Objectives: Ivabradine (IVA), a selective If current inhibitor decreasing the heart rate (HR) in patients with sinus rhythm, has been added to the most recent European Guidelines on heart failure. This selective treatment reduces HR exclusively while fully preserving myocardial contractility and relaxation, atrioventricular conduction, and ventricular repolarization, as well as blood pressure. The aim of this study was to evaluate the improvement of quality of life (QOL) in patients with chronic heart failure (CHF) treated with IVA versus two β-blockers (bisoprolol and carvedilol). Methods: We evaluated if a 1-month treatment with IVA (5 mg b.i.d.) or β-blockers (carvedilol 6.25 mg b.i.d. or bisoprolol 1.25 mg b.i.d.) improves the QOL (assessed by SF-36 questionnaire) in patients with CHF with reduced left ventricular ejection fraction (<50%). SF-36 was tested in 221 CHF patients (mean age 64 ± 6 years) randomized into two groups (IVA group - 110 patients; β-blockers group - 111 patients). Data of QOL questionnaire and HR were collected by an interview during a clinical visit both at prescription time (basal) and after 1 month of therapy with IVA or β-blockers. QOL life and HR results after 1-month of therapy (T1) with IVA were compared with basal values (T0). Results: The IVA versus β-blockers treatment was associated with a significant improvement of physical functioning (p < 0.001 vs. p < 0.01), physical role functioning (p < 0.001 vs. p < 0.01), emotional role functioning (p < 0.01 vs. p < 0.85), and mental health scales (p < 0.001 vs. p < 0.01). HR in the IVA group was significantly lower compared to the group of patients treated with β-blockers (63 vs. 67 bpm; p < 0.001). Conclusions: IVA treatment significantly improves the QOL in patients with CHF without any deleterious impact on hemodynamics, and may be beneficial in these patients without other adverse effects associated with β-blockers.

Background: A great debate in literature exists nowadays on the role of uric acid as a marker of cardiovascular and metabolic organ damage or a risk factor for cardiovascular and metabolic disease. Methods: to determine the relationship among serum uric acid and metabolic syndrome and atherosclerosis, by mean of carotid intima media-thickness, in a cohort of 811 otherwise healthy overweight/obese subjects, without overt atherosclerosis not using any kind of drug. Results: Uric acid levels were positively related to male gender, waist circumference, BMI, systolic and diastolic pressure levels, fasting insulin, fasting glucose, HOMA-IR, triglycerides, total cholesterol, LDL cholesterol, the presence of metabolic syndrome and the number of the components of metabolic syndrome and negative related to HDL cholesterol levels. No correlation was found between uric acid and carotid intima media thickness. At the multiple regression analysis, only triglycerides (positively) and HDL-cholesterol (negatively) maintained an independent association with uric acid, while age, female gender and uric acid showed a significant independent association with metabolic syndrome. Moreover, the analysis of the odd ratios showed that the risk of developing metabolic syndrome was consistent with uric acid levels ranging from 3 mg/dl to 8 mg/dl. Conclusion: the presence of metabolic syndrome does not seem to provide hyperuricemia. By contrast, higher serum uric acid level may predict the risk of metabolic syndrome. Moreover, our results suggest that uric acid cannot be considered a risk factor for early atherosclerosis, at least when assessed using carotid ultrasound.

Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical perturbations in the heart. Interstitial inflammation, oxidative stress, myocardial apoptosis, mitochondria dysfunction, defective cardiac metabolism, cardiac remodeling, hypertrophy and fibrosis with consequent impaired contractility are the most common mechanisms implicated. Epigenetic changes also have an emerging role in the regulation of these crucial pathways. The aim of this review was to highlight the increasing knowledge on the molecular mechanisms of DbCM and the new therapies targeting specific pathways.

Balloon angioplasty may be performed as the first treatment of aortic coarctation to stabilize newborns too sick for immediate surgery. The issue of vascular access is the key to the successful treatment of critical newborns. In our study, we argue that the lesser-known axillary access route is the safest and most effective route of vascular access for balloon angioplasty in infants with aortic coarctation. To support this argument, we present the case of eight unstable newborns with complex heart diseases, who were successfully treated with percutaneous intervention through the axillary artery. This case series is followed by an analysis of the greater efficacy of this technique compared to the more conventional femoral and carotid routes. We conclude by acknowledging the substantial advantages of this lesser-known vascular access and advocate for its more widespread clinical implementation in the treatment of critical newborns.