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Vascular disease was for a long time considered a disease of the old age, but it is becoming increasingly clear that a cumulus of factors can cause early vascular aging (EVA). Inflammation plays a key role in vascular stiffening and also in other pathologies that induce vascular damage. There is a known and confirmed connection between inflammation and atherosclerosis. However, it has taken a long time to prove the beneficial effects of anti-inflammatory drugs on cardiovascular events. Diabetes can be both a product of inflammation and a cofactor implicated in the progression of vascular disease. When diabetes and inflammation are accompanied by obesity, this ominous trifecta leads to an increased incidence of atherothrombotic events. Research into earlier stages of vascular disease, and documentation of vulnerability to premature vascular disease, might be the key to success in preventing clinical events. Modulation of inflammation, combined with strict control of classical cardiovascular risk factors, seems to be the winning recipe. Identification of population subsets with a successful vascular aging (supernormal vascular aging-SUPERNOVA) pattern could also bring forth novel therapeutic interventions.

Even though the new thresholds for defining prediabetes have been around for more than ten years, there is still controversy surrounding the precise characterization of this intermediate glucose metabolism status. The risk of developing diabetes and macro and microvascular disease linked to prediabetes is well known. Still, the prediabetic population is far from being homogenous, and phenotyping it into less heterogeneous groups might prove useful for long-term risk assessment, follow-up, and primary prevention. Unfortunately, the current definition of prediabetes is quite rigid and disregards the underlying pathophysiologic mechanisms and their potential metabolic progression towards overt disease. In addition, prediabetes is commonly associated with a cluster of risk factors that worsen the prognosis. These risk factors all revolve around a common denominator: inflammation. This review focuses on identifying the population that needs to be screened for prediabetes and the already declared prediabetic patients who are at a higher risk of cardiovascular disease and require closer monitoring. [ABSTRACT FROM AUTHOR]

In flammation is involved in initiation, development and complications of the vast majority of non-communicable diseases. Recent research demonstrated that inflammation is involved in pathogenesis of all major cardiovascular diseases. Different endogenous factors (LDL, nucleic acid strands, uric acid - collectively called „Damage Associated Molecular Patterns - DAMPs") activate dedicated receptors („Pattern Recognition Receptors - PRR") on monocytes, macrophages or dendritic cells responsible for the innate immunologic response. They have a major role in natural defense mechanisms against different pathogens and in normal conditions have a protective role. Among PRRs „NOD-like, leucin rich, pyrin containing (NLRP)" receptors are a 14-member family located in the cytoplasm. One of these is the NLRP3 resulting from nuclear transcription under the influence of NF-kB, a second messenger from membrane PRRs to the nucleus. Mostly the same factors responsible for NLRP3 intracellular expression stimulate its oligomerization resulting in a large protein complex, the NLRP3 inflammasome. This activates caspase-1 responsible for IL-1b and IL-18 production and initiates an inflammatory reaction leading to various pathologic processes, such as atherosclerosis, hypertension, diabetes and heart failure. This is the current story as we know it of the NLRP3 inflammasome, a small intracellular component that when inappropriately activated may does more harm than good. [ABSTRACT FROM AUTHOR]