This is the first large-scale multicenter study where a prognostic score, the MECKI score, has been built for systolic HF patients considering CPET data combined with clinical, laboratory and echocardiographic measurements. In the present population, the MECKI score has been successfully validated, performing very high AUC.

L-Carnitine treatment initiated early after acute myocardial infarction and continued for 12 months can attenuate left ventricular dilation during the first year after an acute myocardial infarction, resulting in smaller left ventricular volumes at 3, 6 and 12 months after the emergent event.

We conducted a controlled multicenter trial with central randomization and evaluation of events under blind conditions involving 652 patients with unstable angina. Patients were treated either with conventional therapy alone (group C) (n =338) or with conventional therapy combined with an inhibitor of platelet aggregation, ticlopidine 250 mg b.i.d. (group C+T) (n=314). Patients were assigned randomly within 48 hours of admission and followed up for 6 months. With the "intention-to-treat" approach, the primary end points, vascular death and nonfatal myocardial infarction, were observed in 13.6% of the patients in group C and in 7.3% of the patients in group C+T, which is a reduction in risk of 46.3% (p=0.009). Vascular mortality was 4.7% in patients in group C and 2.5% in patients in group C+T, which is a reduction in risk of 46.8% (p=0.139). The risk of nonfatal myocardial infarction was reduced by 46.1% (p=0.039), with a frequency of 8.9o in patients in group C and 4.8% in patients in group C+T. New Q wave myocardial infarction occurred with a frequency of 6.8% in patients in group C and 3.8% in patients in group C+T, which is a reduction in risk of 44.1% (p=0.091). Fatal and nonfatal myocardial infarction was 10.91% in patients in group C and 5.1% in patients in group C+T, which is a reduction in risk of 53.2% (p=0.006). These findings confirm the importance of platelets in the pathogenesis of unstable angina and the usefulness of antiplatelet treatment for the prevention of cardiovascular events.

AimsWe sought to assess the prevalence and clinical correlates of cardiorenal anaemia (CRA) syndrome in systolic heart failure and the relationship between renal dysfunction and anaemia on hard clinical outcomes. Methods and resultsWe studied 951 patients with chronic heart failure (CHF) and systolic dysfunction. The primary outcome was allcause mortality and urgent heart transplantation (UHT). Cox's regression analyses were used to assess the relation of the variables to the primary outcome. Hazard ratios (HRs) with 95% confidence intervals (CI) were calculated.The prevalence of CRA syndrome was 21.1%. Age (P , 0.001), body mass index (P , 0.001), diabetes (P ¼, 0.001), ischaemic aetiology (P , 0.006), left ventricular ejection fraction (P ¼ 0.018), and treatment with renin-angiotensin system inhibitors (P , 0.001) were independently related to CRA syndrome. During a median follow-up of 3.7 years, the primary outcome occurred in 404 patients (42.5%). Compared with patients with preserved renal function and normal haemoglobin (Hb) levels, those with CRA syndrome had a significantly increased risk for the primary outcome; the univariate and multivariate-adjusted HRs were 4.04 (CI: 3.11-5.24; P , 0.0001) and 2.22 (CI: 1.64-2.98; P , 0.0001), respectively. Three-year UHT-free survival was 86 and 47%, respectively. Among patients with renal dysfunction, the adjusted HR for the primary outcome increased by 17% (CI: 8 -26; P ¼ 0.0001) for each 1 g/dL decrease below an Hb value of 13.0 g/dL. ConclusionHeart failure, renal dysfunction, and anaemia are a fatal combination. Despite a relatively low prevalence, the CRA syndrome contributes to considerable mortality due to CHF.--

In HF patients with permanent atrial fibrillation, exercise performance is reduced as reflected by reduced peak VO(2). The finding of unidentified AT is associated with a poor performance. In atrial fibrillation patients, VO(2) is higher at AT whereas lower at peak. This last observation raises uncertainties about the use of AT data to define performance and prognosis of HF patients with atrial fibrillation.