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Background: The aim of this retrospective study was to identify clinical, humoral and echocardiographic variables predicting rehospitalization and poor quality of life (QOL) in patients with reduced or mid-range ejection fraction heart failure., Methods: From 2009 to 2012, 310 patients were admitted having signs and symptoms of heart failure with reduced ejection fraction. All the patients were followed by phone, calling the patients or the referring general practitioner. The Minnesota Living with Heart Failure Questionnaire (MLHFQ) was used as the instrument to evaluate QOL: MLHFQ less than 24 is a good QOL, 24-45 is moderate QOL and more than 45 is poor QOL. The primary event was poor QOL and/or rehospitalization at 4 years., Results: Seventy-nine patients died at median time of 21 months; 4-year survival was 72 ± 3%. Rehospitalization due to heart failure was recorded in 60 cases. Among 231 survivors, MLHFQ score was good in 99 (42%), moderate in 50 (21%) and poor in 88 (37%). Four-year freedom from death, poor QOL or rehospitalization was 51 ± 3%. Multivariable analysis identified the following risk factors: heart rate at discharge at least 70 bpm, ischemic heart disease, atrial fibrillation, hypercholesterolemia, chronic pulmonary disease, N-terminal pro brain natriuretic peptide at discharge, severe tricuspid regurgitation and mitral regurgitation more than moderate., Conclusion: Clinical, laboratory and echocardiographic profile is crucial to predict long-term QOL of patients admitted for heart failure.

Objective: This study aimed to evaluate the role of angiotensin type 1 receptor gene (AGTR1) polymorphism (A1166C) in left ventricular hypertrophy (LVH) mediated by the angiotensin-converting enzyme (ACE) in endurance athletes., Methods: A group of 74 white, healthy male endurance athletes, aged between 25 and 40 yr, were enrolled in this study. All of them participated primarily in isotonic sports, training for at least >10 h x wk(-1), for at least 5 yr. The ACE genotype (insertion [I] or deletion [D] alleles) was ascertained by polymerase chain reaction (DD in 35, ID in 36, and II in 3). Group II was excluded from the analysis because of its small size. No difference was found between the two groups as regards age, blood pressure, HR, and echocardiographic data., Results: The left ventricular mass index (LVMI) was significantly higher in group DD rather than in group ID (P = 0.029). The group DD showed a slightly higher prevalence of subjects with LVH (LVMI > 131 g x m(-2); 62.9%) than group ID (44.4%, P = 0.120). No association was found between ACE-DD and LVH (odds ratio (OR) = 2.12, 95% confidence interval = 0.82-5.46). Concerning the role of AGTR1 polymorphism, the highest LVMI was found in 15 athletes with ACE-DD and AGTR1-AC/CC genotypes (150 +/- 23 g x m(-2)); the lowest value of LVMI was found in the case of ACE-ID and AGTR1-AA (127 g x m(-2) +/- 18 g x m(-2)), whereas LVMI in subjects with ACE-DD + AGTR1-AA was similar to that in the ACE-ID + AGTR1-AC/CC group (134 +/- 18 g x m(-2) vs 133 +/- 20 g x m(-2), P = 0.880). The presence of ACE-DD + AGTR1 + AC/CC was strongly associated with LVH (OR = 4.6, P = 0.029). Moreover, subjects with LVH showed longer left ventricular isovolumetric relaxation time and higher end-systolic wall stress. The latter was strongly correlated to LVMI (r = 0.588), especially in the presence of ACE-DD + AGTR1 + AC/CC (r = 0.728)., Conclusions: LVMI may be greater in the presence of ACE- DD and AGTR1-AC/CC polymorphisms.

Mitral valve repair for degenerative mitral regurgitation is nowadays one of the most common valvular procedures. Different technical modifications were added to the original Carpentier's method, trying to maximise the stability of the results and to reduce the incidence of immediate complications and of late failure of the correction. Survival is good, even if recent reports showed that recurrence of mitral regurgitation can be higher than expected. Prolapse of the anterior leaflet remains challenging and is related to higher reintervention rates. Nevertheless, the overall success rate is high, and the increasing experience of the different surgical teams approaching this procedure will help maintain satisfactory and stable long-term results.

We describe the case of a 75-year-old female admitted to our ward with a diagnosis of papillary fibroelastoma discovered during routine control. The patient was completely asymptomatic without any previous event of embolization or valve incompetence. We report this rare case of papillary fibroelastoma for its unusual location with large involvement of the anterolateral papillary muscle (its prevalence in the literature is about 1%).

Background: Oxidative stress, resulting from an antioxidant/prooxidant imbalance, seems to be crucial in atherogenesis. Recent evidence has emerged, however, of a surprisingly high content of low-molecular-weight antioxidants in human atherosclerotic plaques, although other antioxidant systems have not been investigated in these lesions., Methods and Results: We studied glutathione-related antioxidant defenses (which play a key role in tissue antioxidant protection) in carotid atherosclerotic plaques of 13 patients subjected to endarterectomy and in normal internal mammary arteries of 13 patients undergoing coronary artery bypass surgery. Selenium-dependent glutathione peroxidase activity was undetectable in the plaques of 7 patients; the other 6 patients with plaques showed a mean enzymatic activity approximately 3.5-fold lower than that of mammary arteries. Glutathione reductase activity was also markedly lower in the plaques than in the arteries. Glutathione transferase instead had comparable activity in the two tissues. Remarkably, 5 of the 7 patients with an undetectable selenium-dependent glutathione peroxidase activity but none of the 6 with a detectable one were characterized by multivascular atherosclerotic involvement (3 patients) or stenosis of the contralateral carotid artery (2 patients)., Conclusions: A weak glutathione-related enzymatic antioxidant shield is present in human atherosclerotic lesions. Although the cause of this phenomenon remains to be determined, the present data suggest that a specific antioxidant/prooxidant imbalance operative in the vascular wall may be involved in atherogenic processes in humans.