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Background: Pulmonary hypertension (PH) is often found in cystic fibrosis (CF) patients affected by end-stage lung disease but its impact on outcome remains unclear. Pulmonary arterial compliance (PAC) is an important determinant of right ventricle (RV) workload and it is a strong predictor of survival in other forms of PH. The aim of this study is to investigate whether PAC is a predictor of long-term prognosis in a population of CF patients affected by advanced lung disease., Methods: Between 2000 and 2014, 178 patients with CF have been evaluated for lung transplantation in our CF Center. Right heart catheterization (RHC) and follow up data were retrievable and analyzed in 141 of them. PAC was defined as the ratio between stroke volume (SV) and pulse pressure (PP) at heart catheterization. The association of PAC with survival was tested at 4 years and compared to other hemodynamic parameters., Results: PH prevalence was 56.4%. Most patients had mild elevation of pulmonary artery pressure (PAP). No difference in mortality was observed in patients with PH compared to patients with normal PAP (HR 0.95: 95% CI 0.49-1.89, p=0.89). At receiver operating characteristic curve (ROC) analysis, the optimal prognostic cut-off point of PAC was 1.95 ml/mmHg. An impaired PAC (≤1.95 ml/mmHg) was a strong independent predictor of long-term mortality (HR 3.44: 95% CI 1.51-7.85: p=0.003)., Conclusions: Impaired PAC is associated with poor prognosis in CF patients awaiting lung transplantation. Other traditional hemodynamic parameters add no prognostic information., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Neonatal fungal valve endocarditis is an uncommon and highly lethal disease. The ideal management strategy is still controversial. Current options include antifungal chemotherapy and surgical intervention, the latter being often limited by risks inherent with valve operations in low body weight infants. We present a case of a premature infant with multiple Candida tricuspid valve mycetomas. Eradication of infection was achieved by combined liposomal amphotericin therapy and complex tricuspid valve repair. Indications, technical aspects, and outcome of treatment in infants are reviewed.

Objective: The purpose of this study was to evaluate infarction-related changes in the infarcted and the non-infarcted myocardium using a baseline assessment of ventricular function obtained prior to the infarction., Background: Experimental studies have shown that both infarcted and non-infarcted myocardium contribute to the process of left ventricular dilatation soon after the infarction, but no data exist on the effect that the infarct has on the pre-infarct ventricular morphology in humans., Methods and Results: 10 patients, out of 721 admitted to our coronary care unit with a first acute myocardial infarction over a 3-year period, had had an echocardiographic examination performed before (354 +/- 407 days) and after (10 +/- 9 days) the infarction which were adequate for quantitative evaluation. Ventricular volume (Simpson) and regional wall motion (Centerline method) were evaluated by biplane apical sections and the endocardial length of the infarct and the non-infarct segments, imaged in a cross-sectional view at the papillary muscle level, were measured. After the infarction end-diastolic and end-systolic ventricular volume increased (P = 0.0003 and P < 0.0001, respectively); diastolic and systolic infarct segment length increased (P = 0.011 and P = 0.0008, respectively), while non-infarct segment had only diastolic lengthening (P = 0.019), without systolic changes. The ejection fraction decreased after the infarction (P < 0.0001), in inverse relation to infarct size and in direct relation to diastolic non-infarct segment lengthening. In the five patients in whom there was a significant diastolic lengthening of non-infarct segment (larger than mean +/- 2 S.D. of the interobserver variability) the decrease in ejection fraction was less than in the patients without significant lengthening of this segment (P = 0.017), despite a similar echocardiographic infarct size index., Conclusion: Ventricular enlargement early after myocardial infarction is due to both infarct expansion and lengthening of non-infarct segment. However, while systolic stretching of the infarct segment is a deleterious process that accounts for the increase in end-systolic volume, diastolic non-infarct segment lengthening is the expression of a functional compensatory mechanism that counteracts the reduction of the ventricular pump function secondary to the infarction.