No abstract

Background: Serum uric acid (UA) has been shown to be an independent predictor of outcome in the general population and in patients with heart failure. There are, however, limited data regarding the prognostic value of UA in the context of acute coronary syndromes (ACS) particularly in medium-term follow up and the available results are contradictory. Materials and methods: Study of consecutive patients admitted with an ACS (with and without ST-segment elevation) at a single-centre coronary care unit. Primary endpoint was all-cause mortality at 1-year follow up. We evaluated if serum UA is an independent predictor of outcome and if it has any added value on top of GRACE risk score for risk prediction. Results: We included 683 patients, mean age 64±13 years, 69% males. In-hospital and 1-year mortality were 4.5 and 7.6% respectively. The best cut-off of UA to predict 1-year mortality was 6.25 mg/dl (sensitivity 59%, specificity 72%) and 30.2% of the patients had an increased UA according to this cut off. Independent predictors of UA were male gender (β= 0.078), body mass index (β=0.163), diuretics before admission (β=0.142), and admission serum creatinine (β=0.403). One-year mortality was significantly higher in patients with increased UA (15.5 vs. 4.2%, p<0.001; log rank, p<0.001). After adjustment, both increased UA as a categorical variable (HR 2.25, 95% CI 1.23-4.13, p=0.008) and as a continuous variable (HR 1.26, 95% CI 1.13-1.41, p<0.001) are independent predictors of mortality. The AUC increases only slightly after inclusion of UA in the model with GRACE risk score (from 0.78 to 0.79, p=0.350). Both models had a good fit; however, model fit worsened after inclusion of UA. Overall, the inclusion of UA in the original was associated with an improvement in both the net reclassification improvement (continuous NRI=44%), and the integrated discrimination improvement (IDI=0.052) suggesting effective reclassification. Conclusions: Serum UA is an independent predictor of all-cause mortality in medium-term after the whole spectrum of ACS and has an added value for risk stratification.

Background: Bicuspid aortic valve is the most common CHD. Its association with early valvular dysfunction, endocarditis, thoracic aorta dilatation, and aortic dissection is well established. Objective: The aim of this study was to assess the incidence and predictors of cardiac events in adults with bicuspid aortic valve. Methods: We carried out a retrospective analysis of cardiac outcomes in ambulatory adults with bicuspid aortic valve followed-up in a tertiary hospital centre. Outcomes were defined as follows: interventional -intervention on the aortic valve or thoracic aorta; medical -death, aortic dissection, aortic valve endocarditis, congestive heart failure, arrhythmias, or ischaemic heart disease requiring hospital admission; and a composite end point of both. Kaplan-Meier curves were generated to determine event rates, and predictors of cardiac events were determined by multivariate analysis. Results: A total of 227 patients were followed-up over 13 ± 9 years; 29% of patients developed severe aortic valve dysfunction and 12.3% reached ascending thoracic aorta dimensions above 45 mm. At least one cardiac outcome occurred in 38.8% of patients, with an incidence rate at 20 years of follow-up of 47 ± 4%; 33% of patients were submitted to an aortic valve or thoracic aorta intervention. Survival 20 years after diagnosis was 94 ± 2%. Independent predictors of the composite end point were baseline moderate-severe aortic valve dysfunction (hazard ratio, 3.19; 95% confidence interval, 1.35-7.54; p < 0.01) and aortic valve leaflets calcification (hazard ratio, 4.72; 95% confidence interval, 1.91-11.64; p < 0.005). Conclusions: In this study of bicuspid aortic valve, the long-term survival was excellent but with occurrence of frequent cardiovascular events. Baseline aortic valve calcification and dysfunction were the only independent predictors of events.

Objective: The role of right ventricular longitudinal strain for assessing patients with repaired tetralogy of Fallot is not fully understood. In this study, we aimed to evaluate its relation with other structural and functional parameters in these patients. Methods: Patients followed-up in a grown-up CHD unit, assessed by transthoracic echocardiography, cardiac MRI, and treadmill exercise testing, were retrospectively evaluated. Right ventricular size and function and pulmonary regurgitation severity were assessed by echocardiography and MRI. Right ventricular longitudinal strain was evaluated in the four-chamber view using the standard semiautomatic method. Results: In total, 42 patients were included (61% male, 32 ± 8 years). The mean right ventricular longitudinal strain was −16.2 ± 3.7%, and the right ventricular ejection fraction, measured by MRI, was 42.9 ± 7.2%. Longitudinal strain showed linear correlation with tricuspid annular systolic excursion (r = − 0.40) and right ventricular ejection fraction (r = − 0.45) (all p < 0.05), which in turn showed linear correlation with right ventricular fractional area change (r = 0.50), pulmonary regurgitation colour length (r = 0.35), right ventricular end-systolic volume (r = − 0.60), and left ventricular ejection fraction (r = 0.36) (all p < 0.05). Longitudinal strain (β = − 0.72, 95% confidence interval −1.41, −0.15) and left ventricular ejection fraction (β = 0.39, 95% confidence interval 0.11, 0.67) were independently associated with right ventricular ejection fraction. The best threshold of longitudinal strain for predicting a right ventricular ejection fraction of <40% was −17.0%. Conclusions: Right ventricular longitudinal strain is a powerful method for evaluating patients with tetralogy of Fallot. It correlated with echocardiographic right ventricular function parameters and was independently associated with right ventricular ejection fraction derived by MRI.