Clinical and epidemiological studies demonstrate that short- and long-term exposure to air pollution increases mortality due to respiratory and cardiovascular diseases. Given the increased industrialization and the increased sources of pollutants (i.e., cars exhaust emissions, cigarette smoke, industry emissions, burning of fossil fuels, incineration of garbage), air pollution has become a key public health issue to solve. Among pollutants, the particulate matter (PM) is a mixture of solid and liquid particles which differently affects human health depending on their size (i.e., PM with a diameter <10 μm reach the lung and PM with a diameter <2.5 μm penetrate deeper into the lung). In particular, the acute exposure to PM and PM increases the rate of cardiovascular deaths. Thus, appropriate interventions to reduce air pollution may promote great benefits to public health by reducing the risk of cardiovascular diseases. Several biological mechanisms have been identified to date which could be responsible for PM-dependent adverse cardiovascular outcomes. Indeed, the exposure to PM and PM induces sustained oxidative stress and inflammation. PM is also able to increase autonomic nervous system activation. Some potential therapeutic approaches have been tested both in pre-clinical and clinical studies, based on the intake of antioxidants from dietary or by pharmacological administration. Studies are still in progress to increase the knowledge of PM activation of intracellular pathways and propose new strategies of intervention.
Inflammation is a key mechanism of cardiovascular diseases. It is an essential component of atherosclerosis and a significant risk factor for the development of cardiovascular events. In the crosstalk between inflammation and cardiovascular diseases, the transcription factor NFκB seems to be a key player since it is involved in the development and progression of both inflammation and cardiac and vascular damage. In this review, we deal with the recent findings of the role of inflammation in cardiac diseases, focusing, in particular, on NFκB as a functional link. We describe strategies for the therapeutic targeting of NFκB as a potential strategy for the failing heart.
Rationale: It has been reported that epicardial adipose tissue (EAT) may affect myocardial autonomic function.Objective: The aim of this study was to explore the relationship between EAT and cardiac sympathetic nerve activity in patients with heart failure.
Methods and Results:In 110 patients with systolic heart failure, we evaluated the correlation between echocardiographic EAT thickness and cardiac adrenergic nerve activity assessed by
Conclusions:This study provides the first evidence of a direct correlation between increased EAT thickness and cardiac sympathetic denervation in heart failure. (Circ Res.
Food supply in the Mediterranean area has been recently modified by big retail distribution; for instance, industrial retail has favored shipments of groceries from regions that are intensive producers of mass food, generating a long supply chain (LSC) of food that opposes short supply chains (SSCs) that promote local food markets. However, the actual functional role of food retail and distribution in the determination of the risk of developing metabolic syndrome (MetS) has not been studied hitherto. The main aim of this study was to test the effects of food chain length on the prevalence of MetS in a population accustomed to the Mediterranean diet. We conducted an observational study in Southern Italy on individuals adhering to the Mediterranean diet. We examined a total of 407 subjects (41% females) with an average age of 56 ± 14.5 years (as standard deviation) and found that being on the Mediterranean diet with a SSC significantly reduces the prevalence of MetS compared with the LSC (SSC: 19.65%, LSC: 31.46%; p: 0.007). Our data indicate for the first time that the length of food supply chain plays a key role in determining the risk of MetS in a population adhering to the Mediterranean diet.
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