1,721,428 research outputs found
Therapeutic approaches for reducing C-reactive protein (CRP) levels and the associated cardiovascular risk.
No full textSeveral inflammatory mediators regulate the evolution of atherosclerosis. C-reactive protein (CRP) is an acutephase reactant, with a direct effect in inflammatory processes characterizing atherosclerosis. For this reason, CRP is actually considered as a factor, rather than simply a cardiovascular risk marker. The recent demonstration of CRP production not only by the liver, but also within atherosclerotic plaques by activated vascular cells, suggests a possible dual role, as both systemic and tissue molecule. Although more studies are needed, some therapeutic approaches to reduce CRP levels have been performed with encouraging results. Behavioral or pharmacologic interventions have been shown to reduce both CRP levels and the associated risk of cardiovascular acute events. Therefore, although most of national Cardiovascular Associations do not suggest high sensitivity CRP screening of the entire adult population as a public-health measure to stratify the cardiovascular risk, serum hs-CRP levels could be a promising target for therapies focused on reducing cardiovascular risk
Does non-alcoholic fatty liver disease (NAFLD) increase cardiovascular risk?
No full textNon alcoholic fatty liver disease (NAFLD) is defined as fat accumulation exceeding 5% to 10% by the weight of the liver, in the absence of other causes of steatosis. NAFLD is strongly associated with metabolic diseases, such as metabolic syndrome. At present, insulin resistance, elevated concentrations of free fatty acids and oxidants, and an imbalance between different cytokines have been identified as the common pathophysiological elements underlying both NAFLD and metabolic syndrome. Emerging evidence also considers NAFLD as the hepatic manifestation of metabolic syndrome and supports a possible direct role of fat liver in cardiovascular risk assessment. Further investigations are needed to better understand the role of NAFLD, as an independent active factor in metabolic syndrome and associated cardiovascular disease
Editorial: update on inflammatory processes governing atherosclerotic plaque vulnerability and reperfusion injury
No full textUpdate on therapeutic strategies to increase adiponectin function and secretion in metabolic syndrome
No full textChanges in diagnostic criteria have impacted on the definition of the metabolic syndrome. The central aetiological importance of insulin resistance has lessened, while the role of other cardiovascular risk factors has progressively increased. Inflammatory mediators have also been identified as crucial targets for more selective therapies in metabolic syndrome. Among several pro-inflammatory factors, adiponectin has been shown to be associated with reduced cardiovascular risk in metabolic syndrome patients. Here, we review new therapeutic approaches, which could potentially increase adiponectin levels in metabolic syndrome
Update on statin-mediated anti-inflammatory activities in atherosclerosis
No full textAnti-inflammatory activities of statins in atherosclerosis have been well documented by both basic research and clinical studies. Statins have been introduced in the 1980s as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors to block cholesterol synthesis and lower cholesterol serum levels. In the last three decades, statins have been shown to possess several anti-inflammatory and antioxidant activities resulting in the beneficial reduction of atherosclerotic processes and cardiovascular risk in both humans and animal models. Inflammatory intracellular pathways involving kinase phosphorylation and protein prenylation are modulated by statins. The same intracellular mechanisms might also cause statin-induced myotoxicity. In the present review, we will update evidence on statin-mediated regulation of inflammatory pathways in atherogenesis
Statins, ACE inhibitors and ARBs in cardiovascular disease
No full textAtherosclerotic cardiovascular disease (CVD) is the main cause of death in developed and developing countries. It is well accepted that several diseases - including hypertension, dyslipidemia and diabetes mellitus - increase CVD. More recently also chronic inflammatory diseases, such as rheumatoid arthritis, have been shown to accelerate CVD. This association further supports a responsible role for inflammatory processes in all stages of CVD pathophysiology. Clinically, CVD ranges through different acute and chronic syndromes with ischemic symptoms in distal tissues, including heart, cerebral region or peripheral arteries. Several treatments for reducing CVD are under investigation. In this review we focus on statins, angiotensin-converting-enzyme (ACE) inhibitors, and angiotensin-II receptor blockers (ARBs), updating therapeutic evidence from the last clinical trials with particular relevance to diabetic patients
Update on the treatments of non-alcoholic fatty liver disease (NAFLD).
No full textNon-alcoholic fatty liver disease (NAFLD) is the most frequent cause of liver damage and alteration of hepatic enzymes. NAFLD is strongly associated with metabolic syndrome and obesity. It is characterized by fat accumulation in the liver that may progress throughout hepatic steatosis and inflammation (non-alcoholic steatohepatitis [NASH]) toward cirrhosis and liver failure. In the last decade several studies suggested that NAFLD is an independent cardiovascular risk factor that increases cardiovascular mortality. At present, several studies investigating possible therapeutic approaches are ongoing. The present review is focused on the current and promising treatments of NAFLD
Methylene blue: potential use of an antique molecule in vasoplegic syndrome during cardiac surgery.
No full textVasoplegic syndrome is a common complication of cardiopulmonary bypass, appearing with an incidence ranging between 5 and 25%. It is characterized by significant hypotension, high or normal cardiac output and low systemic vascular resistance. This syndrome is hypothesized to be caused by the inflammation-mediated dysregulation of endothelial homeostasis and subsequent endothelial dysfunction. In vasoplegic syndrome, the inhibition of the nitric oxide/cyclic guanosine monophosphate pathway with concomitant administration with traditional ionotropes may represent a promising therapeutic option. Methylene blue, an inhibitor of nitric oxide synthase and guanylate cyclase, may contribute to the improvement of refractory hypotension associated with endothelial dysfunction in vasoplegia. In this article, we will update evidence on the potential therapeutic use of methylene blue in vasoplegic syndrome
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