Search

Background and aims Elevated serum uric acid (sUA) concentrations have been associated with worse prognosis in heart failure (HF) but little is known about elderly patients. We aimed to assess long-term additive prognostic value of sUA in elderly patients hospitalized for HF. Methods and results Clinical and echocardiographic characteristics of 310 consecutive elderly patients hospitalized for HF were collected. During index period, 206 had sUA concentrations available, which were obtained within 24 h prior to discharge; 10 patients were lost to follow-up, leaving 196 patients available. Patients had a median age of 77 (IQR 69–83) years, and were mostly male (64.5%). sUA ranges for tertiles I–III were: 1.5–6.1, 6.2–8.3, and 8.4–18.9 mg/dl, respectively. During a median follow-up of 27 months (IQR 10.5–39.5), 122 combined events occurred (87 deaths and 73 HF rehospitalizations). Four-year event-free survival for the combined endpoint was 46 ± 7% for tertile I, 34 ± 7% for tertile II, and 21 ± 5% for tertile III (P = 0.001). By multivariable Cox backward analysis, sUA was retained as a significant predictor. Compared with the lowest sUA tertile, tertile III showed a strong association with outcome, also after adjustment for other predictors (HR 1.84, 95% CI 1.16–2.93; P = 0.01). Importantly, addition of sUA to the other significant predictors of outcome resulted in improved risk classification (net reclassification improvement 0.19, P = 0.017). Conclusions High sUA at discharge is a strong predictor of adverse outcome in elderly hospitalized for HF, and it significantly improves risk classification. Measuring sUA can be a simple and useful tool to identify high-risk elderly hospitalized for HF.

Myocardial reflectivity, as assessed by calibrated integrated backscatter (cIB) analysis, is a non-invasive surrogate for the amount of left ventricular (LV) fibrosis. The aim of this study was to assess the myocardial reflectivity pattern in patients with heart failure and preserved ejection fraction (HFpEF), and to evaluate its relationship with longitudinal systolic deformation of LV by 2D-speckle tracking echocardiography, and degree of diastolic dysfunction. Transthoracic echocardiography, myocardial Doppler-derived systolic (Sm) and early diastolic velocity (E'), global longitudinal strain (GLS), and tissue characterization by cIB, were obtained in 86 subjects, 46 with HFpEF, and 40 controls. GLS was significantly impaired in HFpEF patients (-15.4 ± 3.5 % vs -21.5 ± 2.9 % in controls; P

Metabolic syndrome results in a pro-thrombotic, pro-inflammatory condition that markedly favours the development of diabetes and cardiovascular disease. In patients with metabolic syndrome, many interrelated factors are thought to contribute to the development of vascular alterations; however, insulin resistance is regarded as the most relevant. In fact, in addition to its well-known activity on glucose metabolism, insulin exerts a wide spectrum of non-metabolic actions, including vasodilation, inhibition of platelet aggregation and thrombosis, anti-oxidant and anti-inflammatory effects, which result in anti-atherosclerotic and vascular protective effects. In this setting, clustering of multiple cardiovascular risk factors may reinforce their pro-atherogenic potential. Metabolic syndrome is also accompanied by endothelial dysfunction, and it has become appreciated that microvascular damage is a common finding in these subjects. In diabetic patients, impairment of microcirculation is recognized at the level of all circulatory districts, including coronary microvessels, and it has an important prognostic impact. Diabetes is accompanied by profound changes in energy metabolism, increased oxidative stress, derangement of adipokines synthesis, reduced mobilization and function of endothelial progenitor cells, which may lead to microvascular dysfunction. Features of the insulin resistance syndrome, including altered glucose tolerance, are more frequent in patients with microvascular angina. Taken together, these observations suggest that diabetes, along with each of the various components of the metabolic syndrome, has the capability of profoundly altering coronary microvascular reactivity, thus predisposing to myocardial ischemia even in the absence of coronary artery stenosis. When these alterations combine in the same patient to give rise to full-blown metabolic syndrome, their negative effects on myocardial perfusion are synergistically potentiated. While the pathophysiology of this condition has become to be substantially unravelled, much research is still needed to achieve a tailored therapeutic approach.

Myocardial performance index (MPI), or Tei index, is an indicator of systolic and diastolic myocardial function. MPI increases in case of cardiac dysfunction; however, whether reversal of left ventricular dysfunction is also reflected by concomitant improvement (i.e., decrease) of MPI is unknown.Fifty-two patients with chronic ischemic cardiomyopathy and viable myocardium by dobutamine stress echocardiography were studied by echocardiography before and more than 4 months after cardiac revascularization. Patients were in optimal medical therapy, which remained unchanged following revascularization.At baseline, ejection fraction (EF: 32 ± 6%) and wall motion score index (WMSI: 2.37 ± 0.32) were impaired, and MPI averaged 0.71 ± 0.19. Revascularization markedly improved EF (44 ± 10%, P0.0001) and WMSI (1.77 ± 0.44, P0.0001). MPI also improved (0.59 ± 0.26, P0.0001), and its decrease was significantly correlated with the improvement in EF (r =-0.68, P0.0001) and to the extent of viable myocardium (r =-0.45, P = 0.0007). Responders to revascularization (≥5% increase in EF at follow-up, n = 40% and 77%) achieved a significant improvement in MPI at follow-up in contrast with nonresponders (-23 ± 25% vs. 0.02 ± 0.18%, P = 0.001). Improvement in MPI was largely driven by a significant reduction in isovolumic contraction time (P0.001) with consequent prolongation of the ejection phase.In patients with chronic ischemic cardiomyopathy, MPI improves along with recovery of function, reflecting the intrinsic improvement of viable segments induced by revascularization.