Left ventricular diastolic dysfunction (LVDD) is an important precursor to many different cardiovascular diseases. Diastolic abnormalities have been studied extensively in the past decade, and it has been confirmed that one of the mechanisms leading to heart failure is a chronic, low-grade inflammatory reaction. The triggers are classical cardiovascular risk factors, grouped under the name of metabolic syndrome (MetS), or other systemic diseases that have an inflammatory substrate such as chronic obstructive pulmonary disease. The triggers could induce myocardial apoptosis and reduce ventricular wall compliance through the release of cytokines by multiple pathways such as (1) immune reaction, (2) prolonged cell hypoxemia, or (3) excessive activation of neuroendocrine and autonomic nerve function disorder. The systemic proinflammatory state causes coronary microvascular endothelial inflammation which reduces nitric oxide bioavailability, cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocytes favoring hypertrophy development and increases resting tension. So far, it has been found that inflammatory cytokines associated with the heart failure mechanism include TNF-α, IL-6, IL-8, IL-10, IL-1α, IL-1β, IL-2, TGF-β, and IFN-γ. Some of them could be used as diagnosis biomarkers. The present review aims at discussing the inflammatory mechanisms behind diastolic dysfunction and their triggering conditions, cytokines, and possible future inflammatory biomarkers useful for diagnosis.

As it had been already stated by latest research, inflammation is a condition which sits at the very base of atherogenesis, which is the major consequence of the metabolic syndrome. It was stated that adipose tissue impacts all organs by the synthesis of adipokines. Visfatin/NAMPT is a biomarker that was recently discovered in mice (2005). In the beginning it was believed to have insulin-like properties, but afterwards research has found important links between Visfatin and inflammation, endothelial dysfunction and atherosclerosis in coronary artery disease. It was also linked to plaque instability in acute coronary syndromes. More studies are needed though, to clearly state whether Visfatin/NAMPT has a positive or negative role because, up until now, the only sure fact is that its serum levels correlate with the presence of an inflammatory state.

Fig. 1.Sirtuin enzymatic activities: Sirtuins are NAD + -dependent deacetylases and mono-ADP-ribosyltransferases that regulate a wide array of proteins involved in metabolism and cell survival.The α-acetyl lysine residues of the target protein serve as substrates for sirtuindeacetylation, which generate 2' -OAADPr as a by-product. NAM, nicotinamide [8]