ABSTRACT
Background: Heart failure with preserved ejection fraction (HFpEF) is very frequently associated to sleep breathing disorders (SDB). Red blood cell distribution width (RDW) has been shown to be a potential inflammatory index linked to the degree of hypoxia and oxidative stress. Aim: To identify the existence of a possible relationship between sleep apnea, oxygen saturation (SaO2) and RDW in a population of subjects affected by acute HFpEF (AHFpEF). Methods: AHFpEF patients with known history of SDB were enrolled and performed blood chemistry, echocardiography, and 24-h polysomnography (PSG). Results: A total of 34 acute HFpEF patients (mean age 72.8 +/-8.63) were enrolled in the study. A control group of 24 non-HF patients were considered. Compared to controls, HFpEF patients showed a higher mean apnea hypopnea index (AHI), with prevalence of central apneas. A moderate to severe desaturation pattern was observed in AHFpEF vs. controls. RDW was significantly higher in AHFpEF patients vs. controls (mean value 14.7 +/-2.6 % vs. 9.1 +/-2.2, p < 0.05). In AHFpEF, RDW showed a positive correlation with time of SaO2 < 90% (r = 0.35, p = 0.04), and with mean length of apneic events (60 +/-28 s, r = 0.29, p = 0.03). Conclusion: In patients with AHFpEF and SDB, a dependence relationship between RDW and duration of oxygen desaturation was observed, as if oxidative stress and inflammation related to RDW increase could also be linked to severity of sleep disorders in this population.
ABSTRACT
The Anderson-Fabry disease is a rare, X-linked, multisystemic, progressive lysosomal storage disease caused by α-galactosidase A total or partial deficiency. The resulting syndrome is mainly characterized by early-onset autonomic neuropathy and life-threatening multiorgan involvement, including renal insufficiency, heart disease, and early stroke. The enzyme deficiency leads to tissue accumulation of the glycosphingolipid globotriaosylceramide and its analogues, but the mechanisms linking such accumulation to organ damage are only partially understood. In contrast, enzyme replacement and chaperone therapies are already fully available to patients and allow substantial amelioration of quality and quantity of life. Substrate reduction, messenger ribonucleic acid (mRNA)-based, and gene therapies are also on the horizon. In this review, the clinical scenario and molecular aspects of Anderson-Fabry disease are described, along with updates on disease mechanisms and emerging therapies.
ABSTRACT
Experimental and clinical evidence reported that some polyphenol-rich natural products may offer opportunities for the prevention and treatment of type 2 diabetes, due to their biological properties. Natural products have been suggested to modulate carbohydrate metabolism by various mechanisms, such as restoring ß-cell integrity and physiology and enhancing insulin-releasing activity and glucose uptake. Endothelium is fundamental in regulating arterial function, whereas insulin resistance plays a pivotal role in pathophysiological mechanisms of prediabetic and diabetic states. Glucose and insulin actions in the skeletal muscle are improved by insulin-dependent production of nitric oxide, favoring capillary recruitment, vasodilatation, and increased blood flow. Endothelial dysfunction, with decreased nitric oxide bioavailability, is a critical step in the development of atherosclerosis. Furthermore, insulin resistance has been described, at least in part, to negatively affect endothelial function. Consistent with this, conditions of insulin resistance are usually linked to endothelial dysfunction, and the exposure of the endothelial cells to cardiovascular risk factors such as hypertension, dyslipidemia, and hyperglycemia is associated with reduced nitric oxide bioavailability, resulting in impaired endothelial-dependent vasodilatation. Moreover, endothelial dysfunction has been described as an independent predictor of cardiovascular risk and events. Cocoa and cocoa flavonoids may positively affect the pathophysiological mechanisms involved in insulin resistance and endothelial dysfunction with possible benefits in the prevention of cardiometabolic diseases.
