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Introduction As survival rates of patients born with univentricular heart defects and palliated by the Fontan operation increase, Fontan failure is more frequently encountered in the adult years. The evidence for use of serological markers, including the brain natriuretic peptide (BNP), at the time of acute Fontan failure exacerbations has been limited in this patient population. Hypothesis We hypothesize that among patients with a Fontan circulation admitted for decompensation, serological markers, particularly BNP, will have a different profile when compared to the general heart failure population. Methods This was a single center retrospective study of Fontan patients who were admitted for acute decompensated Fontan failure. The patients underwent a 1:2 propensity match for age, gender and renal function with non-Fontan patients for each hospital encounter. Admission laboratory values and echocardiographic findings were collected and verified. Student's t-test and chi-square test were used for comparison between the two patient groups. A logistic regression model assessed association of patients’ variables with a length of stay greater than 3 days. Results Our study cohort consisted of 54 encounters for 20 Fontan patients with median age of 34 years and 108 encounters for 108 non-Fontan patients with a median age of 35 years. BNP levels were significantly lower in Fontan patients admitted for decompensation (p Conclusion Compared to the general heart failure population with structurally normal hearts, the BNP values in Fontan patients admitted due to decompensation are lower on admission with a smaller change from the last known outpatient value. Alternative laboratory studies profile should likely be used for risk stratification in this patient population.

Background: Cryptogenic stroke is a dreadful outcome for patients with patent foramen ovales (PFO's). Higher incidences of cryptogenic strokes are reported in patients with PFO's and inherited thrombophilias (ITs) such as the Prothrombin and Factor V Leiden mutations. Since carriers of IT's are