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.

Relationship between TRAIL and Left Ventricular Ejection Fraction in Patients with ST-Elevation Myocardial Infarction Treated with Primary Percutaneous Coronary Intervention.

BACKGROUND: Apoptosis plays an important role in the myocardial injury after acute myocardial infarction and in the subsequent development of heart failure. AIM: To clarify serum kinetics of apoptotic markers TRAIL and sFas and their relation to left ventricular ejection fraction (LVEF) in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). METHODS: In 101 patients with STEMI treated with pPCI, levels of TRAIL and sFas were measured in series of serum samples obtained during hospitalization and one month after STEMI. LVEF was assessed at admission and at one month. Major adverse cardiovascular events (MACE, i.e., death, re-MI, and hospitalization for heart failure and stroke) were analysed during a two-year followup. RESULTS: Serum level of TRAIL significantly decreased one day after pPCI (50.5pg/mL) compared to admission (56.7pg/mL), subsequently increased on day 2 after pPCI (58.8pg/mL), and reached its highest level at one month (70.3pg/mL). TRAIL levels on days 1 and 2 showed a significant inverse correlation with troponin and a significant positive correlation with LVEF at baseline. Moreover, TRAIL correlated significantly with LVEF one month after STEMI (day 1: r=0.402, p<0.001; day 2: r=0.542, p<0.001). On the contrary, sFas level was significantly lowest at admission (5073pg/mL), increased one day after pPCI (6370pg/mL), and decreased on day 2 (5548pg/mL). Significantly highest sFas level was marked at one month (7024pg/mL). sFas failed to correlate with LVEF at baseline or at one month. Both TRAIL and sFas showed no ability to predict improvement of LVEF one month after STEMI or a 2-year MACE (represented by 3.29%). CONCLUSION: In STEMI treated with pPCI, TRAIL reaches its lowest serum concentration after reperfusion. Low TRAIL level is associated with worse LVEF in the acute phase of STEMI as well as one month after STEMI. Higher TRAIL level appears to be beneficial and thus TRAIL seems to represent a protective mediator of post-AMI injury.

Apoptosis in ischemic heart disease.

Apoptosis plays an important role in the myocardial loss after acute myocardial infarction and participates in the process of subsequent left ventricular remodeling and development of symptomatic heart failure. Finding a sensitive apoptotic marker that would help in prognostic stratification of patients after acute myocardial infarction and offer new therapeutic strategies is thus of a great importance. Several studies suggest that tumor necrosis factor-related apoptosis inducing ligand (TRAIL) represents a very promising marker of prognosis in patients with acute myocardial infarction. This review article provides an overview of current knowledge on the role of apoptosis in ischemic heart disease and highlights potentially beneficial apoptotic markers in clinical practice.

Prognostic value of TNF-related apoptosis inducing ligand (TRAIL) in acute coronary syndrome patients.

BACKGROUND: Apoptosis plays an important role in the development of heart failure. The aim of the prospectively designed study was to assess whether the concentration of apoptotic markers apoptosis-stimulating fragment (Fas, CD95/APO-1) and tumor necrosis factor-related apoptosis inducing ligand (TRAIL) can predict prognosis in patients with acute coronary syndromes. METHODS: The concentrations of soluble Fas and TRAIL were determined in 295 patients with acute coronary syndromes. The status of all patients was evaluated at 6 months. The primary goal was a composite end-point of death and hospitalization for heart failure. The secondary end-points were re-MI, death alone and stroke alone. RESULTS: During the median follow-up of 6 months, 26 patients experienced the composite end-point. Using multivariate logistic regression, the concentration of TRAIL was the strongest significant and independent predictor of composite end-point (OR 0.11 (95% CI 0.03-0.45), p = 0.002). Low concentration was associated with poor prognosis of patients. Other significant predictors of composite end-point were serum creatinine (OR 7.7 (95% CI 1.1-54.5, p = 0.041) and complete revascularization (OR 0.19 (95% CI 0.05-0.78, p = 0.02). Independent significant predictors of death in the multivariate analysis were the concentration of TRAIL (OR 0.053 (95% CI 0.004-0.744), p = 0.029), older age (OR 1.20 (95% CI 1.02-1.41, p = 0.026) and serum creatinine (OR 15.1 (95% CI 1.56-145.2), p = 0.0193). Re-MI or stroke could not be predicted by any combination of obtained parameters. CONCLUSIONS: Low concentrations of soluble TRAIL represent a strong predictor of a poor prognosis in patients with acute coronary syndrome. The predictive value of TRAIL concentration is independent of age, ejection fraction, index peak troponin level, concentration of BNP or serum creatinine.