No abstract

Twenty-six fetuses with prenatal diagnosis of LVA (50% male subjects) and 16 with LVD (38% male subjects) were identified. Fetal age at diagnosis was 23.8 ± 6.1 weeks. Mean maternal age was 30.6 ± 6.1 years old. LVA was larger (375 ± 237 vs 60 ± 71 mm(2); p = 0.002), and LVA/LVD was frequently observed in an apical location (62%). Associated cardiac/extracardiac defects were reported in 13/42 (31%). Symptomatic patients presented with arrhythmias (LVA 16% vs LVD 0%), hydrops fetalis (LVA 27% vs LVD 18.8%), or rupture (LVA 4% vs LVD 38%; p = 0.02). Size changes of the LVA/LVD during pregnancy were reported in 17%. Fetal death occurred in nine cases (21.4%); termination of pregnancy was performed in six cases (14.3%). All other babies were delivered at term. During follow-up (mean 29.1 ± 38.2 months), the rate of adverse events was significantly increased in patients with LVA (40 vs 0%; p = 0.04) CONCLUSION: The rate of fetal complications including fetal death is high. Long-term outcome among the survivors is significantly worse in patients with LVA.

Background: specific polymorphisms of genes regulating intracellular redox balance and oxidative stress are related to atherogenesis. Some studies have identified a relationship between progression of atherosclerosis and C242T mutation in CYBA gene coding for p22phox, a subunit of the NADH/NADPH oxidase system. Design: we investigated whether the C242T nucleotide transition is associated with the presence of coronary artery disease (CAD) in a population of 494 Caucasian Italians undergoing coronary angiography to diagnose the cause of chest pain. Results: the frequency of the T mutant allele that we found in 276 patients with angiographically documented CAD was significantly higher compared to what we observed in 218 subjects with normal coronary arteries (Controls) (respectively: 0.400 and 0.332, p < 0.01). The prevalence of the T allele was even stronger when we compared: 1) early onset (age ≤55) vs late onset (age ≥65) single-vessel CAD patients (respectively: 0.75 and 0.48, p < 0.05), and 2) the subgroup of CAD patients with at least one ≥98% stenosis in a coronary vessel vs those with no ≥98% stenosis in a coronary vessel (respectively: 0.425 and 0.365, p < 0.05). Conclusions: these results support the increased risk of developing early CAD and of having rapid progression of coronary stenosis in subjects carrying the C242T nucleotide transition among the Italian population.

Dilated cardiomyopathy (DCM) and inflammatory DCM (DCMi) refer to a heterogeneous group of conditions in which autoimmunity plays a major role and progressive cardiac chamber dilatation and remodeling finally leads to congestive heart failure [1]. Numerous autoantibodies against myocyte structural and functional proteins, muscarinic and b1-adrenergic receptors have been detected in patients affected from DCM/DCMi [1,2], and animal models have proved the pathogenic roles of autoantibodies [3,4]. In addition, plasmapheresis of cardiac autoantibodies in patients with DCM/DCMi and subsequent immunoglobulin (Ig) G substitution resulted in significant increase in cardiac index, left ventricular ejection fraction (LVEF), improvement in endothelial function [5], and symptom relief [6][7][8][9].Because immunoadsorption (IA) outcomes on patients' physical status perception and emotional well-being has never been investigated, this observational study was aimed to prospectively assess the effects of IA on heart-related quality of life (QOL), cardiac performance, and clinical parameters in a large cohort of unselected patients.

AimsCongestive heart failure (CHF) can be thought of as a state of chronic immune activation. Polymorphonuclear neutrophil (PMN) apoptosis is one of the mechanisms responsible for the resolution of inflammation. A reduced PMN apoptotic rate in CHF patients may generate a persistent inflammatory response and hence mediate tissue damage in this group of patients. We aimed to measure levels of spontaneous apoptosis of circulating PMNs in CHF patients and in controls, and to examine whether NYHA class, left ventricular ejection fraction (LV-EF), and laboratory parameters of inflammation, endothelial damage, and of liver and renal function, could predict the rate of PMN apoptosis in CHF patients. Methods and resultsA total of 29 CHF patients and 26 controls were studied. Propidium iodide and flow cytometry were used to assess PMN apoptosis. Delay in PMN apoptosis was expressed as percentage (expressed as median, first and third quartiles) of surviving PMNs in the study subjects. We found an increased percentage of surviving PMNs [38(27.1 -47.1)] in CHF patients compared with controls [19.4 (15.8-25.2)] (P , 0.05). The PMN survival rate in the CHF group was correlated to NYHA class, and plasma levels of C-reactive protein and alkaline phosphatase, while it was inversely correlated to LV-EF and protein levels. A positive relationship between PMN survival and increased ex vivo endothelial apoptosis was found. ConclusionIncreased PMN lifespan in patients with worsening CHF could be used as a novel measurement of tissue and endothelial damage in this group of patients.--