM-1 were analysed by a sandwich ELISA test in the cohort of 76 patients with allergic asthma bronchiale and 39 healthy controls. Our results revealed more than 3.5 times higher levels of sTREM-1 in AB patients (92.3 pg/mL ± 125.6) compared with healthy subjects (25.7 pg/mL ± 9.2; P = 0.0001). Higher levels of sTREM-1 were found also in patients with exacerbated AB (170.5 pg/mL ± 78.2) compared with nonexacerbated AB patients (59.1 ± 78.2; P < 0.0001), patients with respiratory tract obstruction (176.4 pg/mL ± 177.8), than those without obstruction (51.99 pg/mL ± 64.0; P < 0.0001) and patients with anti-IgE therapy (P < 0.0001). Levels of sTREM-1 correlated with number of leucocytes (P = 0.002), and absolute number of neutrophils (P = 0.001). Elevated plasma levels of sTREM-1 reflect the severity, state of exacerbation, presence of respiratory tract obstruction in AB patients and together with increased number of neutrophils point to the role of neutrophils in inflammation accompanying AB.

Relationship of self-reported exercise tolerance with inflammatory markers in women with stable ischemic heart disease.

OBJECTIVE: Ischemic heart disease (IHD) is associated with decreased exercise tolerance and it is subjectively reported as angina pectoris or dyspnea. Inflammation and pro- inflammatory cytokines are related to progression of IHD, but their level is seldom analyzed in association with self reported exercise tolerance. METHODS: Women aged 35-75 years with stable IHD from Homocysteine Slovakia study (N=175) were analyzed for monocyte chemoatractant protein-1 (MCP-1), interleukin 6 (IL-6), transforming growth factor ß1 (TGF ß1), Mannan binding lectin (MBL), heat shock proteins 60 (HSP60), carbonyl protein (CP), high sensitivity C-reactive protein (hsCRP) and oxidized glutathione (GSSG) in relation to exercise induced dyspnea or angina pectoris (AP) (≤200 m). RESULTS: Patients with dyspnea had higher HSP60 (77.3±107.2 vs 43.7±48.9 ng/ml; p=0.014) and IL-6 (2.9±1.3 vs 1.9±0.6 pg/ml; p=0.04) levels. IL-6 and HSP60 demonstrated direct correlation with dyspnea (rho=0.39; p=0.02 resp. rho=0.22; p=0.01). AP≤200 m patients showed only decreased protein carbonyl a marker of protein oxidation and increased oxidative stress (CP 61.7±27.3 vs. 72.1±23.1 pg/ml; p=0.001). CP indirectly correlates with AP≤200 m (rho=-0.25; p=0.001). CONCLUSIONS: We have found associations of pro-inflammatory cytokines and inflammation markers with dyspnea or angina pectoris, but the relationship was not consistent in our patients with stable ischemic heart disease.

Association of MCP-1 -2518 A/G single nucleotide polymorphism with the serum level of CRP in Slovak patients with ischemic heart disease, angina pectoris, and hypertension.

The aim of our work was to find if MCP-1 -2518 (A/G) single nucleotide polymorphism (SNP) influences somehow the serum concentrations of high-sensitive CRP (hsCRP) both in patients suffering from ischemic heart disease (IHD), myocardial infarction (MI), angina pectoris (AP), and hypertension (HT) and in control group of healthy subjects. Totally, 263 patients with the diagnosis of IHD, out of them 89 with MI, 145 with AP, 205 with HT, and also 67 healthy subjects were included in the study. First, we estimated the serum levels of hsCRP. We found that patients with AP had significantly higher serum level of hsCRP than both control group of healthy subjects (P = .043) and IHD patients without AP (P = .026). The presence of the mutant G allele statistically significantly correlated with the higher serum levels of hsCRP in patients with IHD (P = .016), AP (P = .004), and HT (P = .013). Higher correlations were found in men (AP: P = .019; HT: P = .047). In all cases the highest levels of hsCRP were found both in patients and healthy controls with homozygous GG genotype.

Atrial conduction delay and its association with left atrial dimension, left atrial pressure and left ventricular diastolic dysfunction in patients at risk of atrial fibrillation.

BACKGROUND: Atrial conduction delay and its association with left atrial dimension, left atrial pressure and left ventricular (LV) diastolic dysfunction in patients at risk of atrial fibrillation (AF) may be assessed by high-resolution electrocardiography of P wave. OBJECTIVES: To determine how left atrial size, left atrial pressure and LV diastolic dysfunction, measured noninvasively by transthoracic echocardiography, influence atrial conduction time. METHODS: Signal-averaged electrocardiography of P wave and echocardiogram were performed on 70 patients (average age of 63+/-10 years; 37 male and 33 female), divided into three groups: group A, patients with paroxysmal AF (n=29); group B, patients with type 2 diabetes mellitus and arterial hypertension, but without AF (n=23); and group C, healthy control patients (n=18). Standard statistical methods were used. RESULTS: Filtered P wave duration, measured by signal-averaged electrocardiography, was significantly prolonged in group A and group B compared with control group C (138+/-12 ms and 125+/-9 ms versus 117+/-8 ms; P